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. 2026 Jun 30;40(4):2025–2032. doi: 10.21873/invivo.14355

Dynamics of the Interleukin-10 Family of Cytokines in Chronic Otitis Media Patients upon 1,8-Cineol Treatment

ANKE LEICHTLE 1,#, JONAS FLECKNER 1,#, KIRSTIN PLÖTZE-MARTIN 1, ZUZANA PENXOVÁ 1, KARL-LUDWIG BRUCHHAGE 1, RALPH PRIES 1
PMCID: PMC13322011  PMID: 42379782

Abstract

Background/Aim

The monoterpene 1,8-Cineol is a natural plant-based anti-inflammatory agent that is used to treat different respiratory diseases with regard to its mucolytic and anti-microbial properties. 1,8-Cineol has recently been shown to support the natural microbial colonization of the middle ear, the intestinal bacterial community, as well as the clinical inflammatory situation of patients with chronic otitis media (COM). The aim of this study was to understand better the influence of 1,8-Cineol treatment on the systemic balances of inflammatory mediators of the interleukin-10 (IL-10) family of cytokines.

Patients and Methods

Plasma concentrations of cytokines IL-10, IL-19, IL-20, Il-22, IL-24 and IL-26 were analyzed in patients with COM with regard to 1,8-Cineol (CNL-1976®) treatment using ELISA measurements.

Results

Data revealed significantly increased concentrations of cytokines IL-19 and IL-26 in plasma samples from patients with COM compared to healthy donors as well as a significant positive correlation between IL-10 and IL-19. Of note, patients with COM revealed significantly reduced plasma levels of IL-26 in response to 14 days of 1,8-Cineol administration.

Conclusion

1,8-Cineol treatment actively modulates the systemic inflammatory environment in patients with chronic otitis media. By resetting disrupted cytokine balances, this plant-based agent offers a promising, target-specific therapeutic strategy for managing persistent middle ear inflammation and potentially mitigating associated systemic comorbidities.

Keywords: Otitis media, IL-10 cytokines, IL-19, IL-26, 1, 8-Cineol, CNL-1976

Introduction

Chronic otitis media (COM) is a prevalent inflammatory disease of the middle ear and responsible for hearing impairment, difficulties in conversations and social distancing (1, 2). COM-associated inflammation alters the permeability of cochlear membranes and thereby allows bacteria and their associated toxins to enter the inner ear (3, 4). Otitis media with effusion is well known as an initial manifestation of granulomatosis with polyangiitis, which is a vascular autoimmune disease of the respiratory tract, kidneys, and other organs (5). Moreover, a connection between COM and rheumatoid arthritis has been described (6). Several medical publications detail also the association between granulomatosis with polyangiitis (GPA) and otitis media with effusion (OME) as an initial symptom (5, 7). Failure to seek treatment may lead to serious otogenic complications such as mastoiditis, labyrinthitis, thrombosis of venous sinus or intracranial complications (8, 9). COM therapy includes antibiotic administration and can also require surgical intervention with complete removal of the inflammation and a subsequent reconstruction of the tympanic membrane or the implantation of hearing devices (10, 11).

Recently, the anti-inflammatory plant-based monoterpene 1,8-Cineol (CNL-1976®) has been shown to support the natural bacterial distribution of the middle ear, the intestinal microbial community as well as the clinical inflammatory situation of patients with COM (12).

The monoterpene 1,8-Cineol is often used as the clinically approved drug Soledum® to treat different respiratory diseases and leads to significantly decreased secretion levels of pro-inflammatory cytokines such as interleukin-1β (IL-1β), IL-5, or IL-6 from lymphocytes and monocytes (13-17). In fact, imbalances of pro- and anti-inflammatory cytokines are mainly responsible for the development of chronic inflammations (18-20).

The family of IL-10 cytokines consists of six members: IL-10, IL-19, IL-20, IL-22, IL-24, IL-26, and is more distantly also related to cytokines IL-28A, IL-28B, and IL-29, all of which are also known as type III interferons (21).

Interleukin-26 is one of the most recently identified members of the IL-10 cytokine family (22). Initial studies revealed elevated expression levels in human chronic inflammatory diseases including psoriatic and rheumatoid arthritis (RA), asthma and chronic obstructive pulmonary disease (COPD), leading to a proposal that it may constitute a novel inflammatory regulator (23-27).

However, the dynamics of circulating IL-10 related cytokines in the context of COM and the influence of 1,8-Cineol have not been investigated so far.

