Entamoeba histolytica: acute granulomatous intestinal lesions in normal and neutrophil-depleted mice

Rivero-Nava, Laura; Aguirre-Garcı́a, Jesús; Shibayama-Salas, Mineko; Hernández-Pando, Rogelio; Tsutsumi, Vı́ctor; Calderón, Jorge

doi:10.1016/s0014-4894(02)00106-6

Cited by 28 publications

(22 citation statements)

References 19 publications

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“…Other studies have indicated that neutrophils have a protective role in amebiasis. Neutrophils limit the size of amebic liver abscesses in wild-type and SCID mice (34,36) and appear to hasten parasite clearance from the intestine in BALB/c mice, albeit the effect was observed only at 6 h since all mice cleared the infection thereafter (27). Our data support the latter findings and strongly suggest that neutrophils play a protective role in intestinal amebiasis.…”

Section: Discussionsupporting

confidence: 83%

Resistance to IntestinalEntamoeba histolyticaInfection Is Conferred by Innate Immunity and Gr-1⁺Cells

et al. 2005

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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 parasiteinduced upregulation of proinflammatory and neutrophil chemotaxis transcripts and there was downregulation of transforming growth factor ␤ 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.

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Section: Discussionsupporting

confidence: 83%

Resistance to IntestinalEntamoeba histolyticaInfection Is Conferred by Innate Immunity and Gr-1⁺Cells

et al. 2005

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“…The hypothesis that destroyed leukocytes would be important agents for the development of hepatic necrosis is also discussed (Tsutsumi et al, 1984). However, the depletion of neutrophils in mice inoculated with E. histolytica trophozoites did not affect the frequency of ulcerative lesions in the large intestine (Rivero-Nava et al, 2002). On the other hand, the products of trophozoites contribute to amplify the inflammatory reaction.…”

Section: Discussionmentioning

confidence: 90%

“…There are many molecules involved in the tissue destruction by amoebas (Leippe et al, 1993;Lopez-vancell et al, 2000;Que & Reed, 2000;Aguirre-Garcia et al, 2002), but amoebiasis pathogenesis is still not totally understood. In this context, the development of new strategies for the study of amoebic lesions may identify other functions of E. histolytica virulence, adding data to better understand the disease.…”

Section: Discussionmentioning

confidence: 99%

Morphometric study of the hepatic lesions experimentally induced in hamsters byEntamoeba disparandE. histolytica

Costa

Brito

Gomes³

et al. 2007

Parasite

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Summary :Evolution of experimental hepatic lesions produced in hamsters with Entamoeba histolytica and E. dispar was evaluated quantitatively and qualitatively through morphometry and immunohistochemistry. Animals infected with E. dispar developed hepatic lesions quantitatively and qualitatively similar to those produced by E. histolytica on the first three days of infection. On the 6 th and 8 th days of infection, E. histolytica produced larger tissue damage than E. dispar. A gradual decrease was observed in the number of trophozoites along the infection. A negative correlation was observed between the reduced number of trophozoites and the larger area of necrosis in both groups, confirming the importance of trophozoites killed in the lesion genesis. Regarding the genetic similarity between E. histolytica and E. dispar, comparison strategy between lesions produced by these species may culminate in identifying virulence factors of E. histolytica. Résumé : ÉTUDE MORPHOMÉTRIQUE DES LESIONS HÉPATIQUES INDUITES EXPÉRIMENTALEMENT CHEZ LES HAMSTERS

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“…In an attempt to show the critical contribution of neutrophils to innate immune defense against P. aeruginosa after initial GI colonization, we tried to eliminate any potential Cy-induced GI mucosal damage and lymphopenia by using an alternative means of neutropenia induction. Neutrophil depletion by monoclonal antibody treatment (RB6-8C5 MAb) has been used in number of animal models of infection (7,9,12,43,51). RB6-8C5 MAb reacts with a common epitope on Ly-6G and Ly-6C, previously known as the myeloid differentiation antigen Gr-1 (19).…”

Section: Discussionmentioning

confidence: 99%

Virulence ofPseudomonas aeruginosain a Murine Model of Gastrointestinal Colonization and Dissemination in Neutropenia

