Abstract
Background
Bacterial infection and colonization are gradually associated with disease severity and prognosis in bronchiectasis. The impact of chronic Pseudomonas aeruginosa (PA) infection on the clinical features and disease progression in stable bronchiectasis remains unclear. This study aims to investigate the association between chronic PA infection and lung function as well as prognosis in stable bronchiectasis.
Methods
This prospective cohort study enrolled patients with stable bronchiectasis, with or without chronic PA infection, in Shanghai between January 2020 and December 2023. We compared the baseline data including clinical characteristics, laboratory findings, and lung function. During follow-up until December 2024, we monitored lung function at the first follow-up visit and recorded the time to first exacerbation.
Results
A total of 391 patients with stable bronchiectasis were enrolled, including 118 (30.2%) with chronic PA infection. These patients showed significantly higher age, BMI < 18.5 kg/m2, disease duration, affected lobes, modified Reiff score, BSI, E-FACED score, exacerbations and related hospitalizations in the prior year, resolved chronic PA infection, purulent sputum, cough, wheezes, crackles, CRP, and CD4⁺T cell counts < 500. Conversely, BMI, other bacterial colonization, and CD4⁺T cell was lower in chronic PA infection group.
Among 210 patients who completed at least one lung function follow-up, forced vital capacity (FVC), FVC%predicted, forced expiratory volume in 1 s (FEV1), FEV1%predicted, and FEV₁/FVC ratio at the first follow-up were significantly lower than baseline. After propensity score matching, 87 patients (32 chronic PA infection, 55 without chronic PA infection) were included. The chronic PA infection group showed significantly greater declines in ΔFEV1 and ΔFEV1/FVC ratio. Survival analysis revealed a significantly shorter median time to first exacerbation in patients with chronic PA infection than in those without (202 days vs. 328 days). Chronic PA infection was associated with exacerbation of bronchiectasis (HR = 1.571; 95%CI: 1.014–2.432).
Conclusion
Chronic PA infection in stable bronchiectasis was associated with high disease severity, accelerated lung function decline and increased exacerbation risk. These results suggested that chronic PA infection contributes to the progression of bronchiectasis.
Supplementary Information
The online version contains supplementary material available at 10.1186/s12890-026-04145-x.
Keywords: Bronchiectasis, Pseudomonas aeruginosa, Chronic infection, Lung function, Propensity score matching
Introduction
Bronchiectasis is a chronic inflammatory airway disease triggered by a variety of etiologies and characterized by recurrent suppurative infections. It features repeated injury and/or obstruction of the small and medium-sized bronchi, destruction of the bronchial wall structure, and abnormal and permanent dilatation of the bronchi. Clinically, it primarily manifests as chronic cough, sputum production, hemoptysis, with or without wheezing and dyspnea [1]. Bronchiectasis is prevalent among Asian populations, affects 1.2% of adults in China. Its incidence increased 2.31-fold between 2013 and 2017 and continues to rise. By 2030, the projected rate is estimated to reach 448.93 per 100,000, posing a substantial healthcare and economic burden [2]. Bronchiectasis is frequently marked by acute exacerbations, with post-exacerbation mortality reaching 30% [3].
Recurrent microbial infection of the lower airways represents a hallmark clinical feature of bronchiectasis and a major driver of disease progression [4]. Pseudomonas aeruginosa (PA) is an opportunistic pathogen capable of causing various invasive infections. It can also exist in a state of chronic infection within the bronchiectasis population, engaging in long-term interaction with the host that lead to progressive tissue damage [5].PA is reported as the most frequently isolated pathogenic microorganism in sputum cultures from bronchiectasis patients during both stable state and acute exacerbations. Its presence is significantly associated with accelerated lung function decline, increased frequency of exacerbations, higher hospitalization rates, and elevated mortality. PA infection plays a critical role in the disease course and clinical outcomes of bronchiectasis patients [6, 7]. Furthermore, PA infection is an independent predictor of the frequent exacerbator phenotype in bronchiectasis. Its associations with high disease severity, poor quality of life, and increased mortality in this phenotype are well-established [8].
Patients with stable bronchiectasis are susceptible to progression to acute exacerbation influenced by various factors, among which chronic PA infection serves as a significant contributor to this transition. Previous studies have predominantly focused on the frequency and severity of acute exacerbations and the management of PA infection in patients during exacerbations. To date, there has been no report on the clinical characteristics, lung function changes, and prognosis among Chinese patients with stable bronchiectasis who have chronic PA infection. Thus, we conducted a prospective cohort study observing and following patients with stable bronchiectasis at Longhua Hospital Affiliated to Shanghai University of Traditional Chinese Medicine from January 2020 to December 2024. Participants were continuously monitored for 12 months, with records of the timing and frequency of acute exacerbations. By comparing clinical features, lung function changes, and short-term outcomes between stable bronchiectasis patients with and without chronic PA infection, this study aims to clarify the correlation between chronic PA infection and clinical manifestations in stable bronchiectasis. The findings may provide insights for individualized management during the stable phase of bronchiectasis.
