ArticleClinical and diagnostic laboratory immunology2004
Leukotriene B4 receptor (BLT-1) modulates neutrophil influx into the peritoneum but not the lung and liver during surgically induced bacterial peritonitis in mice.
Article in Clinical and diagnostic laboratory immunology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 24 citations in OpenAlex.
- Collagen binding adhesin restricts Staphylococcus aureus skin infection.Nature communications · 2026Article
- Contributory Role of BLT2 in the Production of Proinflammatory Cytokines in Cecal Ligation and Puncture-Induced Sepsis.Molecules and cells · 2021Article
- Polyunsaturated fatty acids, specialized pro-resolving mediators, and targeting inflammation resolution in the age of precision nutrition.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2021Review
- Biochemical and immunological characterization of a novel monoclonal antibody against mouse leukotriene B4 receptor 1.PloS one · 2017Article
- Leukocyte function-associated antigen-1 deficiency impairs responses to polymicrobial sepsis.World journal of clinical cases · 2015Article
- Deficiency of the leukotriene B4 receptor, BLT-1, protects against systemic insulin resistance in diet-induced obesity.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- Peritoneal damage: the inflammatory response and clinical implications of the neuro-immuno-humoral axis.World journal of surgery · 2010Review
- Blockade of CD137 signaling counteracts polymicrobial sepsis induced by cecal ligation and puncture.Infection and immunity · 2009Article
- Mechanisms of mortality in early and late sepsis.Infection and immunity · 2006Article
- Leukotriene BOncoimmunologyArticle
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7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Leukotriene B4 (LTB4) is a rapidly synthesized, early neutrophil chemoattractant that signals via its cell surface receptor, BLT-1, to attract and activate neutrophils during peritonitis. BLT-1-deficient (BLT-1(-/-)) mice were used to determine the effects of LTB4 on neutrophil migration and activation, bacterial levels, and survival after cecal ligation and puncture (CLP). Male BLT-1(-/-) or wild-type (WT) BALB/c mice underwent CLP. Tissues were harvested for determination of levels of bacteria, myeloperoxidase (MPO), LTB4, macrophage inflammatory protein 2 (MIP-2), and neutrophil (polymorphonuclear leukocyte [PMN]) numbers at 4 and 18 h after CLP. PMN activation was determined by an assessment of phagocytosis ability and CD11b expression. Survival was also determined. BLT-1(-/-) mice had decreased numbers of PMNs in the peritoneum at both 4 and 18 h after CLP but increased numbers of PMNs in the blood at 18 h compared with WT mice. Liver and lung MPO levels were significantly higher in BLT-1(-/-) mice at both 4 and 18 h after CLP, with increased bacterial levels in the blood, the liver, and peritoneal fluid at 4 h. Bacterial levels remained higher in peritoneal fluid at 18 h, but blood and liver bacterial levels at 18 h were not different from levels at 4 h. PMN phagocytosis and CD11b levels were decreased in BLT-1(-/-) mice. LTB4 levels were similar between the groups before and after CLP, but MIP-2 levels were decreased both locally and systemically in BLT-1(-/-) mice. Survival was significantly improved in BLT-1(-/-) mice (71%) compared with WT mice (14%) at 48 h post-CLP. Thus, LTB4 modulates neutrophil migration into the mouse peritoneum, but not the lung or liver, after CLP. Despite higher bacterial and PMN levels at remote sites, there was increased survival in BLT-1(-/-) mice compared to WT mice. Decreased PMN activation may result in less remote organ dysfunction and improved survival.
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