{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T13:55:39Z","timestamp":1791122139760,"version":"4.1.0"},"reference-count":43,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"5","license":[{"start":{"date-parts":[[2015,9,1]],"date-time":"2015-09-01T00:00:00Z","timestamp":1441065600000},"content-version":"tdm","delay-in-days":9070,"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":[[1990,11]]},"abstract":"<jats:sec>\n            <jats:title\/>\n            <jats:p>We investigated lipopolysaccharide-induced tumor necrosis factor production <jats:italic toggle=\"yes\">in vitro<\/jats:italic> by peripheral blood monocytes from patients with various liver diseases. Tumor necrosis factor production was found to be significantly reduced in patients with chronic hepatitis B (n = 17; 135 \u00b1 30 pg tumor necrosis factor\/ml; mean \u00b1 S.E.M.) and patients with chronic non-A, non-B hepatitis (n = 15; 212 \u00b1 22 pg tumor necrosis factor\/ml) compared with healthy control individuals (n = 47; 411 \u00b1 40 pg tumor necrosis factor\/ml; p &lt; 0.0005 and p &lt; 0.01, respectively). This reduced tumor necrosis factor production was not only seen with an optimal stimulating concentration of lipopolysaccharide (100 ng\/ml) but also with suboptimal concentrations (0.1 ng\/ml). In contrast to patients with chronic viral hepatitis, monocytes from patients with alcohol-induced cirrhosis (n = 26; 444 \u00b1 49 pg tumor necrosis factor\/ml), primary biliary cirrhosis (n = 7; 412 \u00b1 81 pg tumor necrosis factor\/ml) and alcohol-induced fatty liver changes (n = 5; 401 \u00b1 62 pg tumor necrosis factor\/ml) produced normal amounts of tumor necrosis factor when stimulated with an optimal concentration of lipopolysaccharide. Lipopolysaccharide (0.1 ng lipopolysaccharide\/ml)\u2014 stimulated peripheral blood monocytes of patients with chronic hepatitis B (n = 15; 102 \u00b1 32 pg\/ml) or non-A, non-B hepatitis (n = 13; 97 \u00b1 16 pg\/ml) could not be induced to produce more tumor necrosis factor either when prestimulated with \u03b3-interferon (170 \u00b1 45 pg\/ml and 149 \u00b1 32 pg\/ml, respectively), a lymphokine known to activate monocytes, or with the cyclooxygenase inhibitor indomethacin to reduce the suppressive effect of prostaglandin E<jats:sub>2<\/jats:sub> (148 \u00b1 40 pg\/ml and 153 \u00b1 45 pg\/ml, respectively). In contrast, patients with alcoholic cirrhosis (n = 11; 178 \u00b1 31 ng tumor necrosis factor\/ml) showed significant increase of tumor necrosis factor production by lipopolysaccharide-stimulated monocytes when prestimulated with \u03b3-interferon (n = 11; 395 \u00b1 80 pg tumor necrosis factor\/ml; p &lt; 0.025) or indomethacin (n = 11; 393 \u00b1 82 pg tumor necrosis factor\/ml; p &lt; 0.05). A significant reduction in lipopolysaccharide-induced tumor necrosis factor production by peripheral blood monocytes was observed in acute hepatitis B but not in acute hepatitis A or non-A, non-B hepatitis. These investigations suggest that lipopolysaccharide-induced tumor necrosis factor production by peripheral blood monocytes is impaired in patients with chronic viral hepatitis and acute hepatitis B. (HEPATOLOGY 1990;12:1118-1124).