ArticleInfection and immunity2002
Apoptosis in acute shigellosis is associated with increased production of Fas/Fas ligand, perforin, caspase-1, and caspase-3 but reduced production of Bcl-2 and interleukin-2.
Article in Infection and immunity, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 60 citations in OpenAlex.
- Shigellosis.Lancet (London, England) · 2025Review
- Optimizing Low Fishmeal Diets with Vitamin C Supplementation: A Comprehensive Study on Growth, Immunity, and Heat Stress Resistance in Largemouth Bass (Antioxidants (Basel, Switzerland) · 2025Article
- FAS mediates apoptosis, inflammation, and treatment of pathogen infection.Frontiers in cellular and infection microbiology · 2025Review
- Pathogenicity and virulence ofVirulence · 2023Review
- An automated microscopy workflow to study Shigella-neutrophil interactions and antibiotic efficacy in vivo.Disease models & mechanisms · 2023Article
- Comprehensive Pan-Cancer Analyses of Pyroptosis-Related Genes to Predict Survival and Immunotherapeutic Outcome.Cancers · 2022Article
- Review
- Review
- Macrophage Apoptosis Triggered by IpaD from Shigella flexneri.Infection and immunity · 2016Article
- Shigella manipulates host immune responses by delivering effector proteins with specific roles.Frontiers in immunology · 2015Review
- Shigella impairs T lymphocyte dynamics in vivo.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Preventing acute gut wall damage in infectious diarrhoeas with glycosylated dendrimers.EMBO molecular medicine · 2012Article
- Quantitative RT-PCR profiling of the rabbit immune response: assessment of acute Shigella flexneri infection.PloS one · 2012Article
- Innate immune signaling in defense against intestinal microbes.Immunological reviews · 2012Review
- Selective deletion of CD8(+) cells upregulated by caspases-1 via IL-18 in mice immunized with major outer membrane protein of Shigella dysenteriae 1 following infection.Journal of clinical immunology · 2010Article
- Adaptive immune responses during Shigella dysenteriae type 1 infection: an in vitro stimulation with 57 kDa major antigenic OMP in the presence of anti-CD3 antibody.Molecular and cellular biochemistry · 2010Article
- Spa15 of Shigella flexneri is secreted through the type III secretion system and prevents staurosporine-induced apoptosis.Infection and immunity · 2009Article
- Neutrophil apoptosis and the resolution of infection.Immunologic research · 2009Review
- Microbial pathogen-induced necrotic cell death mediated by the inflammasome components CIAS1/cryopyrin/NLRP3 and ASC.Cell host & microbe · 2007Article
- Flagellin suppresses epithelial apoptosis and limits disease during enteric infection.The American journal of pathology · 2006Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 5 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Shigella dysenteriae type 1-induced apoptotic cell death in rectal tissues from patients infected with Shigella dysenteriae type 1 was studied by the terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling (TUNEL) technique and annexin V staining. Expression of proteins and cytokines participating in the apoptotic process (caspase-1, caspase-3, Fas [CD95], Fas ligand [Fas-L], perforin, granzyme A, Bax, WAF-1, Bcl-2, interleukin-2 [IL-2], IL-18, and granulocyte-macrophage colony-stimulating factor) in tissue in the acute and convalescent stages of dysentery was quantified at the single-cell level by in situ immunostaining. Apoptotic cell death in the lamina propria was markedly up-regulated at the acute stage (P < 0.05), where an increased number of necrotic cells were also seen. Phenotypic analysis of apoptotic cells revealed that 43% of T cells (CD3), 10% of granulocytes (CD15), and 5% of macrophages (CD56) underwent apoptosis. Increased activity of caspase-1 persisted in the rectum up to 1 month after onset. More-extensive expression of Fas, Fas-L, perforin, caspase-3, and IL-18, but not IL-2, at the acute stage than at the convalescent stage was observed. Increased expression of caspase-3 and IL-18 in tissues with severe inflammation compared to expression in those with mild inflammation was evident, implying a possible role in the perpetuation of inflammation. Significantly reduced cell death during convalescence was associated with a significant up-regulation of Bcl-2, Bax, and WAF-1 expression in the rectum compared to that in the acute phase of infection. Thus, induction of apoptosis at the local site in the early phase of S. dysenteriae type 1 infection was associated with a significant up-regulation of Fas/Fas-L and perforin and granzyme A expression and a down-regulation of Bcl-2 and IL-2, which promote cell survival.
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