IGA MODULATES NEUTROPHIL INFLAMMATORY POTENTIAL FOLLOWING CHEMOTAXIS

Abstract

Objective: Respiratory mucosal defense provided by secretory IgA (SIgA) may not only act to prevent colonization and invasive infection by "immune exclusion" but may also modulate the immunoinflammatory response by PMNs and macrophages. We compared PMN activation in different cell populations in response to stimulation by lipopolysaccharide (LPS) or heat-killed bacteria. The relative ability of SIgA or IgG to modulate this response was also studied in-vitro. Methods: Monocytes from healthy volunteers were cocultured with LPS or heat-killed E. coli (HK-EC). Either IgA or IgG was added to subsets and culture supernatants obtained. PMNs were then placed in the apical (Ap) chamber of a 10 well chemotaxis chamber containing cell culture supernatants in the basal (Ba) chamber. This resulted in two PMN populations, an apical or non-migrated population and a basal or migrated population, based on chemotactic activities. Neutrophil CD11b expression, superoxide anion production (O2−) and elastase release were determined in both groups. Results: Mean ± SD (n = 4 each)TableResults were similar in experiments conducted with HK-EC. Conclusion: PMN migration was associated with enhanced inflammatory potential. This effect was abrogated by IgA but not IgG. SIgA is important in modulating immunoinflammatory response to LPS and other stimuli. Maintenance of normal IgA levels may limit the severity of acute lung injury and adult respiratory distress syndrome in the clinical setting.