Fig. 1.

Patients with interstitial lung disease (ILD), including idiopathic pulmonary fibrosis (IPF) and pulmonary hypertension (PH), display augmented expression of CXCR2 in myeloid-derived suppressor cells (MDSCs) and pulmonary microvascular endothelial cells (PMVECs). A: changes in percentage of live CD11b⁺CD33⁺HLA-DR⁻ MDSCs in healthy controls (HC; n = 7) and ILD with (n = 6) and without PH (n = 8) peripheral blood samples. B and C: differences in percentage of CD11b⁺CD33⁺HLA-DR⁻CD14⁺ cells (monocytic MDSCs, Mo-MDSCs) and CD11b⁺CD33⁺HLA-DR⁻CD14⁻CD15⁺ cells (polymorphonuclear MDSCs, PMN-MDSCs) between HC and ILD groups. D and E: expression of CXCR2 (mean fluorescence intensity; MFI) in Mo-MDSCs and PMN-MDSCs between group samples. F–I: immunofluorescent staining and signal intensity quantification for interleukin-8 (IL-8), CD31, and CXCR2 in histologic lung samples from healthy controls (HC; n = 6) and IPF patients with (n = 5) and without (n = 6) PH (×4; scale bar 500 μm). J: PMVECs isolated from HC (n = 3), IPF (n = 16), and IPF with PH (n = 9) patients’ lungs with expression, by RT-PCR, of CXCR2 exposed to normoxic (Nx) or hypoxic (Hx; 1% O₂) conditions. K: concentration (pg/mL) of IL-8, by ELISA, in conditioned media of isolated groups’ PMVECs exposed to Nx or Hx. All flow data are presented as median ± interquartile range, and immunofluorescent and molecular analysis is presented as means ± SE. The Mann-Whitney U test or the Kruskal-Wallis rank-sum test was used for nonnormal data comparison. P < 0.05 was considered significant.