<\/jats:p>\n          <\/jats:sec>","DOI":"10.1002\/hep.1840120507","type":"journal-article","created":{"date-parts":[[2007,3,3]],"date-time":"2007-03-03T23:47:02Z","timestamp":1172965622000},"page":"1118-1124","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":17,"title":["Impaired lipopolysaccharide-inducible tumor necrosis factor production in vitro by peripheral blood monocytes of patients with viral hepatitis"],"prefix":"10.1097","volume":"12","author":[{"given":"Christian","family":"M\u00fcller","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christoph C.","family":"Zielinski","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"10.1002\/hep.1840120507-BIB1","doi-asserted-by":"crossref","first-page":"213","DOI":"10.1016\/S0065-2776(08)60846-9","volume":"42","author":"Beutler","year":"1988","journal-title":"Adv Immunol"},{"key":"10.1002\/hep.1840120507-BIB2","doi-asserted-by":"crossref","first-page":"584","DOI":"10.1038\/320584a0","volume":"320","author":"Beutler","year":"1986","journal-title":"Nature"},{"key":"10.1002\/hep.1840120507-BIB3","doi-asserted-by":"crossref","first-page":"413","DOI":"10.1093\/infdis\/157.3.413","volume":"157","author":"Tracey","year":"1988","journal-title":"J Infect Dis"},{"key":"10.1002\/hep.1840120507-BIB4","doi-asserted-by":"crossref","first-page":"1786","DOI":"10.4049\/jimmunol.138.6.1786","volume":"138","author":"Scheurich","year":"1987","journal-title":"J Immunol"},{"key":"10.1002\/hep.1840120507-BIB5","doi-asserted-by":"crossref","first-page":"2639","DOI":"10.4049\/jimmunol.140.8.2639","volume":"140","author":"Hackett","year":"1988","journal-title":"J Immunol"},{"key":"10.1002\/hep.1840120507-BIB6","doi-asserted-by":"crossref","first-page":"786","DOI":"10.1084\/jem.166.3.786","volume":"166","author":"Kehrl","year":"1987","journal-title":"J Exp Med"},{"key":"10.1002\/hep.1840120507-BIB7","doi-asserted-by":"crossref","first-page":"3676","DOI":"10.4049\/jimmunol.139.11.3676","volume":"139","author":"Ghiara","year":"1987","journal-title":"J Immunol"},{"key":"10.1002\/hep.1840120507-BIB8","doi-asserted-by":"crossref","first-page":"850","DOI":"10.1016\/S0140-6736(72)92212-X","volume":"2","author":"Giustino","year":"1972","journal-title":"Lancet"},{"key":"10.1002\/hep.1840120507-BIB9","first-page":"257","volume":"57","author":"Hanson","year":"1984","journal-title":"Clin Exp Immunol"},{"key":"10.1002\/hep.1840120507-BIB10","doi-asserted-by":"crossref","first-page":"510","DOI":"10.1016\/0016-5085(81)90013-5","volume":"80","author":"Kawanishi","year":"1981","journal-title":"Gastroenterology"},{"key":"10.1002\/hep.1840120507-BIB11","first-page":"361","volume":"45","author":"Serdengecti","year":"1981","journal-title":"Clin Exp Immunol"},{"key":"10.1002\/hep.1840120507-BIB12","first-page":"17","volume":"20","author":"Newble","year":"1975","journal-title":"Clin Exp Immunol"},{"key":"10.1002\/hep.1840120507-BIB13","doi-asserted-by":"crossref","first-page":"638","DOI":"10.1002\/hep.1840030503","volume":"3","author":"Brattig","year":"1983","journal-title":"Hepatology"},{"key":"10.1002\/hep.1840120507-BIB14","doi-asserted-by":"crossref","first-page":"202","DOI":"10.1002\/hep.1840020203","volume":"2","author":"Thomas","year":"1982","journal-title":"Hepatology"},{"key":"10.1002\/hep.1840120507-BIB15","doi-asserted-by":"crossref","first-page":"928","DOI":"10.1002\/hep.1840100606","volume":"10","author":"M\u00fcller","year":"1989","journal-title":"Hepatology"},{"key":"10.1002\/hep.1840120507-BIB16","doi-asserted-by":"crossref","first-page":"205","DOI":"10.1136\/adc.64.2.205","volume":"64","author":"M\u00fcller","year":"1989","journal-title":"Arch Dis Child"},{"key":"10.1002\/hep.1840120507-BIB17","doi-asserted-by":"crossref","first-page":"168","DOI":"10.1016\/S0046-8177(86)80290-8","volume":"17","author":"Paronetto","year":"1986","journal-title":"Hum Pathol"},{"key":"10.1002\/hep.1840120507-BIB18","first-page":"50","volume-title":"The liver and portal hypertension","author":"Child","year":"1984","unstructured":". 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