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Chunk #35 — Discussion

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The opposite effects of acute and chronic alcohol on lipopolysaccharide-induced inflammation are linked to IRAK-M in human monocytes.
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Unlike monocytes and Kupffer cells, chronic alcohol ingestion decreased TNF-α production (48) in alveolar macrophages that was related to oxidative stress, decreased glutathione availability, and decreased GM-CSF receptors (35). Because GM-CSF has been shown to result in loss of TLR tolerance, it is tempting to speculate that the persistent TNF-α hyporesponsiveness of alveolar macrophages after chronic alcohol use could be related to the decreased GM-CSFR signaling (35).