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- W2410068364 abstract "Abstract Lactic acid (LA) is elevated in tumors, asthma, and wound healing, environments that also include mast cells and IL-33. However, how LA affects mast cell function is unknown. Therefore we evaluated how LA modifies the IL-33-mediated mast cell response. When bone marrow derived mast cells were cultured with LA, we noted reduced IL-33-mediated cytokine production, an effect that was both monocarboxylate transporter (MCT)1- and pH-dependent. LA selectively decreased IL-33-induced TAK1, JNK, ERK, and NFkB phosphorylation, but not p38 activation. Additionally, LA increased HIF-1α expression. Since HIF-1α has been shown to regulate the pro-inflammatory microRNA miR-155, we examined miR-155 expression. miR-155-5p was reduced by LA, an effect that was reversed by HIF-1α antagonism. More importantly, miR-155-5p overexpression abolished the suppressive effects of LA. Additionally, the negative regulator SOCS1, a known miR-155 target, was elevated by LA addition. This suggests that LA employs HIF-1a to suppress miR-155, indirectly increasing SOCS-1 and limiting cytokine production. These data were recapitulated in vivo, since C57BL/6 mice injected with LA showed less IL-33-induced plasma cytokine levels than control mice. Lastly, LA suppressed IL-33-mediated human skin mast cell activation, an effect that was also MCT1-dependent. Our data demonstrate that lactic acid, present in inflammatory and malignant microenvironments, alters mast cell function to suppress inflammation." @default.
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- W2410068364 date "2016-05-01" @default.
- W2410068364 modified "2023-09-27" @default.
- W2410068364 title "Lactic acid inhibits IL-33-mediated mast cell inflammatory responses via HIF-1α suppressing miR-155 expression" @default.
- W2410068364 doi "https://doi.org/10.4049/jimmunol.196.supp.202.8" @default.
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