Methods
Study design and participants
This prospective study consecutively recruited patients with bronchiectasis in a stable phase from Longhua Hospital Affiliated with Shanghai University of Traditional Chinese Medicine between January 2020 and December 2023. Written informed consent was obtained from all participants. Eligible patients were aged 18 to 75 years, had a high-resolution computed tomography (HRCT)-confirmed diagnosis of bronchiectasis, were in a clinically stable state at enrollment, and completed at least one year of follow-up. The comprehensive exclusion criteria were as follows: (1) co-existing autoimmune diseases or severe immunodeficiency; (2) severe organ dysfunction; (3) active pulmonary tuberculosis or nontuberculous mycobacterial infection; (4) bronchiectasis due to cystic fibrosis; (5) concurrent malignancy; (6) psychiatric or cognitive disorders; (7) hospitalization in the preceding 4 weeks; (8) with incomplete clinical data. The study was approved by the Ethics Committee of Longhua Hospital Affiliated to Shanghai University of Traditional Chinese Medicine (Approval No. 2019LCSY058 and 2024LCSY144).
Bronchiectasis was confirmed by HRCT scans demonstrating a bronchoarterial ratio > 1, lack of tapering, and airways visibility within 1 cm of the pleural surface or touching mediastinal pleura, along with clinical symptoms consistent with bronchiectasis [1]. An acute exacerbation of bronchiectasis was defined according to the European Multicentre Bronchiectasis Research Collaboration/US Bronchiectasis Research Registry (EMBARC/BRR) definitions working group as a deterioration in three or more key symptoms for at least 48 h: worsened cough, change in sputum volume, increased sputum purulence, dyspnea and/or reduced exercise tolerance, fatigue and/or malaise, and hemoptysis, and that necessitate a change in bronchiectasis treatment [9, 10]. The stable state of bronchiectasis was defined as a clinically stable condition without new symptoms and with no requirement for antibiotics or oral corticosteroids for pulmonary exacerbation in the preceding 4 weeks [11].
Study measurement
Electronic medical records were reviewed at enrollment and during follow-up to collect comprehensive clinical data, including: (1) Demographics and baseline characteristics: sex, age, height, weight, body mass index (BMI), bronchiectasis duration, smoking history, alcohol use, number of exacerbations in the prior year, exacerbation-related hospitalizations in the prior year, resolved chronic PA infection, resolved infection with other bacteria, previous hemoptysis, clinical manifestations (sputum characteristics, cough, hemoptysis, wheezes, crackles) and comorbid conditions; (2) Laboratory tests: blood routine, C-reactive protein (CRP), biochemistry, and immune function parameters; (3) Chest HRCT: number of lobes affected, bronchiectasis types; disease severity assessed using the modified Reiff score, bronchiectasis severity index (BSI), and E-FACED score.
Patients were categorized into chronic PA infection and without chronic PA infection groups based on the presence of chronic PA infection during the stable state. Definitions of chronic PA infection were highly heterogeneous, with previous study defining it as 2 positive cultures at least 3 months apart over 12 months during the stable state of bronchiectasis [12].
Patients were prospectively followed for 12 months via outpatient visits or telephone interviews, with monthly assessments for all participants. The first lung function test result and the time to first exacerbation during the follow-up period were recorded. Follow-up concluded in December 2024. Loss to follow-up was defined as failure to contact the patient for three consecutive follow-up points or patient refusal to continue.
Lung function test
All lung function tests were conducted in the outpatient pulmonary function laboratory of Longhua Hospital Affiliated with Shanghai University of Traditional Chinese Medicine. To minimize inter-operator variability, all tests were performed by two certified and experienced respiratory therapists. Procedures strictly followed the American Thoracic Society (ATS) and European Respiratory Society (ERS) standards [13]. Prior to each test, volume calibration was carried out using a 3-liter calibration syringe, with linearity verification of flow performed at low, medium, and high flow rates to ensure instrument accuracy. Spirometry (JAEGER MasterScreen-body + diffusion + APS, Germany) was conducted to determine the lung function and bronchodilator reversibility [14]. Subjects were seated and wore a nose clip during testing, which was performed 15 min after salbutamol inhalation. Expiratory maneuvers were required to be free from interruption, coughing, or air leakage [15]. Additionally, exhalation time needed to reach at least 6 s or a clear volume plateau. Each patient performed at least three acceptable forced expiratory maneuvers to ensure data reproducibility. The following parameters were obtained: forced vital capacity (FVC), FVC% predicted, forced expiratory volume in 1 s (FEV₁), FEV₁% predicted, and the FEV₁/FVC ratio. ΔFVC, ΔFEV₁, ΔFVC%predicted, ΔFEV₁%predicted and ΔFEV₁/FVC ratio was defined as (the first follow-up measurement) - (the baseline measurement).
