Endothelial nitric oxide synthase limits the inflammatory response in mouse cutaneous leishmaniasis.

摘要: Abstract Endothelial nitric oxide synthase (eNOS) was originally discovered in the cardiovascular system, where it contributes to regulation of blood pressure and inhibition platelet adhesion. Considering that vascular endothelium is critical for initiation inflammatory processes eNOS has been detected certain types immune cells, we investigated function C57BL/6 mice infected with Leishmania major , a protozoan parasite causes chronic, but self-healing skin disease. −/− developed more severe (but ultimately resolving) lesions strikingly higher numbers parasites compared wildtype controls. In accordance our finding naive T lymphocytes Th1 cells (as well as Th2 cells) did not express after stimulation required differentiation vitro lymph node from L. -infected released comparable amounts IFN-γ proliferated equally well. Immunohistological analyses revealed expression inducible NO draining nodes completely preserved absence eNOS. However, were characterized by massive infiltrates granulocytes, which similar macrophages failed From these data, conclude during cutaneous leishmaniasis eNOS-derived NO, presumably endothelial counteracts recruitment are known host trojan horses parasites, thereby limits severity lesions.