Alveolar macrophages phenotype in patients with asthma and its combination with gastroesophageal reflux disease with pulmonary manifestations

Abstract

Immune response disorders are one of the main components in pathogenesis of asthma (A) and pulmonary manifestations of gastroesophageal reflux disease (GERD). They depend largely on the balance of functional phenotypes of alveolar macrophages (AM) and their regulation. Objective: assessment of alveolar macrophages (AM) and immune response phenotype imbalance in A and its combination with gastroesophageal reflux disease (GERD) with pulmonary manifestations as compared to healthy volunteers (HV) with use of several phenotype criteria: receptors and cytokine production. Methods: In AM culture medium in patients with A (n=16, 49,30±3,64 y.o.), combination A+GERD (n=16, 49.25±3.60 y.o.) and healthy volunteers (HV) (n=10, 51,83±3,52 y.o.) AM phenotype was assessed by flow cytometry (Beckman Coulter FC500) by pro-and anti-inflammatory (M1/M2) cytokine production and CD markers expression of M1 and M2 AM phenotypes (CD25, CD80 and CD163, CD206, respectively). Results: Analysis of AM phenotype that pooled M1/M2 ratio of AM CD markers and cytokine production in A and A+GERD was 1.59 and 1.61, 0.91 and 0.84 vs. HV (1.00 and 1.00), respectively. The results indicates shift of AM towards M1 phenotype vs HV in A and towards M2 phenotype vs HV – in combination of GERD and A. Conclusions: Analysis of AM with use of several phenotype criteria revealed the shift towards proinflammatory M1 in asthma patients, that probably reflect common proinflammatory component and is expected to be in charge with future asthma exacerbation. In GERD and asthma combination AM phenotype was shifted towards M2 that can probably be due to GERD overlay.