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Eric Houpt

Publications and source records attributed to Eric Houpt.

4 recordsLinked to original sources

Global impact of diarrheal diseases that are sampled by travelers: the rest of the hippopotamus.

Travelers who experience diarrhea (i.e., "turista") are exposed to the same pathogens and illnesses that pose some of the greatest threats to life and development among malnourished children in developing areas around the world, where inadequate water and poor sanitation remain. This article focuses on new findings about the impact, diagnosis, and control of these illnesses and the genetic predispositions of persons who acquire them. Despite the reductions in mortality due to dehydrating diarrhea, the morbidity associated with diarrheal illnesses continues unabated. Furthermore, we increasingly recognize the lasting detrimental effects of enteric infections that occur during early childhood on later physical and cognitive development and, in patients with acquired immunodeficiency syndrome, on the absorption of antiretroviral drugs. Genetic predispositions to inflammation and potential protection associated with such alleles as ApoE4, which are not suspected of being involved in diarrhea, remind us of how much we have to learn about the effect and interactions of enteric tropical infectious diseases with regard to our host genome. New diagnostic methods hold promise for improved recognition and, hopefully, control of enteric infections worldwide.

Diarrhea↗

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

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 beta 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.

Animals↗

Prevention of intestinal amebiasis by vaccination with the Entamoeba histolytica Gal/GalNac lectin.

Prevention of intestinal infection by Entamoeba histolytica would block both invasive disease and parasite transmission. The amebic Gal/GalNAc lectin mediates parasite adherence to the colonic surface and fecal anti-lectin IgA is associated with protection from intestinal reinfection in children. We tested if vaccination with the E. histolytica Gal/GalNAc lectin could prevent cecal infection in a C3H mouse model of amebic colitis. Two trials using native lectin purified from the parasite and two trials using a 64 kDa recombinant fragment ("LecA") were performed with a combined intranasal and intraperitoneal immunization regimen using cholera toxin and Freund's adjuvants, respectively. Two weeks after immunization mice were challenged intracecally with trophozoites, and 4-12 weeks after challenge mice were sacrificed for histopathologic evaluation of infection. Vaccination prevented intestinal infection with efficacies of 84 and 100% in the two native lectin trials and 91 and 34% in the two LecA trials. Mice with detectable pre-challenge fecal anti-lectin IgA responses were significantly more resistant to infection than mice without fecal anti-lectin IgA responses. These results show for the first time that immunization with the Gal/GalNAc lectin can prevent intestinal amebiasis in mice and suggest a protective role for fecal anti-lectin IgA in vivo.

Administration, Intranasal↗

Amebiasis.

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Amebicides↗