Therefore, cytokines IL-10, IL-19, IL-20, IL-22, IL-24 and IL-26 were measured in plasma samples from patients with COM before and after 14 days of anti-inflammatory 1,8-Cineol treatment to better understand the underlying dynamics with regards to the individual clinical situation.

Patients and Methods

Ethics statement. Patients were medically examined and treated at the Department of Otorhinolaryngology, University Hospital Schleswig-Holstein, Campus Lübeck. All patients have given their written informed consent. The present study has been approved by the local ethics committee of the University of Lübeck (approval number 22-040) and carried out in accordance with the ethical principles for medical research formulated in the WMA (World Medical Association) Declaration of Helsinki.

Characteristics of examined patients. All patients (n=25) included in the study suffered from rhinosinusitis and persistent COM, both of which share the same respiratory epithelium (28). The average age of the patients with COM was 53 years (30 to 68 years). All patients had received prior antibiotic therapy and developed microbial resistance against many or all available classical antibiotics. Therefore, we treated them with 1,8-Cineol. 1,8-Cineol (CNL-1976®) was used in terms of the clinically approved drug Soledum® Kapseln forte (capsules) (Cassella-med GmbH & Co. KG, Cologne, Germany). For therapeutic use, patients are treated with Soledum® Kapseln forte (3×200 mg Cineol/day), over 14 days for oral administration without additional antibiotic treatments during this time period.

Cytokine analysis. Enzyme-linked immunosorbent assays (ELISA) were used to analyze plasma concentrations of cytokines IL-10, IL-19, IL20, IL-22 (R&D Systems, Minneapolis, MN, USA), IL-24 (Antibodies online, Aachen, Germany) and IL-26 (Invitrogen, Carlsbad, CA, USA) according to the manufacturers’ protocols.

Statistical analysis. GraphPad Prism Version 7.0f (GraphPad Software, Inc., San Diego, CA, USA) was used for statistical analyses. The mean and standard error (SEM) are shown and differences between groups were calculated by testing for Gaussian distribution (normality tests), applying parametric (Student’s t-test), or non-parametric 1-way ANOVA with Bonferroni post hoc test. Correlation analyses were performed using multivariate regression with the Pearson correlation coefficient. p<0.05 (*), p<0.01 (**), and p<0.001 (***). Additional statistical details such as sample size are given in the respective figure legends, when appropriate.

Results

Plasma levels of IL-19 and IL-26 are significantly elevated in COM. Concentrations of cytokines IL-10, IL-19, IL-20, IL-22, IL-24, and IL-26 were analysed in plasma samples from patients with otitis media. Data revealed significantly increased plasma concentrations of cytokines IL-19 and IL-26 in patients with COM compared to healthy donors (HD) (Figure 1). Measurements of IL-10, IL-20, IL-22, and IL-24 revealed no overall significant differences compared to HD but showed clearly increased levels in specific individuals (Figure 1).

Figure 1.

Figure 1

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ELISA measurements of IL-10, IL-19, IL-20, IL-22, IL-24, and IL-26 concentrations in plasma samples from patients with otitis media (COM) (n=25) compared to healthy donors (HD; n=7). *p<0.05.

Further correlation analyses revealed a highly significant positive correlation between the measured plasma levels of IL-10 and IL-19 (p<0.001) in patients with COM, but no significant correlations between all other measured cytokines (Figure 2).

Figure 2.

Figure 2

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Correlation analysis between measured IL-10 and IL-19 concentrations in plasma samples from patients with chronic Otitis media. The Pearson correlation coefficient (r) and p-values are given. ***p<0.001 (***).

Response to 1,8-Cineol treatment. An evaluation of the clinical course revealed an improved clinical outcome of 13 patients with otitis media from our cohort after 14 days of 1,8-Cineol (CNL-1976®) treatment, who showed no response to the previous standard therapeutic regimen. In addition to improved ear symptoms, treatment with 1,8-Cineol also led to an improvement in accompanying rhinosinusitis symptoms.

To assess whether specific profiles of interleukin-10 related cytokines would change in response to 1,8-Cineol treatment, we analyzed plasma samples before herbal drug administration compared to plasma samples after 14 days of 1,8-Cineol treatment. Data revealed significantly reduced plasma levels of IL-26 in response to 1,8-Cineol as well as modestly reduced plasma concentrations of cytokines IL-10, IL-19 and IL-24 (Figure 3).

