In vivo Disruption of the Fas Pathway Abrogates Gastric Growth Alterations Secondary to Helicobacter Infection

• Published in: The Journal of infectious diseases Vol. 182; no. 3; pp. 856 - 864
• Main Authors: Houghton, JeanMarie, Bloch, Lisa Macera, Goldstein, Marsha, von Hagen, Stanley, Korah, Reju M.
• Format: Journal Article
• Language: English
• Published: Chicago, IL University of Chicago Press 01.09.2000
• Subjects: Animals; Apoptosis; Bacterial diseases; Biological and medical sciences; Cell growth; Experimental bacterial diseases and models; Fas antigen; fas Receptor - genetics; fas Receptor - physiology; Gastric Mucosa - metabolism; Gastric Mucosa - pathology; Gastric parietal cells; Helicobacter; Helicobacter infections; Helicobacter Infections - metabolism; Helicobacter Infections - pathology; Infections; Infectious diseases; Ligands; Lymphocytes; Major Articles; Male; Medical sciences; Messenger RNA; Mice; Mice, Inbred C57BL; Mice, Inbred MRL lpr; Mice, Knockout; Receptors; RNA, Messenger - metabolism; Signal Transduction; Stomach - metabolism; Stomach - pathology; Spirillales; Helicobacter; Rodentia; Spirillaceae; Host agent relation; Infection; Signal transduction; Vertebrata; Experimental disease; Mammalia; Mouse; Bacteriosis; Bacteria; Apoptosis
• ISSN: 0022-1899; 1537-6613
• DOI: 10.1086/315788

Helicobacter infection is associated with gastric cell growth alterations, plausibly predisposing to ulcer disease and gastric adenocarcinoma. Previous investigations from our laboratory have implicated the involvement of the Fas pathway in Helicobacter-induced apoptotic signaling in vitro. In this report we use C57BL/6J00064 mice to examine the direct role of Fas signaling in Helicobacter-medmted growth alterations in vivo. Helicobacter infection upregulated gastric cell Fas antigen (Fas Ag) mRNA and increased surface receptor expression, along with concomitant altered apoptotic and proliferative response, measured by terminal deoxytransferase-deoxyuridine 5-triphosphate nick end labeling and 5-bromo-2'-deoxuridine immunohistochemistry, respectively. In addition, histopathological alterations, including parietal cell loss and gastric atrophy, were noted. In contrast, infection in$B6.MRL-FAS_lpr$,a Fas Ag knockout mouse in the C57BL/6 background, did not result in increased apoptosis, proliferation, or histological alterations, a finding that argues strongly for the role of Fassignaling pathway in orchestrating diverse growth responses to Helicobacter infection.