ArticleScientific reports2012
Disparate roles of marrow- and parenchymal cell-derived TLR4 signaling in murine LPS-induced systemic inflammation.
Article in Scientific reports, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 28 citations in OpenAlex.
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- Niacin Ameliorates Neuro-Inflammation in Parkinson's Disease via GPR109A.International journal of molecular sciences · 2019Article
- The In Vitro Immunomodulatory Effects Of Gold Nanoparticles Synthesized FromInternational journal of nanomedicine · 2019Article
- Human SR-BI and SR-BII Potentiate Lipopolysaccharide-Induced Inflammation and Acute Liver and Kidney Injury in Mice.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Article
- Natural small molecule FMHM inhibits lipopolysaccharide-induced inflammatory response by promoting TRAF6 degradation via K48-linked polyubiquitination.Scientific reports · 2015Article
- Imaging S1P1 activation in vivo.Experimental cell research · 2015Review
- P38/MAPK contributes to endothelial barrier dysfunction via MAP4 phosphorylation-dependent microtubule disassembly in inflammation-induced acute lung injury.Scientific reports · 2015Article
- Astragaloside IV inhibits NF- κ B activation and inflammatory gene expression in LPS-treated mice.Mediators of inflammation · 2015Article
- Abandon the mouse research ship? Not just yet!Shock (Augusta, Ga.) · 2014Article
- Toll-like receptor 4 in bone marrow-derived cells contributes to the progression of diabetic retinopathy.Mediators of inflammation · 2014Article
- Chloroquine relieves acute lung injury in rats with acute hemorrhagic necrotizing pancreatitis.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2013Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Systemic inflammatory response syndrome (SIRS) occurs in a range of infectious and non-infectious disease processes. Toll-like receptors (TLRs) initiate such responses. We have shown that parenchymal cell TLR4 activation drives LPS-induced systemic inflammation; SIRS does not develop in mice lacking TLR4 expression on parenchymal cells. The parenchymal cell types whose TLR4 activation directs this process have not been identified. Employing a bone marrow transplant model to compartmentalize TLR4 signaling, we characterized blood neutrophil and cytokine responses, NF-κB1 activation, and Tnf-α, Il6, and Ccl2 induction in several organs (spleen, aorta, liver, lung) near the time of LPS-induced symptom onset. Aorta, liver, and lung gene responses corresponded with both LPS-induced symptom onset patterns and plasma cytokine/chemokine levels. Parenchymal cells in aorta, liver, and lung bearing TLR4 responded to LPS with chemokine generation and were associated with increased plasma chemokine levels. We propose that parenchymal cells direct SIRS in response to LPS.
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