ArticleImmunology1997
The involvement of macrophage-derived tumour necrosis factor and lipoxygenase products on the neutrophil recruitment induced by Clostridium difficile toxin B.
Article in Immunology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 46 citations in OpenAlex.
- Clostridioides difficile : A suspected pro-carcinogenic bacterium for gastrointestinal tumors.Chinese medical journal · 2026Review
- The complete catalog of antimicrobial resistance secondary active transporters inComputational and structural biotechnology journal · 2024Article
- Vitamin DAutophagy · 2022Article
- Article
- From Nursery to Nursing Home: Emerging Concepts in Clostridioides difficile Pathogenesis.Infection and immunity · 2020Review
- Enterotoxic Clostridia:Microbiology spectrum · 2019Review
- The role of toxins in Clostridium difficile infection.FEMS microbiology reviews · 2017Review
- Article
- The enterotoxicity of Clostridium difficile toxins.Toxins · 2010Review
- Clostridium difficile toxin B differentially affects GPCR-stimulated Ca2+ responses in macrophages: independent roles for Rho and PLA2.Journal of leukocyte biology · 2010Article
- Review
- Essential role of the glucosyltransferase activity in Clostridium difficile toxin-induced secretion of TNF-alpha by macrophages.Microbial pathogenesis · 2009Article
- STAT4 isoforms differentially regulate Th1 cytokine production and the severity of inflammatory bowel disease.Journal of immunology (Baltimore, Md. : 1950) · 2008Article
- Essential role of toxin A in C. difficile 027 and reference strain supernatant-mediated disruption of Caco-2 intestinal epithelial barrier function.Clinical and experimental immunology · 2008Article
- Clostridium difficile toxins: mechanism of action and role in disease.Clinical microbiology reviews · 2005Review
- Intestinal secretory factor released by macrophages stimulated with Clostridium difficile toxin A: role of interleukin 1beta.Infection and immunity · 1998Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Clostridium difficile (Cd) toxins appear to mediate the inflammatory response in pseudomembranous colitis and/or colitis associated with the use of antibiotics. In contrast to Cd Toxin A (TxA), Cd Toxin B (TxB) has been reported not to promote fluid secretion or morphological damage in rabbits and hamsters and also does not induce neutrophil chemotaxis in vitro. However, TxB is about 1000 times more potent than TxA in stimulating the release of tumour necrosis factor-alpha (TNF-alpha) by cultured monocytes. In the present study, we investigated the ability of TxB to promote neutrophil migration into peritoneal cavities and subcutaneous air-pouches of rats. We also examined the role of resident peritoneal cells in this process as well as the inflammatory mediators involved. TxB caused a significant and dose-dependent neutrophil influx with a maximal response at 0.1 microgram/cavity after 4 hr. Depleting the peritoneal resident cell population by washing the peritoneal cavity or increasing this population by pretreating the animals with thioglycollate blocked and amplified the TxB-induced neutrophil migration, respectively. Pretreating the animals with MK886 (a lipoxygenase inhibitor), NDGA (a dual cyclo- and lipoxygenase inhibitor) or the glucocorticoid, dexamethasone, but not with indomethacin (a cyclo-oxygenase inhibitor), or BN52021 (a platelet-activating factor antagonist), inhibited the neutrophil migration evoked by TxB. Pretreatment with dexamethasone or the administration of anti-TNF-alpha serum into the air-pouches also significantly reduced the TxB-induced neutrophil migration. Supernatants from TxB-stimulated macrophages induced neutrophil migration when injected into the rat peritoneal cavity. This effect was attenuated by the addition of either MK886 or dexamethasone to the macrophage monolayer and by preincubating the supernatants with anti-TNF-alpha serum. TxB also stimulated the release of TNF-alpha by macrophages. Overall, these results suggest that TxB induces an intense neutrophil migration which is mediated by macrophage-derived TNF-alpha and lipoxygenase products.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.