Journal
INFECTION AND IMMUNITY
Volume 71, Issue 6, Pages 3572-3577Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/IAI.71.6.3572-3577.2003
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Funding
- NCI NIH HHS [CA 16885, R01 CA067529, R56 CA016885, R01-CA 67529, R01 CA016885] Funding Source: Medline
- NIAID NIH HHS [T32 AI 07019, T32 AI007019] Funding Source: Medline
- NIDDK NIH HHS [P30-DK34989-17, P30 DK034989] Funding Source: Medline
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Susceptible strains of mice that are naturally or experimentally infected with murine intestinal helicobacter species develop hepatic inflammatory lesions,that have previously been described as chronic active hepatitis. The inflammatory infiltrates in some models of chronic autoimmunity or inflammation resemble tertiary lymphoid organs hypothesized to arise by a process termed lymphoid organ neogenesis. To determine whether hepatic inflammation caused by infection with helicobacter could give rise to tertiary lymphoid organs, we used fluorescence-activated cell sorting, immunohistochemistry, and in situ hybridization techniques to identify specific components characteristic of lymphoid organs in liver tissue sections and liver cell suspensions from helicobacter-infected mice. Small venules (high endothelial venules [HEVs]) in inflammatory lesions in Helicobacter species-infected livers were positive for peripheral node addressin. Mucosal addressin cell adhesion molecule also stained HEVs and cells with a staining pattern consistent with scattered stromal cells. The chemokines SLC (CCL 21) and BLC (CXCL13) were present, as were B220-positive B cells and T cells. The latter included a naive (CD45lo-CD62Lhi) population. These findings suggest that helicobacter-induced chronic active hepatitis arises through the process of lymphoid organ neogenesis.
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