Journal article
The roles of complement receptor 3 and Fcγ receptors during Leishmania phagosome maturation
Journal of leukocyte biology, Vol.93(6), pp.921-932
06/2013
DOI: 10.1189/jlb.0212086
PMCID: PMC3656333
PMID: 23543768
Abstract
Opsonophagocytosis influences phagosomal trafficking of Leishmania without altering the intracellular fate.
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 FcγRs. Here, we investigated the role of CR3 and FcγR engagement on the maturation of
Leishmania
-containing phagosomes using CD11b−/− and FcγR−/− 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 FcγR 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.
Details
- Title: Subtitle
- The roles of complement receptor 3 and Fcγ receptors during Leishmania phagosome maturation
- Creators
- Rachel Polando - Department of Biological Sciences, Eck Institute for Global Health, University of Notre Dame, Notre Dame, Indiana, USA; andUpasna Gaur Dixit - Internal Medicine andCristina R Carter - Department of Biological Sciences, Eck Institute for Global Health, University of Notre Dame, Notre Dame, Indiana, USA; andBlake Jones - Department of Biological Sciences, Eck Institute for Global Health, University of Notre Dame, Notre Dame, Indiana, USA; andJames P Whitcomb - Department of Biological Sciences, Eck Institute for Global Health, University of Notre Dame, Notre Dame, Indiana, USA; andWibke Ballhorn - Department of Biological Sciences, Eck Institute for Global Health, University of Notre Dame, Notre Dame, Indiana, USA; andMelissa Harintho - Department of Biological Sciences, Eck Institute for Global Health, University of Notre Dame, Notre Dame, Indiana, USA; andChristopher L Jerde - Department of Biological Sciences, Eck Institute for Global Health, University of Notre Dame, Notre Dame, Indiana, USA; andMary E Wilson - Microbiology and Epidemiology, University of Iowa and the Veterans Affairs Medical Center, Iowa City, Iowa, USAMary Ann McDowell - Department of Biological Sciences, Eck Institute for Global Health, University of Notre Dame, Notre Dame, Indiana, USA; and
- Resource Type
- Journal article
- Publication Details
- Journal of leukocyte biology, Vol.93(6), pp.921-932
- DOI
- 10.1189/jlb.0212086
- PMID
- 23543768
- PMCID
- PMC3656333
- NLM abbreviation
- J Leukoc Biol
- ISSN
- 0741-5400
- eISSN
- 1938-3673
- Publisher
- Society for Leukocyte Biology; Bethesda, MD, USA
- Grant note
- R01 AI045540; R01 AI067874; R01 AI076233; R01AI056242 / National Institutes of Health
- Language
- English
- Date published
- 06/2013
- Academic Unit
- Microbiology and Immunology; International Programs; Epidemiology; Internal Medicine
- Record Identifier
- 9984001201102771
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