
Polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs) can set up an immunosuppressive microenvironment in the lung via arginase-1 (ARG-1) bronchiectasis, which is linked to clinical outcomes and response to antibiotic treatment among patients with bronchiectasis, suggests a study.
Patients with bronchiectasis showed accumulations of PMN-MDSCs in the lung and blood when compared with healthy individuals. Most neutrophils in the lung of those with bronchiectasis consisted of LOX-1+ PMN-MDSCs.
PMN-MDSCs could suppress the proliferation of T cells by secreting high levels of the enzyme ARG-1. Of note, a negative association was observed between the frequencies of PMN-MDSCs in sputum and the time to next exacerbation in patients with bronchiectasis.
Furthermore, treatment with antibiotics could substantially reduce the frequencies of PMN-MDSC in the airway of bronchiectasis patients.
These findings indicate a potential role of PMN-MDSCs in bronchiectasis progression, according to the investigators.
In this study, the investigators performed flow cytometry and immunofluorescence staining to analyse the frequencies and presence of PMN-MDSCs, LOX-1+ neutrophils, and ARG-1+ PMN-MDSCs in peripheral blood mononuclear cells, sputum, and lung tissues. They established T-cell proliferation assays to assess the immunosuppressive activities of PMN-MDSCs.
In addition, the underlying mechanism of PMN-MDSC-mediated immunosuppression was examined via RNA sequencing. Finally, the investigators analysed the association of PMN-MDSC with the time to next exacerbation and treatment response to antibiotic therapy.