Journal
JOURNAL OF LEUKOCYTE BIOLOGY
Volume 93, Issue 6, Pages 921-932Publisher
OXFORD UNIV PRESS
DOI: 10.1189/jlb.0212086
Keywords
CD11b; mannose receptor; deficient; LAMP1; EEA1
Categories
Funding
- U.S. National Institutes of Health [R01 AI045540, R01 AI067874, R01 AI076233, R01AI056242]
- American Heart Association [0435333Z]
- Merit Review grant from the Department of Veterans Affairs
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Leishmania are intracellular parasites adapted to surviving in macrophages, whose primary function is elimination of invading pathogens. Leishmania entry into host cells is receptor-mediated. These parasites are able to engage multiple host cell-surface receptors, including MR, TLRs, CR3, and Fc gamma Rs. Here, we investigated the role of CR3 and Fc gamma R engagement on the maturation of Leishmania-containing phagosomes using CD11b-/- and Fc gamma R-/- macrophages, and assessing EEA1 and lysosome-associated proteins is necessary for the phagosome maturation delay, characteristic of Leishmania infection. Leishmania-containing phagosomes do not fuse with lyosomes until 5 h postinfection in WT mice. Phagolysosome fusion occurs by 1 h in CD11b and Fc gamma R common chain KO macrophages, although receptor deficiency does not influence Leishmania entry or viability. We also investigated the influence of serum components and their effects on phagosome maturation progression. Opsonization with normal mouse serum, complement-deficient serum, or serum from Leishmania-infected mice all influenced phagosome maturation progression. Our results indicate that opsonophagocytosis influences phagosomal trafficking of Leishmania without altering the intracellular fate.
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