Acute inflammation causes epithelial invasion and mucosal destruction in experimental shigellosis.
Open Access
- 1 October 1994
- journal article
- Published by Rockefeller University Press in The Journal of Experimental Medicine
- Vol. 180 (4) , 1307-1319
- https://doi.org/10.1084/jem.180.4.1307
Abstract
The gram-negative pathogen Shigella flexneri causes bacillary dysentery, an invasive disease of the human colonic mucosa. A major characteristic of the infectious process is the occurrence of an acute inflammatory reaction of mucosal tissues which is generally consequence of primary invasion and destruction of colonic epithelial cells by the pathogen. Confirming in vitro demonstration that S. flexneri is unable to invade the apical pole of colonic cells and that polymorphonuclear (PMN) cells may assist them in reaching the basal side of epithelial cells where they can invade, we have provided here in vivo evidence that S. flexneri enters the epithelial barrier essentially through the dome of lymphoid follicles at the early stage of infection and that subsequent invasion and destruction of the epithelium is primarily due to immigration of leukocytes, particularly PMN that destroy cohesion of the epithelial barrier. These conclusions are based on experiments carried out in infected rabbit ligated intestinal loops, with some animals treated by an anti-CD18 monoclonal antibody that blocked immigration of leukocytes into infected tissues.Keywords
This publication has 26 references indexed in Scilit:
- Neutrophils are essential for early anti-Listeria defense in the liver, but not in the spleen or peritoneal cavity, as revealed by a granulocyte-depleting monoclonal antibody.The Journal of Experimental Medicine, 1994
- Migration of neutrophils through epithelial monolayersTrends in Cell Biology, 1994
- Unipolar localization and ATPase activity of IcsA, a Shigella flexneri protein involved in intracellular movementJournal of Bacteriology, 1993
- In vivo biologic and immunohistochemical analysis of interleukin-1 alpha, beta and tumor necrosis factor during experimental endotoxemia. Kinetics, Kupffer cell expression, and glucocorticoid effects.1991
- Cytokine response by monocytes and macrophages to free and lipoprotein-bound lipopolysaccharideInfection and Immunity, 1990
- Death in Shigellosis: Incidence and Risk Factors in Hospitalized PatientsThe Journal of Infectious Diseases, 1990
- Identification of icsA, a plasmid locus of Shigella flexneri that governs bacterial intra- and intercellular spread through interaction with F-actin.Proceedings of the National Academy of Sciences, 1989
- Interleukin 1 induces a shock-like state in rabbits. Synergism with tumor necrosis factor and the effect of cyclooxygenase inhibition.Journal of Clinical Investigation, 1988
- Entry of Shigella flexneri into HeLa cells: evidence for directed phagocytosis involving actin polymerization and myosin accumulationInfection and Immunity, 1987
- Multiplication of Shigella flexneri within HeLa cells: lysis of the phagocytic vacuole and plasmid-mediated contact hemolysisInfection and Immunity, 1986