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• W2022339604 abstract "Circulating levels of leptin are elevated in type-2 diabetes mellitus (T2DM) and leptin plays a role in immune responses. Elevated circulating IL-18 levels are associated with clinical complications of T2DM. IL-18 regulates cytokine secretion and the function of a number of immune cells including T-cells, neutrophils and macrophages and as such has a key role in immunity and inflammation. Pro-inflammatory monocytes exhibiting elevated cytokine secretion are closely associated with inflammation in T2DM, however, little is known about the role of leptin in modifying monocyte IL-18 secretion. We therefore aimed to investigate the effect of leptin on IL-18 secretion by monocytes. We report herein that leptin increases IL-18 secretion in THP-1 and primary human monocytes but has no effect on IL-18 mRNA. Leptin and LPS signalling in monocytes occurs by overlapping but distinct pathways. Thus, in contrast to a strong stimulation by LPS, leptin has no effect on IL-1β mRNA levels or IL-1β secretion. In addition, LPS stimulates the secretion of IL-6 but leptin did not whereas both treatments up regulate IL-8 secretion from the same cells. Although leptin (and LPS) has a synergistic effect with exogenous ATP on IL-18 secretion in both THP-1 and primary monocytes, experiments involving ATP assays and pharmacological inhibition of ATP signalling failed to provide any evidence that endogenous ATP secreted by leptin-stimulated monocytes was responsible for enhancement of monocyte IL-18 secretion by leptin. Analysis of the action of caspase-1 revealed that leptin up regulates caspase-1 activity and the effect of leptin on IL-18 release is prevented by caspase-1 inhibitor (Ac-YVAD-cmk). These data suggest that leptin activates IL-18 processing rather than IL-18 transcription. In conclusion, leptin enhances IL-18 secretion via modulation of the caspase-1 inflammasome function and acts synergistically with ATP in this regard. This process may contribute to aberrant immune responses in T2DM and other conditions of hyperleptinemia." @default.
• W2022339604 created "2016-06-24" @default.
• W2022339604 creator A5003077380 @default.
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• W2022339604 date "2014-02-01" @default.
• W2022339604 modified "2023-09-25" @default.
• W2022339604 title "Leptin enhances the secretion of interleukin (IL)-18, but not IL-1β, from human monocytes via activation of caspase-1" @default.
• W2022339604 cites W1484335948 @default.
• W2022339604 cites W1514081838 @default.
• W2022339604 cites W1547420341 @default.
• W2022339604 cites W1561511271 @default.
• W2022339604 cites W1605844554 @default.
• W2022339604 cites W1824528611 @default.
• W2022339604 cites W1925191409 @default.
• W2022339604 cites W1927491384 @default.
• W2022339604 cites W1967855498 @default.
• W2022339604 cites W1984553097 @default.
• W2022339604 cites W1985016679 @default.
• W2022339604 cites W1987535382 @default.
• W2022339604 cites W1993026721 @default.
• W2022339604 cites W1994621482 @default.
• W2022339604 cites W1995898826 @default.
• W2022339604 cites W1995970556 @default.
• W2022339604 cites W2007506634 @default.
• W2022339604 cites W2008768221 @default.
• W2022339604 cites W2010072332 @default.
• W2022339604 cites W2011128327 @default.
• W2022339604 cites W2012270515 @default.
• W2022339604 cites W2015808968 @default.
• W2022339604 cites W2020626901 @default.
• W2022339604 cites W2023710365 @default.
• W2022339604 cites W2026155294 @default.
• W2022339604 cites W2028017703 @default.
• W2022339604 cites W2040248629 @default.
• W2022339604 cites W2049735903 @default.
• W2022339604 cites W2050209877 @default.
• W2022339604 cites W2051529467 @default.
• W2022339604 cites W2053446303 @default.
• W2022339604 cites W2055528092 @default.
• W2022339604 cites W2056843503 @default.
• W2022339604 cites W2059926508 @default.
• W2022339604 cites W2060282267 @default.
• W2022339604 cites W2064876520 @default.
• W2022339604 cites W2065330071 @default.
• W2022339604 cites W2065391130 @default.
• W2022339604 cites W2069038722 @default.
• W2022339604 cites W2076854360 @default.
• W2022339604 cites W2090859543 @default.
• W2022339604 cites W2099790921 @default.
• W2022339604 cites W2107216319 @default.
• W2022339604 cites W2107277218 @default.
• W2022339604 cites W2110603890 @default.
• W2022339604 cites W2112884350 @default.
• W2022339604 cites W2116594981 @default.
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• W2022339604 cites W2120247510 @default.
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• W2022339604 cites W2125510262 @default.
• W2022339604 cites W2130200649 @default.
• W2022339604 cites W2133895102 @default.
• W2022339604 cites W2142431039 @default.
• W2022339604 cites W2149168766 @default.
• W2022339604 cites W2149371927 @default.
• W2022339604 cites W2154579584 @default.
• W2022339604 cites W2161526125 @default.
• W2022339604 cites W2162035041 @default.
• W2022339604 cites W2162668563 @default.
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• W2022339604 doi "https://doi.org/10.1016/j.cyto.2013.10.008" @default.
• W2022339604 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24275551" @default.
• W2022339604 hasPublicationYear "2014" @default.
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