The local inflammatory response to Leishmania chagasi infantum infection (134.89)

Abstract

Abstract Leishmania chagasi infantum (Lci) causes human visceral leishmaniasis. To study the nature of the early inflammatory response, we introduced metacyclic wild type and mCherry-transgenic parasites intradermally in ears of BALB/c mice. Inflammatory cells were collected from the dermal tissue and draining lymph nodes (dLN) at various times post-infection. FACS analysis revealed a rapid and abundant influx of neutrophils in the infected ears, which peaked between 6 and 24 hrs, but diminished by 48 hrs after infection. The neutrophil influx was dose dependent and specific for the local infection site. NK cells peaked at 24-48 hrs in the ear and 48-72 hrs in the dLN. Total cellularity of the dLN increased significantly after infection, primarily due to an expansion in the B cell population. mCherry parasites were observed infecting nearly 50% of neutrophils in the ear lesions during the earliest times (6-24 hrs), whereas parasites predominantly infected macrophages by 48 hrs. These data suggest intradermal Lci infection induces a rapid innate immune response in the local site and support the hypothesis that infected neutrophils provide one of the first major points of Leishmania entry into the infected host.