Elevated levels of IL-17 have been observed in ALD, correlating with the severity of hepatic inflammation and liver damage.66 IL-17 is heavily implicated in the recruitment of neutrophils to the liver, where it promotes alcohol-induced HCC by synergising with other inflammatory mediators.99 IL-17 amplifies the production of pro-inflammatory cytokines, including TNF- and IL-6, further driving the progression of liver injury.66 100 In patients with ALD, particularly those with AH and cirrhosis, IL-17-secreting cells, such as T lymphocytes and neutrophils, are abundant and significantly contribute to the inflammatory response.66 Studies have shown that HSCs expressing the IL-17 receptor can recruit neutrophils on IL-17 stimulation,66 promoting liver inflammation through the secretion of inflammatory mediators such as IL-8 and growth-related oncogene alpha.66 Blocking IL-17 has demonstrated protective effects in mouse models of alcohol-induced liver injury,67 including a reduction in voluntary alcohol consumption in alcohol-dependent mice,67 suggesting that targeting IL-17 could be a promising therapeutic strategy to attenuate liver inflammation and injury in ALD
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M.CattonC.et al
However, SapM shares only 16% identity with the closest classical alkaline phosphatase, Ec-AlkP, and lacks the characteristic catalytic motif present in alkaline phosphatases, DSA (D101, S102 and A103 in Ec-AlkP), where S is the nucleophile residue 25
However, these are not the only consequences of dysbiosis