Statistical analysis
In this study, data analysis was conducted using SPSS software (version 26.0 Chicago, IL, USA) for Windows. The normality of data distribution was assessed with the Kolmogorov–Smirnov test. Normally distributed continuous variables are presented as mean ± standard deviation (SD). Differences between groups were compared using the independent samples t-test. Differences within groups were compared using the paired t-test. Non-normally distributed continuous variables are expressed as median (inter-quartile range, IQR), and the Mann-Whitney U test was used for between-group comparisons. The qualitative or dichotomized variables are summarized as absolute numbers and percentages of the total case. Group differences for categorical variables were analyzed using the Chi-square test or Fisher’s exact test, depending on the data suitability. Propensity score matching (PSM) analysis was employed to control for potential confounding factors and reduce bias. The probability of acute exacerbation was analyzed by plotting a Kaplan-Meier curve in a time-to-event analysis. The Log-rank test was applied to compare survival curves between the two groups. The hazard ratio (HR) and 95% confidence interval (CI) were calculated for the independent variables. All tests were two-sided, and a P value of less than 0.05 was considered indicative of statistical significance.
Results
Study profile and demographic data
Between January 2020 and December 2023, 391 eligible participants were recruited into and ultimately included in this cohort analysis. Of these, 118 patients (30.2%) were classified as the chronic PA infection group, while 273 patients (69.8%) comprised the group without chronic PA infection (Fig. 1). Demographic and partial clinical data of participants were showed in Table 1. Patients in the chronic PA infection group were significantly older and had a lower BMI compared to the group without chronic PA infection. The proportion of patients with BMI < 18.5 kg/m2 was significantly higher in the chronic PA infection group. Additionally, these patients had a longer duration of bronchiectasis, a greater number of lobes affected, and higher modified Reiff, BSI, and E-FACED scores. The chronic PA infection group also exhibited significantly more exacerbations and more exacerbation-related hospitalizations within the previous years. This group had a higher proportion of patients with a history of chronic PA infection that was successfully eradicated. In contrast, other bacterial infection was less frequent in this group. Clinical manifestations such as purulent sputum, cough, wheezes, and crackles were also significantly more common in the chronic PA infection group (P < 0.05).
Fig. 1.
The workflow for patients with stable bronchiectasis recruited in the study
Table 1.
Demographic and clinical characteristics of 391 study participates
| Clinical variables | Without chronic PA infection (n = 273) |
Chronic PA infection (n = 118) |
Statistic | P-value |
|---|---|---|---|---|
| Age, years, mean ± SD | 61.00 ± 11.11 | 63.60 ± 7.99 | t=-2.61 | 0.010 |
| Gender, Male/Female, n (%) | 96 (35.16)/ 177 (64.84) | 42 (35.59)/ 76 (64.41) | χ²=0.007 | 0.935 |
| BMI, kg/m2, median (IQR) | 18.64 (17.44, 19.68) | 17.93 (16.92, 18.91) | Z=-4.711 | < 0.001 |
| BMI < 18.5 kg/m², n (%) | 128(46.9) | 82(69.5) | χ²=16.933 | < 0.001 |
|
Ex-smoker or current smoker, n (%) |
45 (16.48) | 23 (19.49) | χ²=0.519 | 0.471 |
| Alcohol abuse, n (%) | 126 (46.2) | 66 (55.9) | χ²=3.152 | 0.076 |
| Bronchiectasis duration, years, median (IQR) | 13 (8, 17) | 15 (11, 20.25) | Z=-3.744 | < 0.001 |
