ArticleClinical and vaccine immunology : CVI2010
Beneficial dysregulation of the time course of inflammatory mediators in lipopolysaccharide-induced tumor necrosis factor alpha factor-deficient mice.
Article in Clinical and vaccine immunology : CVI, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Neutrophils loaded NADMaterials today. Bio · 2025Article
- MicroRNAs regulate innate immunity against uropathogenic and commensal-like Escherichia coli infections in the surrogate insect model Galleria mellonella.Scientific reports · 2020Article
- Increasing Tau 4R Tau Levels Exacerbates Hippocampal Tau Hyperphosphorylation in the hTau Model of Tauopathy but Also Tau Dephosphorylation Following Acute Systemic Inflammation.Frontiers in immunology · 2020Article
- Gram Negative Bacterial Inflammation Ameliorated by the Plasma Protein Beta 2-Glycoprotein I.Scientific reports · 2016Article
- Dysregulated Inflammatory Signaling upon Charcot-Marie-Tooth Type 1C Mutation of SIMPLE Protein.Molecular and cellular biology · 2015Article
- Pivotal role of NOD2 in inflammatory processes affecting atherosclerosis and periodontal bone loss.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Mutation of SIMPLE in Charcot-Marie-Tooth 1C alters production of exosomes.Molecular biology of the cell · 2013Article
- Minocycline ameliorates LPS-induced inflammation in human monocytes by novel mechanisms including LOX-1, Nur77 and LITAF inhibition.Biochimica et biophysica acta · 2012Article
- Article
- Whole-body deletion of LPS-induced TNF-α factor (LITAF) markedly improves experimental endotoxic shock and inflammatory arthritis.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Age-related alterations in retinal neurovascular and inflammatory transcripts.Molecular vision · 2011Article
- Bioinformatics analysis of macrophages exposed to Porphyromonas gingivalis: implications in acute vs. chronic infections.PloS one · 2010Article
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Authors and funding
3 authors.
Funding
Abstract
To begin to understand the surprising survival of macrophage-specific lipopolysaccharide-induced tumor necrosis factor alpha factor-deficient (macLITAF(-/-)) animals after a lethal dose of lipopolysaccharide (LPS), as reported earlier, the present follow-up study focuses on the role of LITAF in the regulation of inflammatory cytokines secreted in response to lethal or sublethal doses of LPS administered to wild-type (WT) and macLITAF(-/-) mice. A time course study of kinase expression in peritoneal macrophages revealed increased phosphorylation of prosurvival kinases Akt, Erk1/2, and ribosomal S6 kinase (RSK) in macLITAF(-/-) mice compared to that in WT mice (n = 8), confirming their role in LPS-mediated diseases. macLITAF(-/-) mice (n = 8) survived a lethal dose of LPS plus d-galactosamine (d-GalN), expressing lower serum levels of pro- and anti-inflammatory cytokines than the WT levels. To extend our knowledge on LPS-induced inflammatory events, an effective sublethal dose of LPS was administered to the animals (n = 14). WT animals exhibited an acute inflammatory response that decreased after 4 h. Interestingly, macLITAF(-/-) mice exhibited an initial delay in the secretion of proinflammatory cytokines that peaked after 8 h and reached WT levels after 18 h. Anti-inflammatory cytokine secretions were initially delayed but increased after 4 h and remained elevated compared to WT levels, even after 18 h. Our results demonstrate that LITAF deficiency in vivo affects cytokines other than TNF-alpha and influences the balance between the pro- and anti-inflammatory cytokines, which protects the animals from the deleterious effects of an LPS-induced inflammatory response, resulting in a beneficial host regulation of inflammatory cytokines and in enhanced survival. Therapeutic intervention aimed at reducing LITAF via kinase modulators may prove useful in preventing LPS-induced mortality.
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