Editing Leishmania (section)

===Uptake and survival===
[[File:Leishmaniasis life cycle diagram en.svg|thumb|579px|center|Lifecycle of ''Leishmania'']]

Upon [[microbial]] infection, PMNs move out from the bloodstream through the vessels' endothelial layer, to the site of the infected tissue (dermal tissue after fly bite). They immediately initiate the first immune response and phagocytize the invader by recognition of foreign and activating surfaces on the parasite. Activated PMN secrete [[chemokines]], [[Interleukin 8|IL-8]] particularly, to attract further [[granulocytes]] and stimulate phagocytosis. Further, ''L. major'' increases the secretion of IL-8 by PMNs. This mechanism is observed during infection with other [[obligate intracellular parasites]], as well. For microbes like these, multiple intracellular survival mechanisms exist. Surprisingly, the coinjection of apoptotic and viable pathogens causes by far a more fulminate course of disease than injection of only viable parasites. When the anti-inflammatory signal [[phosphatidylserine]] usually found on apoptotic cells, is exposed on the surface of dead parasites, ''L. major'' switches off the [[oxidative burst]], thereby preventing killing and degradation of the viable pathogen.

In the case of ''Leishmania'', progeny are not generated in PMNs, but in this way they can survive and persist untangled in the primary site of infection. The promastigote forms also release ''Leishmania'' chemotactic factor (LCF) to actively recruit neutrophils, but not other [[leukocytes]], for instance [[monocytes]] or [[NK cells]]. In addition to that, the production of [[interferon gamma]] (IFNγ)-inducible protein 10 (IP10) by PMNs is blocked in attendance of ''Leishmania'', what involves the shut down of inflammatory and protective immune response by NK and [[Th1 cell]] recruitment. The pathogens stay viable during phagocytosis since their primary hosts, the PMNs, expose apoptotic cell-associated molecular pattern (ACAMP) signaling "no pathogen".