| Bronchiectasis type, n (%) | χ²=3.290 | 0.193 | ||
| Cylindrical | 168 (61.54) | 61 (51.69) | ||
| Varicose | 70 (25.64) | 38 (32.20) | ||
| Cystic | 35 (12.82) | 19 (16.10) | ||
| Number of lobes affected, median (IQR) | 3 (2, 4) | 4 (3, 5) | Z=-6.732 | < 0.001 |
| Modified Reiff score, median (IQR) | 3 (2, 6) | 5 (4, 8) | Z=-5.964 | < 0.001 |
| BSI score, median (IQR) | 6 (4, 6) | 6 (5.5, 8) | Z=-4.859 | < 0.001 |
| E-FACED score, median (IQR) | 1 (0, 1) | 2 (1, 3) | Z=-3.132 | 0.002 |
| Number of exacerbations in the prior year, median (IQR) | 1 (0, 2) | 2 (0, 3) | Z=-5.218 | < 0.001 |
| Exacerbation-related hospitalizations in the prior year, n (%) | 85 (31.14) | 54 (45.76) | χ²=7.694 | 0.006 |
| Resolved chronic PA infection, n (%) | 69 (25.3) | 80 (67.8) | χ²=63.160 | < 0.001 |
|
Resolved infection with other bacteria, n (%) |
87 (31.9) | 16 (13.6) | χ²=14.234 | < 0.001 |
| Hemoptysis in the prior year, n (%) | 49 (17.95) | 49 (41.53) | χ²=24.383 | < 0.001 |
| Clinical manifestations, n (%) | ||||
| Purulent sputum | 127 (46.5) | 100 (84.7) | χ²=49.438 | < 0.001 |
| Cough | 140 (51.3) | 83 (70.3) | χ²=12.210 | < 0.001 |
| Hemoptysis | 26 (9.5) | 12 (10.2) | χ²=0.039 | 0.843 |
| Wheezes | 75 (27.5) | 60 (50.8) | χ²=19.914 | < 0.001 |
| Crackles | 126 (46.2) | 87 (73.7) | χ²=25.261 | < 0.001 |
| Previous infection history, n (%) | ||||
| Pulmonary tuberculosis | 72 (26.37) | 37 (31.36) | χ²=1.017 | 0.313 |
| Pneumonia | 42 (15.38) | 26 (22.03) | χ²=2.535 | 0.111 |
| Pertussis | 17 (6.23) | 7 (5.93) | χ²=0.012 | 0.911 |
| Measles | 4 (1.47) | 6 (5.08) | χ²=4.331 | 0.037 |
| Comorbid conditions, n (%) | ||||
| Chronic sinusitis | 30 (10.99) | 16 (13.56) | χ²=0.524 | 0.469 |
| Allergic rhinitis | 17 (6.23) | 3 (2.54) | χ²=2.305 | 0.129 |
| GERD | 11 (4.03) | 4 (3.39) | χ²=0.091 | 0.762 |
| Diabetes | 77 (28.21) | 33 (27.97) | χ²=0.002 | 0.962 |
| Hypertension | 89 (32.60) | 44 (37.29) | χ²=0.807 | 0.369 |
| Coronary heart disease | 127 (46.52) | 62 (52.54) | χ²=1.197 | 0.274 |
| Liver disease | 21 (7.69) | 6 (5.08) | χ²=0.871 | 0.351 |
| Kidney disease | 14 (5.13) | 8 (6.78) | χ²=0.423 | 0.515 |
| Cerebral vascular disease | 95 (34.80) | 44 (37.29) | χ²=0.223 | 0.637 |
| Lung function indices | ||||
| FEV1, L, median (IQR) | 1.52 (1.32, 1.73) | 1.52 (1.30, 1.73) | Z=-0.208 | 0.836 |
| FVC, L, mean ± SD | 1.93 ± 0.42 | 1.90 ± 0.39 | t = 0.673 | 0.502 |
| FEV1%predicted, mean ± SD | 71.73 ± 6.34 | 70.98 ± 6.14 | t = 1.072 | 0.284 |
| FVC%predicted, median (IQR) | 68.00 (62.00, 74.00) | 68.50 (62.00, 74.00) | Z=-0.340 | 0.734 |
| FEV1/FVC, mean ± SD | 79.92 ± 5.97 | 80.42 ± 6.26 | t=-0.748 | 0.455 |
| FeNO, ppb, mean ± SD | 13.12 ± 6.89 | 12.70 ± 6.31 | t = 0.564 | 0.573 |
Abbreviations: PA Pseudomonas aeruginosa, BMI Body mass index, BSI Bronchiectasis Severity Index, GERD Gastroesophageal reflux disease, FEV1 Forced expiratory volume in 1 s, FVC Forced vital capacity, FeNO Fractional exhaled nitric oxide
Laboratory testing data
Table 2 showed the baseline laboratory characteristics of the enrolled patients. Statistically significant differences were identified between the groups for CRP, CD4+T cells, and the proportion of individuals with CD4+T cell counts < 500. Specifically, the chronic PA infection patients demonstrated significantly elevated CRP, decreased CD4+T cell counts, and an increased proportion of patients with CD4+T cells counts < 500 compared to their counterparts without chronic PA infection (P < 0.05). The differences in all other laboratory results were not statistically significant.
Table 2.
