Depressed monocyte production of interleukin‐1 and tumor necrosis factor‐alpha in patients with alcoholic liver cirrhosis

Abstract

Interleukin-1 and tumor necrosis factor-alpha activity by E. coli lipopolysaccharide-triggered monocytes were studied in patients with chronic alcoholic liver disease. Monocytes from cirrhotic patients were shown to have a significant reduction in IL-I and TNF-a activity, compared with that from age-and sex-matched healthy controls. These findings indicate further immunoregulatory disturbances concerning alcoholic liver cirrhosis.

Expression of AXL receptor tyrosine kinase relates to monocyte dysfunction and severity of cirrhosis

“…Although we and others have previously focused on impaired innate immune responses after the onset of AD/ACLF, when infection susceptibility is highest (10, 12, 18, 20), it is barely known when and under which circumstances innate immune dysfunction occurs and infection susceptibility emerges during progression of cirrhosis and portal hypertension. Previous studies addressing phenotype and function of classical (CD14 + CD16 − ) and nonclassical (CD14 + CD16 + ) monocyte subsets in CLD showed inconsistent data regarding cytokine production and phagocytosis (31, 32, 33). We previously showed that inflammatory cytokine production was depressed not only in AD/ACLF but also in stable cirrhosis (18), whereas the underlying mechanism remained unexplained.…”

Production of inflammatory cytokines by peripheral blood monocytes in chronic alcoholism: Relationship with ethanol intake and liver disease

“…However, currently available information about the secretion and expression of inflammatory cytokines in alcoholic patients with liver cirrhosis remains controversial, and production of IL12 by monocytes from these individuals has not been analyzed so far in the literature. Reported studies show that ALC is associated with depressed secretion of IL1 (27,48,49) and TNFa (27,49) by both LPS-stimulated PB monocytes (27) and macrophages (49), which is even more pronounced among patients with severe ALC and malnutrition (48,49). In contrast, others have found an increased secretion of IL1 (50) and TNFa (50,51) by LPS-stimulated PB monocytes from ALC patients.…”

“…By contrast, ex vivo stimulation of peripheral blood (PB) monocytes and macrophages from chronic alcoholic patients without liver disease with LPS has been related to an increased secretion of IL1b, down-regulation of both TNFa and IL12 production by PB monocytes, (23) and TNFa secretion by alveolar macrophages (24). Concerning ALD, both a spontaneous and stimulated increase in the secretion of TNFa by monocytes has been reported in patients with alcoholic hepatitis (25,26), while in alcoholic liver cirrhosis (ALC) downregulation of IL1 and TNFa secretion by monocytes has been demonstrated (27).…”

A Multiplex Assay of 26 Cytokines Secreted by Blood Cells of Patients With Liver Cirrhosis

“…Относительно продукции провоспалительных цитокинов показано, что при алкогольных гепатитах секреция TNFα моноцитами крови действительно повышена [23]. В то же время при ЦП моноциты характерзуются сниженной секрецией IL-1 и TNFα [24]. Сходные данные о низкой спонтанной продукции моноцитами IL-1, IL-6, IL-12 и TNFα у пациентов с алкогольным ЦП были получены Laso F.J. c cоавт [20].…”