{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,10]],"date-time":"2026-03-10T11:30:04Z","timestamp":1773142204603,"version":"3.50.1"},"reference-count":51,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"4","license":[{"start":{"date-parts":[[2015,9,1]],"date-time":"2015-09-01T00:00:00Z","timestamp":1441065600000},"content-version":"tdm","delay-in-days":9284,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[1990,4]]},"abstract":"<jats:sec>\n            <jats:title\/>\n            <jats:p>The objective of this study was to analyze monokine production by peripheral blood mononuclear cells from patients with alcoholic cirrhosis. The capacity of peripheral blood mononuclear cells and purified monocytes from these patients to produce tumor necrosis factor \u03b1, interleukin 1\u03b2, and interleukin 6 was investigated. Spontaneous production of tumor necrosis factor \u03b1, interleukin 6 and interleukin 1\u03b2 was similar in cirrhotic and healthy subjects, but serum levels of interleukin 6 (&lt;2 U\/ml vs. 9.5 \u00b1 3 U\/ml) and tumor necrosis factor \u03b1 (3.1 \u00b1 1.2 pg\/ml vs. 12.0 \u00b1 1.2 pg\/ml) were significantly higher in cirrhotic patients. However, peripheral blood mononuclear cells or purified monocytes from patients with alcoholic liver cirrhosis, stimulated <jats:italic toggle=\"yes\">in vitro<\/jats:italic> with <jats:italic toggle=\"yes\">Escherichia coli<\/jats:italic> lipopolysaccharide, displayed a marked increase of tumor necrosis factor \u03b1, interleukin 1\u03b2 and interleukin 6 secretions compared with healthy controls. A striking feature of this overproduction was its reversibility as assessed by allowing cells to rest <jats:italic toggle=\"yes\">in vitro<\/jats:italic> without lipopolysaccharide for 1 to 7 days before stimulation. In such conditions, tumor necrosis factor \u03b1 and interleukin 6 secretions declined to levels present in healthy subjects in whom production remained stable, whereas interleukin 1\u03b2 secretion markedly decreased in both groups to the point where no difference could be seen. This reversible oversecretion of cytokines after lipopolysaccharide stimulation, along with the lack of abnormality of spontaneous cytokine secretion, suggests that monocytes in these patients may have undergone an <jats:italic toggle=\"yes\">in vivo<\/jats:italic> activation process analogous to a priming phenomenon. The <jats:italic toggle=\"yes\">in vitro<\/jats:italic> activation with lipopolysaccharide may represent the correlate of <jats:italic toggle=\"yes\">in vivo<\/jats:italic> endotoxemia observed during acute events such as sepsis. This might lead\u2013possibly through the recognized cytopathic and cytotoxic effects of excessive production of monokines\u2013to the decompensation of the underlying liver disease. Monokine oversecretion may also play a role in the pathogenesis and perpetuation of the disease and may be associated with clinical and biological features of cirrhosis such as cachexia, muscle wasting and hypergammaglobulinemia.(HEPATOLOGY 1990; 11:628:634.)<\/jats:p>\n          <\/jats:sec>","DOI":"10.1002\/hep.1840110416","type":"journal-article","created":{"date-parts":[[2007,3,3]],"date-time":"2007-03-03T23:15:53Z","timestamp":1172963753000},"page":"628-634","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":151,"title":["Excessive In Vitro Bacterial Lipopolysaccharide\u2013Induced Production of Monokines in Cirrhosis"],"prefix":"10.1097","volume":"11","author":[{"given":"Jacques","family":"Devi\u00e8re","sequence":"first","affiliation":[]},{"given":"Jean","family":"Content","sequence":"additional","affiliation":[]},{"given":"Chantal","family":"Denys","sequence":"additional","affiliation":[]},{"given":"Paul","family":"Vandenbussche","sequence":"additional","affiliation":[]},{"given":"Liliane","family":"Schandene","sequence":"additional","affiliation":[]},{"given":"Joseph","family":"Wybran","sequence":"additional","affiliation":[]},{"given":"Etienne","family":"Dupont","sequence":"additional","affiliation":[]}],"member":"276","reference":[{"key":"10.1002\/hep.1840110416-BIB1","doi-asserted-by":"crossref","first-page":"759","DOI":"10.7326\/0003-4819-60-5-759","volume":"60","author":"Austrian","year":"1964","journal-title":"Ann Intern Med"},{"key":"10.1002\/hep.1840110416-BIB2","doi-asserted-by":"crossref","first-page":"161","DOI":"10.1097\/00005792-197105000-00002","volume":"50","author":"Conn","year":"1971","journal-title":"Medicine"},{"key":"10.1002\/hep.1840110416-BIB3","first-page":"725","volume-title":"Diseases of the liver","author":"Conn","year":"1987","unstructured":". Cirrhosis. In: ed. Diseases of the liver. Sixth ed. Philadelphia: J. B. Lippincott Co., 1987: 725\u2013864."},{"key":"10.1002\/hep.1840110416-BIB4","first-page":"541","volume":"63","author":"Saxena","year":"1986","journal-title":"Clin Exp Immunol"},{"key":"10.1002\/hep.1840110416-BIB5","doi-asserted-by":"crossref","first-page":"577","DOI":"10.1002\/hep.1840070327","volume":"7","author":"Fuji","year":"1987","journal-title":"HEPATOLOGY"},{"key":"10.1002\/hep.1840110416-BIB6","first-page":"377","volume":"72","author":"Devi\u00e8re","year":"1988","journal-title":"Clin Exp Immunol"},{"key":"10.1002\/hep.1840110416-BIB7","first-page":"369","volume":"55","author":"Rodriguez","year":"1984","journal-title":"Clin Exp Immunol"},{"key":"10.1002\/hep.1840110416-BIB8","doi-asserted-by":"crossref","first-page":"992","DOI":"10.1016\/0016-5085(78)90668-6","volume":"75","author":"Wands","year":"1978","journal-title":"Gastroenterology"},{"key":"10.1002\/hep.1840110416-BIB9","doi-asserted-by":"crossref","first-page":"1417","DOI":"10.1084\/jem.167.4.1417","volume":"167","author":"Uyttenhoeve","year":"1988","journal-title":"J Exp Med"},{"key":"10.1002\/hep.1840110416-BIB10","first-page":"221","volume":"77","author":"Devi\u00e8re","year":"1989","journal-title":"Clin Exp Immunol"},{"key":"10.1002\/hep.1840110416-BIB11","first-page":"195","volume-title":"Inflammation: basic principles and clinical correlates","author":"Dinarello","year":"1988","unstructured":"Cytokines: interleukin 1 and tumor necrosis factor (cachectin). In: , , eds. Inflammation: basic principles and clinical correlates. 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