Baseline laboratory characteristics of 391 study participates
| Laboratory testing variables | Without chronic PA infection (n = 273) |
Chronic PA infection (n = 118) |
Statistic | P-value |
|---|---|---|---|---|
| WBC, ×109/L, mean ± SD | 7.82 ± 1.86 | 8.05 ± 2.09 | t=-1.02 | 0.309 |
| NEU, ×109/L, median (IQR) | 2.7 (2.3, 3.4) | 2.7 (2.3, 3.2) | Z=-0.406 | 0.685 |
| EOS, ×109/L, median (IQR) | 0.27 (0.13, 0.39) | 0.22 (0.12, 0.34) | Z=-1.73 | 0.084 |
| CRP, mg/L, median (IQR) | 8.00 (6.00, 10.90) | 12.55 (7.28, 18.32) | Z=-5.00 | < 0.001 |
| Albumin, g/L, median (IQR) | 38.00 (34.00, 44.00) | 37.00 (34.00, 44.00) | Z=-0.04 | 0.965 |
| CD4+T cell counts, µL, median (IQR) | 497 (438, 557) | 481.5 (416.5, 536) | Z=-2.673 | 0.008 |
| CD4+T cell counts < 500, n (%) | 139 (50.6) | 73 (61.9) | χ²=3.979 | 0.046 |
| CD8+T cell counts, µL, median (IQR) | 486.00 (427.00, 552.00) | 482.50 (400.00, 536.50) | Z=-1.68 | 0.093 |
| CD4+/CD8+ ratio, mean ± SD | 1.03 ± 0.19 | 1.03 ± 0.19 | t=-0.22 | 0.824 |
| CD19+B cell counts, µL, median (IQR) | 235.00 (188.00, 310.00) | 267.00 (192.00, 335.00) | Z=-1.71 | 0.088 |
| CD16+CD56+NK cell counts, µL, median (IQR) | 365.00 (256.00, 483.00) | 409.00 (276.00, 515.50) | Z=-1.52 | 0.128 |
Abbreviations: WBC White blood cell, NEU Neutrophil, EOS Eosinophil, CRP C-reactive protein
Lung function changes at enrollment and first follow-up
A total of 210 patients completed at least one lung function follow-up, with a median time to the first follow-up of 8 months. No significant difference in follow-up time was observed between the two groups. Compared to baseline, all lung function parameters at follow-up showed changes, with FVC, FEV₁, FEV₁%predicted, FVC%predicted, and the FEV₁/FVC ratio all decreased to varying degrees (P < 0.05) (Table 3).
Table 3.
Comparison of lung function at baseline and first follow-up in 210 patients
| Lung function indices | Baseline (n = 210) | Follow-up (n = 210) | Statistic | P-value |
|---|---|---|---|---|
| FEV1, L, median (IQR) | 1.52 (1.30, 1.76) | 1.40 (1.22, 1.73) | Z=-5.545 | < 0.001 |
| FVC, L, median (IQR) | 1.76 (1.54, 2.16) | 1.64 (1.64, 2.19) | Z=-4.086 | < 0.001 |
| FEV1% predicted, mean ± SD | 71.57 ± 6.29 | 66.98 ± 8.79 | t = 9.501 | < 0.001 |
| FVC% predicted, median (IQR) | 67.00 (61.00, 74.00) | 65.50 (56.00, 77.00) | Z=-4.388 | < 0.001 |
| FEV1/FVC, median (IQR) | 80.00 (75.00, 85.00) | 80.00 (74.00, 84.00) | Z=-7.102 | < 0.001 |
Among the 210 patients with stable bronchiectasis who completed follow-up lung function tests, 58 had chronic PA infection, while 152 did not. Significant baseline differences were observed between groups with and without chronic PA infection, suggesting potential confounding factors. To investigate the link between dynamic lung function changes and chronic PA infection in stable bronchiectasis, we performed PSM analysis on the 210 patients who completed follow-up lung function assessments. Using a 1:3 nearest neighbor matching, without replacement within a caliper width of 0.2, we matched the two cohorts. The density curves of propensity score before and after matching were shown in Supplementary Figure S1 (left and right, respectively). After matching, 87 patients were included, with 32 in the chronic PA infection group and 55 in the non-PA infection group. No significant differences in baseline characteristics were observed between the two groups after matching (P > 0.05) (Supplementary Table S1).
In the matched cohort, changes in lung function from baseline to follow-up were compared between the two groups. The chronic PA infection group showed a mean change in FEV₁ of − 0.06, which was significantly lower than that of the non-PA infection group (–0.04, P = 0.038). Additionally, the median change in FEV₁/FVC was − 1.00 in the chronic PA infection group, significantly lower than that in the non-PA infection group (0.00, P = 0.042) (Table 4).
Table 4.
