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Infection and Immunity, November 1999, p. 6056-6066, Vol. 67, No. 11
Unité de Pathogénie Microbienne
Moléculaire/Unité INSERM 3891 and
Unité de Pharmacologie Cellulaire/Unité INSERM
485,2 Institut Pasteur, 75724 Paris Cedex 15, France; Department of Pathology, Kumamoto University Medical
School, Kumamoto 860, Japan3; and
Department of Microbiology, Skirball Institute, New York
University Medical Center, New York, New York
100164
Received 24 March 1999/Returned for modification 11 May
1999/Accepted 5 August 1999
Infection by the enteric bacterial pathogen Shigella
results in intense mucosal inflammation and destruction of the colonic and rectal epithelium in infected humans. Initial bacterial
translocation occurs through the follicle-associated epithelium.
Previous experiments suggest that interleukin-1 (IL-1) is crucial to
trigger inflammation, particularly in the follicular zones. During the
first 4 hours of infection in a rabbit ligated-loop model of intestinal
invasion, there are two salient characteristics: (i) a high
concentration of IL-1
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Increased Interleukin-1 (IL-1) and Imbalance
between IL-1 and IL-1 Receptor Antagonist during Acute Inflammation in
Experimental Shigellosis
and IL-1
, both in infected Peyer's patch
tissue and in the corresponding efferent mesenteric blood, and (ii) a
very low level of expression of IL-1 receptor antagonist (IL-1ra). These may reflect a combination of regulation of expression and secretion of IL-1
, IL-1
, and IL-1ra by both resident and
recruited phagocytes and the induction of mononuclear phagocyte
apoptosis by Shigella. This low IL-1ra/IL-1 ratio likely
accounts for the rapid, uncontrolled inflammation characteristic of shigellosis.
*
Corresponding author. Mailing address: Unité de
Pathogénie Microbienne Moléculaire/Unité INSERM 389, Institut Pasteur, 25-28 Rue du Docteur Roux, 75724 Paris Cedex 15, France. Phone: (33) (0)1 45 68 83 42. Fax: (33) (0)1 45 68 89 53. E-mail: psanson{at}pasteur.fr.
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