2005

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Pseudomonas aeruginosa bacteremia in cancer patients develops from initial gastrointestinal (GI) colonization with translocation into the bloodstream in the setting of chemotherapy-induced neutropenia and GI mucosal damage. We established a reproducible mouse model of P. aeruginosa GI colonization and systemic spread during neutropenia. Mice received 2 mg of streptomycin/ml of drinking water and 1,500 U of penicillin G/ml for 4 days and then ingested 10 7 CFU of P. aeruginosa per ml of drinking water for 5 days. After GI colonization levels were determined, cyclophosphamide (Cy) was then injected intraperitoneally (i.p.) three times every other day or an antineutrophil monoclonal antibody, RB6-8C5, was injected i.p. once. Dissemination was defined by the presence of P. aeruginosa in spleens of moribund or dead mice. In this mouse model, P. aeruginosa colonizes the GI tract and then disseminates systemically once Cy or RB6-8C5 is administered. The duration and intensity of neutropenia, related to Cy dose, was found to be a means to compare the virulence of different P. aeruginosa strains, as exhibited by comparisons of strains lacking or producing the virulence-enhancing ExoU cytotoxin. The lipopolysaccharide outer core polysaccharide and O side chains were critical in establishing GI colonization, and P. aeruginosa mutants lacking the aroA gene (necessary for synthesizing aromatic amino acids) were able to establish GI colonization but unable to disseminate. Both the colonization and dissemination phases of P. aeruginosa pathogenesis can be studied in this model, which should prove useful for evaluating pathogenesis, therapies, and associated means to control P. aeruginosa nosocomial infections.Pseudomonas aeruginosa causes significant morbidity and mortality in immunocompromised hosts (1, 15, 44), particularly neutropenic cancer patients (16). Although currently gram-positive organisms account for 60 to 70% of all documented infections in febrile neutropenic cancer patients (17, 26), these infections, in general, are typically more indolent, and delays of 24 to 48 h in initiating antibiotic therapy are usually not detrimental (17, 46). Importantly, the incidence of P. aeruginosa bacteremia has decreased in solid tumor patients but not in patients with acute leukemia (8). In fact, despite its lower incidence, P. aeruginosa continues to cause a disproportionate degree of morbidity and mortality in this patient population (6, 15, 16).The presumed mechanism for establishing P. aeruginosa bacteremia in cancer patients involves initial gastrointestinal (GI) colonization with subsequent translocation into the bloodstream in the setting of chemotherapy-induced neutropenia and GI mucosal damage (39). Leukemia patients who develop P. aeruginosa bacteremia have been found to have fecal cultures that are positive for the same strain of P. aeruginosa (18,50). When fecal cultures of these patients showed the presence of other potentially pathogenic gram-negative organisms (e.g., Escherichia coli, Klebsiella sp., etc.), P. ae...

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Entamoeba histolytica: acute granulomatous intestinal lesions in normal and neutrophil-depleted mice

Cited by 28 publications

References 19 publications

Resistance to IntestinalEntamoeba histolyticaInfection Is Conferred by Innate Immunity and Gr-1⁺Cells

Resistance to IntestinalEntamoeba histolyticaInfection Is Conferred by Innate Immunity and Gr-1⁺Cells

Morphometric study of the hepatic lesions experimentally induced in hamsters byEntamoeba disparandE. histolytica

Virulence ofPseudomonas aeruginosain a Murine Model of Gastrointestinal Colonization and Dissemination in Neutropenia

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Entamoeba histolytica: acute granulomatous intestinal lesions in normal and neutrophil-depleted mice

Cited by 28 publications

References 19 publications

Resistance to IntestinalEntamoeba histolyticaInfection Is Conferred by Innate Immunity and Gr-1+Cells

Resistance to IntestinalEntamoeba histolyticaInfection Is Conferred by Innate Immunity and Gr-1+Cells

Morphometric study of the hepatic lesions experimentally induced in hamsters byEntamoeba disparandE. histolytica

Virulence ofPseudomonas aeruginosain a Murine Model of Gastrointestinal Colonization and Dissemination in Neutropenia

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Resistance to IntestinalEntamoeba histolyticaInfection Is Conferred by Innate Immunity and Gr-1⁺Cells

Resistance to IntestinalEntamoeba histolyticaInfection Is Conferred by Innate Immunity and Gr-1⁺Cells