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- W2060948891 abstract "Age-associated defects in both B-lymphocytes and macrophages in elderly result in a reduction in the efficacy of vaccines to many Gram positive bacteria like Streptococcus pneumoniae. Splenic macrophages from aged mice have been shown to have a defect in production of pro-inflammatory cytokines (IL-6, IL-12, IL-1β, TNF-α) but exhibit increased production of IL-10 upon TLR-4 ligation. Here we showed that aged macrophages demonstrate similar cytokine dysregulation phenotype upon stimulation with TLR-2 ligands, or killed S. pneumoniae. We hypothesized that an age-associated increase in activity of phosphatidyl inositol 3-kinase (PI3K)-Akt signaling pathway may be playing a causal role in the age-associated cytokine dysregulation. We found that gene expression of both the regulatory (p85β) and the catalytic (p110δ) subunits of Class IA PI3K is higher in aged than in young splenic macrophages. The age-associated increase in the activity of PI3K was also demonstrated by an upregulation of P-Akt and its downstream target, glycogen synthase kinase-3 (GSK-3). Inhibition of PI3K enhanced induction of pro-inflammatory cytokines, by TLR-2/TLR-1, TLR-2/TLR-6 and TLR-4 ligands as well as heat killed S. pneumoniae (HKSP). Therefore, targeting PI3-Kinase could rescue cytokine dysregulation in aged macrophages and enhance the relevant pro-inflammatory cytokines needed to support B-cell activation and differentiation." @default.
- W2060948891 created "2016-06-24" @default.
- W2060948891 creator A5013597901 @default.
- W2060948891 creator A5050883853 @default.
- W2060948891 creator A5059343866 @default.
- W2060948891 creator A5091572691 @default.
- W2060948891 date "2011-06-01" @default.
- W2060948891 modified "2023-10-18" @default.
- W2060948891 title "Role of phosphoinositide 3-kinase–Akt signaling pathway in the age-related cytokine dysregulation in splenic macrophages stimulated via TLR-2 or TLR-4 receptors" @default.
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- W2060948891 doi "https://doi.org/10.1016/j.mad.2011.05.003" @default.
- W2060948891 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3155631" @default.
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