IgA- and secretory IgA-opsonized S. aureus induce a respiratory burst and phagocytosis by polymorphonuclear leucocytes.

The aim of the present study was to investigate whether corpuscular immune complexes containing human IgA were able to interact with human polymorphonuclear leucocytes (PMN). As a model for corpuscular IgA immune complexes (IgA IC), heat-killed Staphylococcus aureus (S. aureus) opsonized with either purified human serum IgA or purified secretory IgA (sIgA) isolated from human colostrum was used. In order to determine the capacity of IgA and sIgA to opsonize S. aureus the phagocytosis of these IgA IC by PMN was measured. S. aureus opsonized with IgA, sIgA, IgG, heat-inactivated serum or fresh serum was ingested by 23 +/- 8%; 28 +/- 9%; 39 +/- 7%; 31 +/- 10% and 78 +/- 10% of the PMN (S. aureus:PMN = 10:1, n = 4), respectively. These results were significantly different (P less than 0.05) from the percentage obtained with unopsonized S. aureus (9 +/- 3%), indicating that IgA and sIgA induce ingestion of S. aureus. The phagocytic index for PMN incubated with S. aureus opsonized with sIgA (231) was higher than for S. aureus opsonized with IgA (119), indicating a better uptake of S. aureus opsonized with sIgA in our system. Bacteria opsonized with either IgA or sIgA were also capable of triggering H2O2 release of PMN in a dose-dependent manner. The H2O2 release by PMN triggered with S. aureus opsonized with IgA could not be inhibited with a F(ab')2 anti-Fe gamma receptor monoclonal antibody, whereas the H2O2 release triggered with S. aureus opsonized with IgG was fully inhibited. Soluble heat-aggregated IgA (AIgA) also induced H2O2 release of PMN, suggesting that the IgA itself is essential for the induction of a respiratory burst.