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,
Departments of
*
Pathology,
Molecular Biology and Pharmacology, and
Medicine, and
Center for Immunology, Washington University School of Medicine, St. Louis, MO 63110
The bacteria Helicobacter pylori is a major human
pathogen that infects over half of the world’s population. Infection
initiates a series of changes in the gastric mucosa, beginning with
atrophic gastritis and leading in some patients to peptic ulcer
disease, mucosa-associated lymphomas, and gastric adenocarcinoma.
Although this cascade of events clearly occurs, little is known about
the role of the host immune response in disease progression. We have
utilized the C57BL/6 Helicobacter felis mouse model to
critically analyze the role of the adaptive immune response in the
development of Helicobacter-associated gastric
pathology. Infection of B and T cell-deficient RAG-1-/-
mice or T cell-deficient TCR
-/- mice with H.
felis resulted in high levels of colonization, but no
detectable gastric pathology. Conversely, infection of B cell-deficient
µMT mice resulted in severe gastric alterations identical with those
seen in immunocompetent C57BL/6-infected mice, including gastric
mucosal hyperplasia and intestinal metaplasia. These results
demonstrate that the host T cell response is a critical mediator of
Helicobacter-associated gastric pathology, and that B
cells and their secreted Abs are not the effectors of the
immune-mediated gastric pathology seen after H. felis
infection. These results indicate that in addition to specific
Helicobacter virulence factors, the host immune response
is an important determinant of Helicobacter-associated
disease.
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