Changes in lung function from baseline to the first follow-up in the two groups after PSM
| Change in Lung function indices | Without chronic PA infection (n = 55) |
Chronic PA infection (n = 32) |
Statistic | P-value |
|---|---|---|---|---|
| Time to first lung function follow-up, month, median (IQR) | 8.00 (5.50, 9.00) | 8.50 (6.00, 11.00) | Z=-1.32 | 0.185 |
| ΔFEV1, L, mean ± SD | -0.04±0.10 | -0.06±0.08 | t = 1.94 | 0.038 |
| ΔFVC, L, mean ± SD | -0.04±0.10 | -0.05±0.08 | t = 0.43 | 0.667 |
| ΔFEV1%predicted, mean ± SD | -5.00±10.00 | -9.00±9.00 | t = 1.42 | 0.159 |
| ΔFVC%predicted, mean ± SD | -4.00±10.00 | -5.00±8.00 | t = 0.43 | 0.667 |
| ΔFEV1/FVC, median (IQR) | 0.00 (-1.00, 0.00) | -1.00 (-3.00, 0.00) | Z=-2.03 | 0.042 |
Analysis of the one-year exacerbation risk in stable bronchiectasis with chronic PA infection
Significant baseline differences existed between the two groups, indicating the presence of potential confounding variables. Therefore, to analyze the risk of bronchiectasis exacerbation in chronic PA infection patients, we applied PSM analysis to 391 patients to match the two cohorts. PSM was performed using a 1:2 nearest neighbor matching without replacement within a caliper width of 0.2. The density curves of propensity scores before and after matching were shown in Supplementary Figure S2 (left and right, respectively). After matching, no significant differences in baseline characteristics were observed between the two groups (P > 0.05) (Supplementary Table S2).
In the matched cohort, with the time to the first exacerbation as the endpoint event, Kaplan-Meier curves were plotted for the group with and without chronic PA infection. The Log-rank test was used to assess the statistical difference between the survival curves. As shown in Fig. 2, the median time to exacerbation was 328 days in patients without chronic PA infection (group = 0) and 202 days in those with chronic PA infection (group = 1) (Log-rank P = 0.041). The statistical analyses indicate that chronic PA infection (HR = 1.571; 95%CI: 1.014–2.432) was a risk factor for exacerbation of bronchiectasis.
Fig. 2.
Kaplan-Meier curves for one-year exacerbation in stable bronchiectasis patients with and without chronic PA infection. group = 0, without chronic PA infection; group = 1, chronic PA infection
Discussion
This study enrolled a total of 391 patients with stable bronchiectasis, among whom 30.2% were identified as having chronic PA infection. PA is a common opportunistic pathogen and the most frequently identified pathogen in the lower airways of bronchiectasis patients in China. A study by Sun et al. [16] reported a PA isolation prevalence of 20.61% (265/1286) in sputum/bronchoalveolar lavage fluid cultures from bronchiectasis patients. Another retrospective study found that among 522 bronchiectasis patients with positive sputum cultures, the PA detection rate was as high as 36.8% [17]. Overall, our findings are consistent with these previous reports.
The results of this study demonstrated significant differences between the groups with and without chronic PA infection in terms of demographic data, clinical manifestations and disease severity, laboratory findings, imaging characteristics, exacerbation, and lung function parameters. Previous studies have indeed indicated considerable differences in sample species diversity between sputum culture-positive and culture-negative groups in bronchiectasis. These microbiome profiles also correlate significantly with clinical features [7, 18]. In our cohort, marked differences were observed between the two groups regarding age, BMI, duration of bronchiectasis, number of lobes affected, modified Reiff score, presence of purulent sputum, cough, wheezes, and crackles, as well as CD4+T cell and the proportion of patients with CD4+T cell counts < 500. Compared with patients without chronic PA infection, those with chronic PA infection tended to be older, had a longer duration of bronchiectasis, more severe disease, greater extent of structural lung involvement, and more prominent clinical symptoms, accompanied by poorer nutritional status and immune dysfunction. These findings align with previous research [19, 21]. Significant differences in BSI and E-FACED scores were also observed between the two groups, in line with previous retrospective studies [22]. However, since chronic PA infection was the primary exposure variable and is part of both severity scores, we cannot infer a direct causal relationship between this infection and bronchiectasis severity from these results. This potential association requires further investigation.
Furthermore, our results indicated that patients with chronic PA infection had a significantly higher number of patients experiencing exacerbations and hospitalizations in the prior year. This suggests that chronic PA infection may lead to more frequent acute exacerbations in bronchiectasis. A finding was corroborated by Finch et al. [12], who also reported that stable bronchiectasis patients with chronic PA infection experience more frequent exacerbations and have higher hospitalization rates and risks of clinical deterioration.
