Background
Whether polymorphonuclear neutrophils (PMN) exert a protective role upon chlamydial infection by expressing inducible nitric oxide (NO) synthase (iNOS) and producing NO remains unclear.
Conclusions
NO-producing PMN confer a protective role during pulmonary C. psittaci infection in mice, and thus our study sheds new light on PMN function during Chlamydia infection.
Methods
This issue was addressed using BALB/c mice infected with Chlamydia psittaci 6BC strain. Methods included flow cytometry, immunofluorescence, qRT-PCR, and western blot.
Results
The number of PMN was significantly increased during C. psittaci infection, which was accompanied by increased iNOS expression and NO production in the mouse lungs. PMN were the major source of NO during pulmonary C. psittaci infection and inhibited C. psittaci multiplication in an iNOS/NO-dependent manner. Depletion of PMN aggravated C. psittaci-induced disease and increased C. psittaci burden. Nuclear factor-κB (NF-κB) and STAT1 signaling pathways, but not MAPK signaling pathways, were required for the induction of iNOS expression and NO production in PMN by C. psittaci infection. Thus, our findings highlight the protective role of NO-producing PMN in C. psittaci infection. Conclusions: NO-producing PMN confer a protective role during pulmonary C. psittaci infection in mice, and thus our study sheds new light on PMN function during Chlamydia infection.