ArticleLife sciences2010
Aging-related hyperinflammation in endotoxemia is mediated by the alpha2A-adrenoceptor and CD14/TLR4 pathways.
Article in Life sciences, 2010. 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, 16 citations in OpenAlex.
- FOXO1 orchestrates the intestinal homeostasis via neuronal signaling in group 3 innate lymphoid cells.The Journal of experimental medicine · 2023Article
- Disparate Recruitment and Retention of Plasmacytoid Dendritic Cells to The Small Intestinal Mucosa between Young and Aged Mice.Aging and disease · 2021Article
- Different roles of FAT10, FOXO1, and ADRA2A in hepatocellular carcinoma tumorigenesis in patients with alcoholic steatohepatitis (ASH) vs non-alcoholic steatohepatitis (NASH).Experimental and molecular pathology · 2018Article
- Klotho suppresses the inflammatory responses and ameliorates cardiac dysfunction in aging endotoxemic mice.Oncotarget · 2017Article
- Uninephrectomy-Induced Lipolysis and Low-Grade Inflammation Are Mimicked by Unilateral Renal Denervation.Frontiers in physiology · 2016Article
- Modulation of chemokine gradients by apheresis redirects leukocyte trafficking to different compartments during sepsis, studies in a rat model.Critical care (London, England) · 2014Article
- Immunology primer for neurosurgeons and neurologists part 2: Innate brain immunity.Surgical neurology international · 2013Review
- From expression pattern to genetic association in asthma and asthma-related phenotypes.BMC research notes · 2012Article
- Ghrelin-mediated sympathoinhibition and suppression of inflammation in sepsis.American journal of physiology. Endocrinology and metabolism · 2012Review
- Effect of ageing on systemic inflammatory response in acute pancreatitis.International journal of inflammation · 2012Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
aimsSepsis is a major cause of morbidity and mortality in the elderly population. In prior studies, we have shown that in vivo, the inflammatory response in aged animals is exaggerated as compared to young animals and that this response likely accounts for the increased morbidity and mortality. Part of this uncontrolled inflammatory response in sepsis is due to the innate immune response. However, recent studies have shown that the pathogenesis of sepsis is much more complex. The adrenergic autonomic nervous system is now thought to play a key role in modulating the inflammatory response in sepsis. In this study, we hypothesize that not only is the innate immune response enhanced in response to lipopolysaccharide (LPS) in aged animals, but that the adrenergic nervous system also plays a role in the release of excess inflammatory cytokines. MAIN
methodsMale Fischer-344 rats (young: 3 months; aged: 24 months) were used. Endotoxemia was induced by intravenous injection of lipopolysaccharide (LPS, 15 mg/kg BW). Splenic tissues were harvested and mRNA and protein were extracted. The protein expression of CD14 and TLR4, key mediators of LPS in the innate response, as well as alpha-2A adrenergic receptor (alpha(2A)-AR) and phosphodiesterase 4D (PDE4D), as the means by which the autonomic nervous system exerts its effects were analyzed. KEY
findingsSplenic tissue concentrations of alpha(2A)-AR, PDE4D, CD14, and TLR4 were significantly increased in septic aged rats as compared to aged sham rats and septic young rats. The increased expression of alpha(2A)-AR in septic aged rats was further confirmed by immunohistochemical staining of splenic tissues. SIGNIFICANCE: These data support the hypothesis that not only is the innate immune response increased in aged animals during sepsis, but that there is also an upregulated response of the adrenergic autonomic nervous system that contributes to excess proinflammatory cytokine release.
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