Immune and Proliferative Cellular Responses to Helicobacter pylori Infection in the Gastric Mucosa of Mexican Children

Unidad de Investigación en Enfermedades Infecciosas, Hospital de Pediatría, CMN SXXI, Instituto Mexicano del Seguro Social, México City, México.
Helicobacter (Impact Factor: 4.11). 07/2007; 12(3):224-30. DOI: 10.1111/j.1523-5378.2007.00493.x
Source: PubMed


Helicobacter pylori infection occurs mostly during childhood, but few studies on this age group have addressed the innate immune and the proliferative response to this infection. Mexico has a high H. pylori prevalence in children, but a low risk of gastric cancer. The aim of this work was to study the cellular responses of the gastric mucosa to this infection in Mexican children.
Antral and corpus gastric biopsies were obtained from 44 H. pylori-infected children (mean age 12 +/- 3.2 years) and 44 uninfected children (mean age 10 +/- 3 years). Mucosal cellular responses were studied by immunohistochemistry, using anti-Ki67 antibodies for proliferation studies, antihuman tryptase for mast cells, and antihuman CD68 for macrophages. T and B lymphocytes were stained with a commercial integrated system. The intensity of cellular responses was estimated histologically using the software KS300.
Epithelium proliferation and infiltration of macrophages and T and B lymphocytes were significantly higher in H. pylori-infected than in uninfected children. A balanced increase of CD4, CD8, and CD20 lymphocytes was observed in infected children. However, activated mast cells were decreased, and infiltration of neutrophil and mononuclear cells was low. Epithelial proliferation was associated with polymorphonuclear infiltration but not with infiltration of macrophages or lymphocytes. Inflammation and proliferation was higher in CagA (+)-infected children.
Mexican children respond to H. pylori infection with a low inflammatory response, a balanced increase of T and B lymphocytes, and a high regenerative activity.

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Available from: Javier Torres, Oct 22, 2014
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    • "This appears to be a characteristic feature of H. pylori infection, as gastric mucosal cell proliferation is increased in H. pyloriassociated chronic gastritis but not in chronic gastritis where the organism is absent (Lynch et al., 1995). Study by Munoz et al. (2007) also suggests proliferative activity as the epithelial regenerative response to cell damage caused by inflammatory mediators. The initiation of an active inflammatory response. "
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