The mechanisms by which PA infection leads to worsened disease status and increased susceptibility to exacerbations in bronchiectasis have not been fully elucidated. Research in bronchiectasis found that effective isolation from external infectious agents significantly lowered exacerbation rates in patients without chronic bacterial infections, whereas those with PA infection continue to experience disease deterioration. This finding highlight that the chronic presence of PA may itself act as a trigger for bronchiectasis deterioration, even without significant external exposure, under conditions where the host-bacterium balance is tilted toward increased bacterial replication [23]. Moreover, data from a prospective study showed that the presence of specific genomic islands, virulence genes (exoS, exoY), and increased IL-6 levels are superior to immunoglobulin levels in identifying bronchiectasis exacerbations. This finding reveals a key distinction between exacerbations and stable phases in bronchiectasis [24]. Evidence suggests that bronchiectasis induced chronic PA infection can significantly augment airway neutrophilic inflammation and disrupt the balance between neutrophil elastase and its inhibitors. This promotes excessive mucus production, which in turn may contribute to mechanical airway dilation. Furthermore, airway neutrophilic inflammation can lead to epithelial damage and airway remodeling, ultimately driving disease progression and clinical deterioration in bronchiectasis [25, 26]. Data from the European Bronchiectasis Registry indicate that increased sputum purulence and viscosity are closely associated with bacterial infection, disease severity, and the risk of exacerbation [27]. Additionally, Figueiredo et al. [28] reported a direct correlation between sputum color, inflammatory markers, and PA infection in patients with stable bronchiectasis. Consistent with these previous findings, our study observed significantly elevated levels of the inflammatory marker CRP, along with a higher prevalence of purulent sputum, cough, wheezes, and crackles in chronic PA infection group.
We compared lung function parameters between baseline and follow-up in patients with bronchiectasis. A decline were observed at follow-up, to varying extents, in FVC, FEV₁, FEV₁% predicted, FVC% predicted, and the FEV₁/FVC ratio compared to baseline. Lung function impairment in bronchiectasis is considered a result of complex interactions among infection, impaired mucociliary clearance, inflammation, and lung injury [29]. Inflammatory responses damage the airway mucosa, leading to remodeling and worsening airflow obstruction. Impaired ciliary function and abnormal mucus secretion hinder mucus clearance, promoting mucus plug formation and further limiting airflow. Finally, structural airway destruction increases airway resistance and directly compromises ventilation [30]. Qin et al. [31] confirmed that lung function impairment increases significantly with disease progression in bronchiectasis. A similar conclusion was reported in the study by Lapinel et al. [32]. Our findings further support that lung function declines over time in patients with stable bronchiectasis. It should be noted that the observed changes in lung function parameters reflect the average group-level trend, not a uniform decline in all individuals. Furthermore, lung function measurements could have been influenced by acute exacerbations during follow-up. Physiological decline in lung function is known to occur in healthy individuals [33]. However, due to the influence of various host and environmental factors, we cannot definitively compare the magnitude of decline between stable bronchiectasis patients and healthy individuals over the same period.
Microbial colonization and infection are key components in the pathophysiology of bronchiectasis. Infection with pathogens such as PA can exacerbate inflammatory responses and airway structural damage, accelerating lung function decline. This is closely linked to greater disease severity, increased exacerbation frequency, and higher mortality risk [34]. A retrospective study of 156 patients hospitalized for bronchiectasis exacerbations found that 55.6% had airflow obstruction, and those with chronic bacterial infections showed a significant reduction in lung diffusing capacity [35]. Another study in CHEST confirmed that chronic PA infection is an independent risk factor for accelerated lung function decline and is strongly associated with disease progression in bronchiectasis [36]. In our study, the changes in both ΔFEV₁ and ΔFEV₁/FVC was significantly lower in the group with chronic PA infection. Notably, while the difference in FEV1 decline between the two groups reached statistical significance, the absolute magnitude of decline was small. This finding only suggests that chronic PA infection is indeed associated with decline in lung function among patients with bronchiectasis and may indicate a poorer pulmonary function prognosis. Further validation in larger cohorts, combined with clinical and imaging outcomes, is required to confirm these findings.
Previous studies have predominantly focused on the clinical features, exacerbation frequency, disease severity, lung function, and management of PA infection in patients during acute exacerbations of bronchiectasis. However, it remains unclear whether positive PA detection in lower respiratory tract samples is associated with future exacerbations in patients with stable bronchiectasis. Our study addressed this gap by analyzing 391 patients using PSM combined with Kaplan-Meier survival analysis. We found that the median time to exacerbation in chronic PA infection group was 202 days, which was significantly shorter than the group without chronic PA infection. The statistical analyses indicate that chronic PA infection (HR = 1.571; 95%CI: 1.014–2.432) increases the risk of acute exacerbation within the next year for patients with bronchiectasis. This finding is consistent with previous reports [37, 38], suggesting that chronic PA infection was a crucial risk factor for exacerbations. It also underscores the greater disease burden associated with exacerbations in patients with chronic PA infection, highlighting the need for intensified disease management in this population.