Figure 3.

Figure 3

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ELISA measurements of plasma samples from patients with chronic Otitis media (COM) (n=16) and healthy donors (HD, n=7) before (pre) and after (post) 1,8-Cineol administration. Data revealed significantly reduced plasma concentrations of interleukin-26 (IL-26) in patients with COM in response to 1,8-Cineol treatment. *p<0.05; **p<0.01.

Discussion

The present study investigated the dynamics of the IL-10 family of cytokines including IL-10, IL-19, IL-20, IL-22, IL-24, and IL-26 in plasma samples of patients with COM, all of which are known to be associated with different autoimmune and chronic inflammatory diseases (21). Of the six IL-10 family members IL-10, IL-22, and IL-26 are preferentially secreted by immune cells, whereas IL-19, IL-20, and IL-24 can also be produced by tissue cells (20). An anti-inflammatory activity of 1,8-Cineol via a regulation of associated biosynthetic pathways has been shown in different inflammatory diseases (29-32). Greiner and colleagues observed significantly decreased activities of transcription factor NFκB and the c-Jun N-terminal kinase (JNK)/activator protein-1 (AP-1) pathway in the human cancer cell lines U373 and HeLa upon 1,8-Cineol treatment (33).

Our study revealed significantly overall increased plasma concentrations of cytokines IL-19 and IL-26 in patients with COM compared to healthy donors as well as elevated levels of cytokines IL-10, IL-20, IL-22, and IL-24 in certain individuals.

Elevated plasma concentrations of IL-19 and IL-24 have also been observed in diabetic nephropathy, lupus nephritis, and chronic kidney diseases (34-38). Recent data revealed an immune regulatory link between IL-10 and its related family members IL-19 and IL-24 in human filarial infections (39, 40). It has been shown that IL-26 is closely associated with systemic inflammatory processes and lung functions in patients with asthma (41). Recent findings revealed that IL-26 attenuates the differentiation patterns of osteoblasts in patients with osteoarthritis via an activation of NF-κB related pathways (42).

Furthermore, elevated IL-26 concentrations have been found in the serum and synovial fluid from patients with rheumatoid arthritis compared to healthy individuals (26), which is of particular interest due to a known association of COM and rheumatoid arthritis granulomatosis with polyangiitis (GPA) (5-7). Furthermore, correlation analyses revealed a significant positive correlation between the plasma concentrations of cytokines IL-10 and IL-19 in patients with COM. IL-19 has been identified as a human homologue of IL-10 in the year 2000, both of which share 21% amino acid identity (43). Increased serum levels of IL-10 have been shown in the context of acute otitis media caused by Streptococcus pneumonia compared to Haemophilus influenzae and Moraxella catarrhalis (39), which underlines the influence of the individual microbial communities on the course of disease and the inflammatory situation in patients with COM.

Our patients revealed significantly reduced plasma levels of IL-26 in response to 14 days of 1,8-Cineol (CNL-1976®) administration. This is a very promising finding in view of the therapeutic impact, since IL-26 has emerged as a mediator of chronic inflammation, acting as a carrier for inflammatory extracellular DNA, and promoting the generation of Th17 cells in inflammatory processes (25, 44, 45).

In summary, our study provides novel insights into the differential effects of the monoterpene 1,8-Cineol on the systemic balances of inflammatory mediators in patients suffering from rhinosinusitis and persistent COM. Further investigations on larger patient cohorts and over longer periods of time are needed to corroborate our findings and to further correlate these data with the individual clinical situation, the underlying microbial communities and the development of rheumatoid comorbidities.

Conflicts of Interest

The Authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results.

Authors’ Contributions

Conceptualization, A.L., K.L.B., and R.P.; methodology and investigation, J.F., A.L., K.P.-M., Z.P., resources, A.L., K.-L.B., and R.P.; data curation, A.L., J.F., K.-L.B., and R.P.; writing - original draft preparation, J.F., A.L., and R.P.; writing - review and editing, all Authors. All Authors have read and agreed to the published version of the manuscript.

Acknowledgements

The Authors are grateful to the participating patients and all members of the ENT department, University Hospital Schleswig-Holstein, Lübeck for supporting sample collection.

Funding

This research was funded by Cassella-med GmbH & Co. KG, Cologne, Germany.

Artificial Intelligence (AI) Disclosure

No artificial intelligence (AI) tools, including large language models or machine learning software, were used in the preparation, analysis, or presentation of this manuscript.

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