Pathogenicity islands of Shigella.

Molly A Ingersoll (1, 2) , E Groisman (3, 4) , A Zychlinsky (5)

1 Skirball Institute of Biomolecular Medicine
2 Department of Microbiology [New York, NY, USA]
3 HHMI - Howard Hughes Medical Institute [Saint Louis]
4 Department of Molecular Microbiology [St. Louis, MO, USA]
5 MPIIB - Max Planck Institute for Infection Biology

Shigella species are the causative agents of bacillary dysentery. Signs of disease range from mild diarrhea to a severe form of disease including fever, abdominal cramps, and stools containing blood, pus and mucus. Shigella are primarily human pathogens but can produce disease symptoms in other primates (Sansonetti 1992). After ingestion, shigellae traverse the intestinal epithelial barrier through specialized cells, called M-cells, at the level of the colon (Wassef et al. 1989). These cells transport antigens, including enteric pathogens, across the epithelium. Following transcytosis, micro-organisms gain access to lymphoid follicles containing resident tissue macrophages (Jarry et al. 1989; Soestayo et al. 1990). After phagocytosis, shigellae rapidly destroy the membrane of the phagosome and are liberated into the host cell cytoplasm (Finlay and Falkow 1988; Maurelli and Sansonetti 1988).

Domains: Immunology

Molly A Ingersoll, E Groisman, A Zychlinsky. Pathogenicity islands of Shigella.. Current Topics in Microbiology and Immunology, 2002, Pathogenicity Islands and the Evolution of Pathogenic Microbes, 264 (1), pp.49-65. ⟨10.1007/978-3-642-56031-6_4⟩. ⟨pasteur-02439664⟩