Let's take an overview of the etoh abuse
Ingested ethanol (EtOH) rapidly enters the bloodstream and freely enters
various tissue compartments. Chronic ethanol ingestion and metabolism
can lead to an altered cellular redox state due to increased production
of reactive oxygen species (ROS) by Kupffer cells (KC) and translocation
of bacteria and endotoxin (lipopolysaccharide, LPS). LPS signalling
through Toll-like receptor 4 (TLR4) leads to the release of pro-inflammatory cytokines (tumour-necrosis factor- (TNF-) and interleukin-1 (IL-1))
and chemokines (IL-8 and monocyte chemoattractant protein-1). These
events are thought to be crucial in the development of chronic liver
disease. Local production of TNF-
can also induce the local production of the suppressor of cytokine
signalling 3 (SOCS3), which can inhibit STAT (signal transducers and
activators of transcription) signalling and so lead to the resistance of
alcoholic liver disease patients to type-I interferons. Ethanol also
results in the loss of splenic and circulating T and B cells, partly
through apoptosis. In the lung compartment, ethanol suppresses the
production of pro-inflammatory cytokines by the alveolar macrophages
(AM) and of IL-17 by T cells in lung tissue or bronchiole-associated
lymphoid tissue (BALT), which results in a diminished cytokine/chemokine
cascade and hence defective polymorphonuclear leukocyte (PMN)
recruitment and host defence. NF-B, nuclear factor-B.
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