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Campylobacter jejuni--microtubule-dependent invasion
1Laboratory of Enteric and Sexually Transmitted Diseases, FDA-Center for Biologics Evaluation and Research, Bldg 29/420, NIH Campus, Bethesda, MD 20892, USA. kopecko@cber.fda.gov
Trends in Microbiology
|August 22, 2001
Summary
Campylobacter jejuni, a common cause of foodborne illness and Guillain-Barré syndrome, invades the gut using an unusual microtubule-dependent mechanism. This pathway differs significantly from the pathogenesis seen in Shigella species.
Area of Science:
- Microbiology
- Cellular Biology
- Pathogenesis
Background:
- Campylobacter jejuni is a primary bacterial cause of global foodborne illness.
- It is also a significant etiological agent of Guillain-Barré syndrome, a paralytic neurological disorder.
- The precise mechanisms of C. jejuni pathogenesis are under active investigation.
Purpose of the Study:
- To elucidate the molecular and cellular details of the gut-invasion mechanism employed by C. jejuni.
- To characterize the role of microtubules versus actin filaments in C. jejuni-mediated host cell entry.
- To compare the pathogenic strategies of C. jejuni with those of Shigella species.
Main Methods:
- Molecular and cellular biology techniques were applied to a well-characterized strain of C. jejuni.
- Studies focused on analyzing the host cell invasion process.
- Comparative analysis of cytoskeletal element involvement (microtubules and actin filaments) was performed.
Main Results:
- A novel microtubule-dependent, but actin-filament-independent, gut-invasion mechanism was identified in C. jejuni.
- This mechanism is crucial for the initiation of disease by certain C. jejuni strains.
- The identified invasion pathway appears distinct from those utilized by Shigella spp.
Conclusions:
- C. jejuni employs a unique mechanism for gut invasion, relying on host cell microtubules.
- This microtubule-dependent pathway represents a key aspect of C. jejuni pathogenesis.
- Despite causing similar human dysenteric syndromes, C. jejuni and Shigella spp. utilize divergent molecular strategies for disease initiation.