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Published on: October 22, 2013
Campylobacter jejuni activates mitogen-activated protein kinases in Caco-2 cell monolayers and in vitro infected
Amanda MacCallum1, Graham Haddock2, Paul H Everest1
1Institute of Comparative Medicine, Sir Henry Wellcome Building, University of Glasgow Faculty of Veterinary Medicine, Bearsden Road, Glasgow G61 1QH, UK.
Abstract:
The mitogen-activated protein kinases (MAPKs) play a central role in many host signalling pathways. These signalling proteins are known to be involved in host responses against invasive bacteria including generation of chemotactic and inflammatory cytokines. It was hypothesized that Campylobacter jejuni may activate MAPKs, as intestinal infection may induce a clinical and pathological picture of acute colonic inflammation. Infection of Caco-2 cell monolayers (human colonic epithelial cell line) and human colonic tissue with C. jejuni in vitro demonstrated increased MAPK activity for ERK 1/2 (p44/42 MAPK), JNK and p38 MAPKs. Kinase activity and phosphorylated forms were increased in infected Caco-2 cells and human colonic explants, suggesting that these pathways are important in inflammatory responses induced by C. jejuni in man.
Insights
Campylobacter jejuni infection activates mitogen-activated protein kinases (MAPKs) in human intestinal cells. This suggests MAPKs are key players in the inflammatory response to this common bacterial pathogen.
Area of Science:
- Cellular biology
- Immunology
- Microbiology
Background:
- Mitogen-activated protein kinases (MAPKs) are crucial signaling proteins in host cellular pathways.
- MAPKs mediate host responses to bacterial invasion, including cytokine generation and inflammation.
Purpose of the Study:
- To investigate if Campylobacter jejuni activates MAPKs in the human colon.
- To understand the role of MAPKs in the inflammatory response to C. jejuni infection.
Main Methods:
- Infection of Caco-2 cell monolayers (human colonic epithelial cells) with C. jejuni.
- Infection of human colonic tissue explants with C. jejuni.
- Assessing MAPK activity (ERK1/2, JNK, p38) and phosphorylation levels.
Main Results:
- C. jejuni infection significantly increased the activity and phosphorylation of ERK1/2, JNK, and p38 MAPKs.
- Elevated MAPK activity was observed in both Caco-2 cells and human colonic explants.
Conclusions:
- Campylobacter jejuni activates key MAPK signaling pathways in human intestinal cells.
- MAPK activation is implicated in the inflammatory responses triggered by C. jejuni in the human colon.
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