This study collected a wide range of variables from patients with stable bronchiectasis at a tertiary hospital in China, including demographic data, past medical history, comorbidities, laboratory findings, and lung function results. It aimed to characterize the clinical profile, lung function changes, and short-term exacerbation risk in chronic PA infection population. Our findings provide clinicians with detailed data for a more comprehensive understanding of stable bronchiectasis patients with chronic PA infection. This knowledge can optimize disease management, reduce exacerbation risk, and alleviate the economic burden on patients and the strain on healthcare resources. Our study has several limitations. As a single-center, prospective cohort study with a long follow-up period and significant patient dropout, potential biases and errors may exist. Chronic PA infection is associated with accelerated lung function decline and may be important in stable bronchiectasis progression. However, given the limited extent of FEV1 decline observed, the reliability of these findings thus requires further validation. Larger, national multicenter clinical trials is warranted to further confirm our conclusions.
Conclusion
chronic PA infection in stable bronchiectasis was associated with high disease severity, accelerated lung function decline and increased exacerbation risk. These results suggested that chronic PA infection contributes to the progression of bronchiectasis.
Supplementary Information
Supplementary Material 1. Supplementary Table S1. Comparison of baseline characteristics before and after PSM: chronic PA infection and lung function association.
Supplementary Material 2. Supplementary Table S2. Comparison of baseline characteristics before and after PSM: association between chronic PA infection and one-year exacerbation risk in bronchiectasis.
Supplementary Material 3. Supplementary Figure S1. Density curves of propensity scores before and after matching: chronic PA infection and lung function association.
Supplementary Material 4. Supplementary Figure S2. Density curves of propensity scores before and after matching: association between chronic PA infection and one-year exacerbation risk in bronchiectasis.
Acknowledgements
Not applicable.
Abbreviations
- PA
Pseudomonas aeruginosa
- BMI
Body mass index
- BSI
Bronchiectasis severity index
- CRP
C-reactive protein
- FVC
Forced vital capacity
- FEV1
Forced expiratory volume in 1 s
- GERD
Gastroesophageal reflux disease
- FeNO
Fractional exhaled nitric oxide
- PSM
Propensity score matching
- HRCT
High-resolution computed tomography
- SD
Standard deviation
- IQR
Inter-quartile range
- HR
Hazard ratio
- CI
Confidence interval
- WBC
White blood cell
- NEU
Neutrophil
- EOS
Eosinophil
Authors’ contributions
Rui Zhou and Shao-yan Zhang collected the clinical data and performed all analyses. Ben Su, Tao Chen, Xin-yuan Xu, and Yu-xian Chen contributed to statistical analyses. Zheng-yi Zhang and Ding-zhong Wu provided radiological and clinical insights to data interpretation. Rui Zhou and Shao-yan Zhang drafted the manuscript. Lei Qiu and Zhen-hui Lu take full responsibility for the content of the article including study design, the data and analysis. All authors have read and agreed to the published version of the manuscript. All authors have agreed to be personally accountable for the contributions.
Funding
This work was funded by the Major National Science and Technology Projects of China (2024ZD0523000), Shanghai Municipal Science and Technology Commission (23S21900600), Shanghai Municipal Health Commission (20234Y0109), Science and Technology Committee of Xuhui District (23XHYD-25), Shanghai Shenkang Hospital Development Center (SHDC12023106), and Shanghai Pudong New District Pilot Project for the Inheritance, Innovation, and Development of Traditional Chinese Medicine (YC-2023-0901).
Data availability
The original data supported this study can be looked up in our hospital’s electronic medical record system, further inquiries can be directed to the corresponding author. Datasets are not suitable to be deposited to publicly available repositories due to patient privacy.
Declarations
Ethics approval and consent to participate
The study was approved by the Ethics Committee of Longhua Hospital Affiliated to Shanghai University of Traditional Chinese Medicine (Approval No. 2019LCSY058 and 2024LCSY144), in accordance with the Declaration of Helsinki. Written informed consent was obtained from all patients/participants involved in the study.
Consent for publication
Not applicable.
Competing interests
The authors declare no competing interests.
Footnotes
Publisher’s note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
Rui Zhou and Shao-yan Zhang are co-first authors, contributed equally to this work.
Contributor Information
Zhen-hui Lu, Email: Dr_luzh@shutcm.edu.cn.
Lei Qiu, Email: dr_qiulei@shutcm.edu.cn.
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Supplementary Materials
Supplementary Material 1. Supplementary Table S1. Comparison of baseline characteristics before and after PSM: chronic PA infection and lung function association.
Supplementary Material 2. Supplementary Table S2. Comparison of baseline characteristics before and after PSM: association between chronic PA infection and one-year exacerbation risk in bronchiectasis.
Supplementary Material 3. Supplementary Figure S1. Density curves of propensity scores before and after matching: chronic PA infection and lung function association.
Supplementary Material 4. Supplementary Figure S2. Density curves of propensity scores before and after matching: association between chronic PA infection and one-year exacerbation risk in bronchiectasis.
Data Availability Statement
The original data supported this study can be looked up in our hospital’s electronic medical record system, further inquiries can be directed to the corresponding author. Datasets are not suitable to be deposited to publicly available repositories due to patient privacy.