TY - JOUR
T1 - Mucosal lymphoid infiltrate dominates colonic pathological changes in murine experimental Shigellosis
AU - Martino, Maria Celeste
AU - Rossi, Giacomo
AU - Martini, Irene
AU - Tattoli, Ivan
AU - Chiavolini, Damiana
AU - Phalipon, Armelle
AU - Sansonetti, Philippe J.
AU - Bernardini, Maria Lina
N1 - Funding Information:
Received 5 October 2004; accepted 11 February 2005; electronically published 31 May 2005. Financial support: European Commission (grant QLK2-1999-00938); Italian Ministero dell’Istruzione, Università e Ricerca (grant PRIN2002). Reprints or correspondence: Dr. Maria Lina Bernardini, Dipartimento di Biologia Cellulare e dello Sviluppo, Università La Sapienza, Via dei Sardi 70, 00185 Rome, Italy (marialina.bernardini@uniroma1.it).
PY - 2005/7/1
Y1 - 2005/7/1
N2 - Background. Shigella species are invasive human pathogens that cause acute rectocolitis by triggering a dysregulated inflammatory reaction in the colonic and rectal mucosa. Because mice are naturally resistant to shigellosis, there is no mouse model that mimics human disease. We explore the susceptibility of intestinal flora-depleted mice to shigellosis after intragastric infection with Shigella strains. Methods. Mice given 5 g/L streptomycin as a beverage were infected intragastrically with 1 × 108 cfu of either invasive or noninvasive Shigella strains. Results. We found that invasive Shigella strains persist up to 30 days in feces, whereas the persistence of noninvasive Shigella strains was reduced. Colonization primarily involves the colon and the cecum and, to a lesser extent, the ileum. The hallmark of inflammation in the intestinal tissue is a dramatic expansion of the lymphoid follicles, in which a high apoptotic index is recorded. Conclusions. We provide a murine model in which shigellae are able to reach their natural tissue target: the colon. Moreover, the absence of polymorphonuclear leukocyte recruitment and of epithelial cell lesions reveal some aspects of shigellosis that are usually hidden by the prevalence of this cell population. This novel model may contribute to the identification of new targets for vaccines and therapies.
AB - Background. Shigella species are invasive human pathogens that cause acute rectocolitis by triggering a dysregulated inflammatory reaction in the colonic and rectal mucosa. Because mice are naturally resistant to shigellosis, there is no mouse model that mimics human disease. We explore the susceptibility of intestinal flora-depleted mice to shigellosis after intragastric infection with Shigella strains. Methods. Mice given 5 g/L streptomycin as a beverage were infected intragastrically with 1 × 108 cfu of either invasive or noninvasive Shigella strains. Results. We found that invasive Shigella strains persist up to 30 days in feces, whereas the persistence of noninvasive Shigella strains was reduced. Colonization primarily involves the colon and the cecum and, to a lesser extent, the ileum. The hallmark of inflammation in the intestinal tissue is a dramatic expansion of the lymphoid follicles, in which a high apoptotic index is recorded. Conclusions. We provide a murine model in which shigellae are able to reach their natural tissue target: the colon. Moreover, the absence of polymorphonuclear leukocyte recruitment and of epithelial cell lesions reveal some aspects of shigellosis that are usually hidden by the prevalence of this cell population. This novel model may contribute to the identification of new targets for vaccines and therapies.
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U2 - 10.1086/430740
DO - 10.1086/430740
M3 - Article
C2 - 15942903
AN - SCOPUS:20844458270
SN - 0022-1899
VL - 192
SP - 136
EP - 148
JO - Journal of Infectious Diseases
JF - Journal of Infectious Diseases
IS - 1
ER -