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Bacteria-triggered CD4+ T regulatory cells suppress Helicobacter hepaticus-induced colitis

We have previously demonstrated that interleukin (IL)-10–deficient (IL-10 knockout [KO]) but not wild-type (WT) mice develop colitis after infection with Helicobacter hepaticus. Here, we show that infected recombination activating gene (RAG) KO mice develop intestinal inflammation after reconstitution with CD4+ T cells from IL-10 KO animals and that the cotransfer of CD4+ T cells from H. hepaticus–infected but not uninfected WT mice prevents this colitis. The disease-protective WT CD4+ cells are contained within the CD45RBlow fraction and unexpectedly were found in both the CD25+ and the CD25- subpopulations of these cells, their frequency being higher in the latter. The mechanism by which CD25+ and CD25- CD45RBlow CD4+ cells block colitis involves IL-10 and not transforming growth factor (TGF)-ß, as treatment with anti–IL-10R but not anti–TGF-ß monoclonal antibody abrogated their protective effect. In vitro, CD45RBlow CD4+ cells from infected WT mice were shown to produce IL-10 and suppress interferon-{gamma} production by IL-10 KO CD4+ cells in an H. hepaticus antigen–specific manner. Together, our data support the concept that H. hepaticus infection results in the induction in WT mice of regulatory T cells that prevent bacteria-induced colitis. The induction of such cells in response to gut flora may be a mechanism protecting normal individuals against inflammatory bowel disease

Egg excretion in the initial phase of experimental murine schistosomiasis mansoni: stability and association with worm burden Esquistossomose mansoni experimental murina: estabilidade da eliminação dos ovos nas fezes e sua associação com a carga parasitária na fase inicial da infecção

Stability of faecal egg excretion and correlation with results related to worm burden at the initial phase of schistosomiasis mansoni were observed in two groups of mice infected with different Schistosoma mansoni cercarial burdens, by means of analysis of quantitative parasitological studies and schistosome counts after perfusion. Thus, it may be stated that few quantitative parasitological stool examinations could be sufficient to express the infection intensity at the initial phase, on the same grounds that it was already demonstrated at the chronic phase. Furthermore, it is confirmed that the use of the number of eggs passed in the faeces as a tool to estimate the worm burden at the initial phase of schistosome infection is adequate.<br>Através da análise de exames parasitológicos quantitativos seriados e da contagem de esquistossomos após perfusão em dois grupos de camundongos infectados com diferentes cargas de cercárias de Schistosoma mansoni, verificou-se a existência da estabilidade da eliminação de ovos e sua correlação com a carga parasitária na fase inicial da esquistossomose mansoni. Deste modo, pode-se afirmar que poucos exames parasitológicos de fezes quantitativos podem ser suficientes para traduzir a intensidade da infecção também na fase inicial , à semelhança do já demonstrado para a crônica. Além disto, comprova-se a adequação do uso do número de ovos eliminados nas fezes como expressão da carga parasitária na fase inicial da infecção esquistossomótica