Uptake_and_survival Leishmania

lifecycle of leishmania

upon microbial infection, pmns move out bloodstream through vessels’ endothelial layer, site of infected tissue (dermal tissue after fly bite). initiate first immune response , phagocytize invader recognition of foreign , activating surfaces on parasite. activated pmn secrete chemokines, il-8 particularly, attract further granulocytes , stimulate phagocytosis. further, l. major increases secretion of il-8 pmns. mechanism observed during infection other obligate intracellular parasites, well. microbes these, multiple intracellular survival mechanisms exist. surprisingly, coinjection of apoptotic , viable pathogens causes far more fulminate course of disease injection of viable parasites. when anti-inflammatory signal phosphatidylserine found on apoptotic cells, exposed on surface of dead parasites, l. major switches off oxidative burst, thereby preventing killing , degradation of viable pathogen.

in case of leishmania, progeny not generated in pmns, in way can survive , persist untangled in primary site of infection. promastigote forms release leishmania chemotactic factor (lcf) actively recruit neutrophils, not other leukocytes, instance monocytes or nk cells. in addition that, production of interferon gamma (ifnγ)-inducible protein 10 (ip10) pmns blocked in attendance of leishmania, involves shut down of inflammatory , protective immune response nk , th1 cell recruitment. pathogens stay viable during phagocytosis since primary hosts, pmns, expose apoptotic cell-associated molecular pattern (acamp) signaling no pathogen .