ArticleThe American journal of pathology2001
Monocyte/macrophage activation by normal bacteria and bacterial products: implications for altered epithelial function in Crohn's disease.
Article in The American journal of pathology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 98 citations in OpenAlex.
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- Mechanism of Nrf2 in the treatment of ulcerative colitis via regulating macrophage polarization.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2023Review
- Group 3 innate lymphoid cells require BATF to regulate gut homeostasis in mice.The Journal of experimental medicine · 2022Article
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- Inflammatory and immunometabolic consequences of gut dysfunction in HIV: Parallels with IBD and implications for reservoir persistence and non-AIDS comorbidities.EBioMedicine · 2019Review
- Lipopolysaccharide-Induced Increase in Intestinal Epithelial Tight Permeability Is Mediated by Toll-Like Receptor 4/Myeloid Differentiation Primary Response 88 (MyD88) Activation of Myosin Light Chain Kinase Expression.The American journal of pathology · 2017Article
- Intestinal inflammation and the diet: Is food friend or foe?World journal of gastrointestinal surgery · 2016Review
- Giardia duodenalis cathepsin B proteases degrade intestinal epithelial interleukin-8 and attenuate interleukin-8-induced neutrophil chemotaxis.Infection and immunity · 2014Article
- Fibrocytes are involved in inflammation as well as fibrosis in the pathogenesis of Crohn's disease.Digestive diseases and sciences · 2014Article
- Intestinal anti-inflammatory activity of lentinan: influence on IL-8 and TNFR1 expression in intestinal epithelial cells.PloS one · 2013Article
- The immunity of splenic and peritoneal F4/80(+) resident macrophages in mouse mixed allogeneic chimeras.Journal of molecular medicine (Berlin, Germany) · 2007Article
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- Effect of rebamipide on the colonic barrier in interleukin-10-deficient mice.Digestive diseases and sciences · 2007Article
- Enterocyte cytoskeleton changes are crucial for enhanced translocation of nonpathogenic Escherichia coli across metabolically stressed gut epithelia.Infection and immunity · 2006Article
- Polymorphisms of CD14 gene and TLR4 gene are not associated with ulcerative colitis in Chinese patients.Postgraduate medical journal · 2005Article
- Effects of psychological stress on small intestinal motility and bacteria and mucosa in mice.World journal of gastroenterology · 2005Article
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Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intestinal immune cells are less reactive than those in the peripheral blood; however, such cells from patients with Crohn's disease may be more responsive to bacterial products. Our study examined if nonpathogenic bacteria or lipopolysaccharide (LPS), can affect epithelial function in the presence of monocytes/macrophages. Lamina propria mononuclear cells (LPMCs) and peripheral blood monocytes (PBMs) were obtained from patients with Crohn's disease and control patients. Filter-grown T84 epithelial monolayers were co-cultured with nonactivated or LPS-activated LPMCs or PBMs for 48 hours. Epithelial secretory [baseline short-circuit current (Isc) and DeltaIsc to forskolin] and barrier (transepithelial electrical resistance) parameters were measured in Ussing chambers. LPS-activated PBMs from both controls and patients with Crohn's disease significantly increased Isc ( approximately 300%) and reduced transepithelial electrical resistance ( approximately 40%). Epithelial function was not altered after co-culture with control LPMCs +/- LPS. However, LPMCs from patients with Crohn's disease spontaneously secreted tumor necrosis factor-alpha, and induced epithelial changes similar to those produced by LPS-activated PBMs. Co-culture with control Escherichia coli and PBMs induced comparable changes in epithelial physiology, which were abrogated by anti-tumor necrosis factor-alpha antibody. We conclude that LPMCs of patients with Crohn's disease are spontaneously activated, possibly by gram-negative luminal bacteria, and can directly cause significant alterations in epithelial ion transport and barrier functions.
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