Resistance to intestinal Entamoeba histolytica infection is conferred by innate immunity and Gr-1+ cells

Amon Asgharpour, Carol Gilchrist, Duza Baba, Shinjiro Hamano, Eric Houpt

Research output: Contribution to journalArticlepeer-review

68 Scopus citations

Abstract

Establishment of intestinal infection with Entamoeba histolytica depends on the mouse strain; C57BL/6 mice are highly resistant, and C3H/HeJ mice are relatively susceptible. We found that resistance to intestinal infection was independent of lymphocyte activity or H-2 haplotype and occurred in the first hours to days postchallenge according to in vivo imaging. At 18 h postchallenge, the ceca of resistant C57BL/6 mice were histologically unremarkable, in contrast to the severe inflammation observed in susceptible C3H/HeJ mice. Comparison of cecal gene expression in C3H/HeJ and C57BL/6 mice demonstrated that there was parasite-induced upregulation of proinflammatory and neutrophil chemotaxis transcripts and there was downregulation of transforming growth factor β signaling molecules. Pretreatment with dexamethasone abrogated the partial resistance of C3H/HeJ or CBA mice through an innate, lymphocyte-independent mechanism, but it had no effect on the high-level resistance of C57BL/6 mice. Similarly, administration of a neutrophil-depleting anti-Gr-1 monoclonal antibody (RB6-8C5) decreased the partial resistance of CBA mice and led to severe pathology compared to control antibody-treated mice, but it had no effect on C57BL/6 resistance. These data indicate that there are discrete mechanisms of innate resistance to E. histolytica depending on the host background and, in contrast to other reports, imply that neutrophils are protective and not damaging in intestinal amebiasis.

Original languageEnglish
Pages (from-to)4522-4529
Number of pages8
JournalInfection and Immunity
Volume73
Issue number8
DOIs
StatePublished - Aug 2005
Externally publishedYes

Fingerprint

Dive into the research topics of 'Resistance to intestinal Entamoeba histolytica infection is conferred by innate immunity and Gr-1+ cells'. Together they form a unique fingerprint.

Cite this