Keith Wilson
Faculty Member
Last active: 12/19/2020

Host response to Helicobacter pylori infection before initiation of the adaptive immune response.

Algood HM, Gallo-Romero J, Wilson KT, Peek RM, Cover TL
FEMS Immunol Med Microbiol. 2007 51 (3): 577-86

PMID: 17919297 · DOI:10.1111/j.1574-695X.2007.00338.x

Helicobacter pylori persistently colonizes the human stomach. In this study, immune responses to H. pylori that occur in the early stages of infection were investigated. Within the first 2 days after orogastric infection of mice with H. pylori, there was a transient infiltration of macrophages and neutrophils into the glandular stomach. By day 10 postinfection, the numbers of macrophages and neutrophils decreased to baseline levels. By 3 weeks postinfection, an adaptive immune response was detected, marked by gastric infiltration of T lymphocytes, macrophages, and neutrophils, as well as increased numbers of H. pylori-specific T cells, macrophages, and dendritic cells in paragastric lymph nodes. Neutrophil-attracting and macrophage-attracting chemokines were expressed at higher levels in the stomachs of H. pylori-infected mice than in the stomachs of uninfected mice. Increased expression of TNFalpha and IFNgamma (Th1-type inflammatory cytokines) and IL-17 (a Th17-type cytokine) was detected in the stomachs of H. pylori-infected mice, but increased expression of IL-4 (a Th2-type cytokine) was not detected. These data indicate that a transient gastric inflammatory response to H. pylori occurs within the first few days after infection, before the priming of T cells and initiation of an adaptive immune response. It is speculated that inappropriate waning of the innate immune response during early stages of infection may be a factor that contributes to H. pylori persistence.

MeSH Terms (17)

Animals Chemokines Dendritic Cells Helicobacter Infections Helicobacter pylori Interferon-gamma Interleukin-4 Interleukin-17 Lymph Nodes Macrophages Male Mice Neutrophils Stomach T-Lymphocytes Time Factors Tumor Necrosis Factor-alpha

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