ArticleAnnals of surgery2007
Exposure to bacterial DNA before hemorrhagic shock strongly aggravates systemic inflammation and gut barrier loss via an IFN-gamma-dependent route.
Article in Annals of surgery, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 25 citations in OpenAlex.
- The Central Role and Possible Mechanisms of Bacterial DNAs in Sepsis Development.Mediators of inflammation · 2020Review
- Low doses of celecoxib attenuate gut barrier failure during experimental peritonitis.Laboratory investigation; a journal of technical methods and pathology · 2013Article
- Hemorrhage-induced intestinal damage is complement-independent in Helicobacter hepaticus-infected mice.Shock (Augusta, Ga.) · 2010Article
- Orally administered bifidobacteria as vehicles for delivery of agents to systemic tumors.Molecular therapy : the journal of the American Society of Gene Therapy · 2010Article
- Linking oxidative stress to inflammation: Toll-like receptors.Free radical biology & medicine · 2010Review
- Noninflammatory gluten peptide analogs as biomarkers for celiac sprue.Chemistry & biology · 2009Article
- Surgical inflammation: a pathophysiological rainbow.Journal of translational medicine · 2009Review
- Mechanism of cytokine modulation of epithelial tight junction barrier.Frontiers in bioscience (Landmark edition) · 2009Review
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo investigate the role of bacterial DNA in development of an excessive inflammatory response and loss of gut barrier loss following systemic hypotension. SUMMARY BACKGROUND DATA: Bacterial infection may contribute to development of inflammatory complications following major surgery; however, the pathogenesis is not clear. A common denominator of bacterial infection is bacterial DNA characterized by unmethylated CpG motifs. Recently, it has been shown that bacterial DNA or synthetic oligodeoxynucleotides containing unmethylated CpG motifs (CpG-ODN) are immunostimulatory leading to release of inflammatory mediators.
methodsRats were exposed to CpG-ODN prior to a nonlethal hemorrhagic shock. The role of interferon-gamma (IFN-gamma) was investigated by administration of anti IFN-gamma antibodies.
resultsExposure to CpG-ODN prior to hemorrhagic shock significantly augmented shock-induced release of IFN-gamma, tumor necrosis factor-alpha (TNF-alpha) (P < 0.05), interleukin (IL)-6 (P < 0.05), and nitrite levels (P < 0.05), while there was a defective IL-10 response (P < 0.05). Simultaneously, expression of Toll-like receptor (TLR) 4 in the liver was markedly enhanced. Furthermore, intestinal permeability for HRP significantly increased and bacterial translocation was enhanced in hemorrhagic shock rats pretreated with CpG-ODN. Interestingly, inhibition of IFN-gamma in CpG-treated animals reduced TNF-alpha (P < 0.05), IL-6 (P < 0.05), nitrite (P < 0.05), and intestinal permeability following hemorrhagic shock (P < 0.05) and down-regulated expression of TLR4.
conclusionExposure to bacterial DNA strongly aggravates the inflammatory response, disrupts the intestinal barrier, and up-regulates TLR4 expression in the liver following hemorrhagic shock. These effects are mediated via an IFN-gamma-dependent route. In the clinical setting, bacterial DNA may be important in development of inflammatory complications in surgical patients with bacterial infection.
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