Lymphotoxin-alpha (TNF-beta) during sepsis.
T cell release of lymphotoxin-alpha (LT-alpha, or TNF-beta) is stimulated by pyrogenic exotoxins of Gram-positive bacteria and mitogens. In contrast to TNF-alpha, it is unknown whether LT-alpha plays any role in the pathogenesis of sepsis and, in particular, the pathogenesis of Gram-positive sepsis. Sera from patients with sepsis were examined for LT-alpha and compared with normal volunteers and pregnant women. LT-alpha was detected in 33% of sepsis sera (mean 608.4 pg/ml SE 306), 16% of normal sera (mean 167 pg/ml SE 87) and 23% of sera from pregnant women (mean 714 pg/ml SE 191). These differences were not significant and there were no differences within sepsis sera when grouped by the type of causative organism, or disease severity. LT-alpha detected by immunoassay in serum was not bioactive, in contrast to that produced in cell culture. Recombinant soluble TNF receptors (rSTNFR) neutralized the bioactivity of recombinant LT-alpha at rSTNFR concentrations which did not interfere with immunoreactivity and which are known to prevail in vivo. Hence, LT-alpha is unlikely to have a critical role in the pathogenesis of sepsis. Much of the potential bioactivity of this lymphokine may be abrogated by TNFR in serum.
Sriskandan
S
S
Department of Infectious Diseases & Bacteriology, Royal Postgraduate Medical School, London, UK.
Moyes
D
D
Lemm
G
G
Cohen
J
J
D000818:Animals; D015703:Antigens, CD; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D007739:L Cells; D008233:Lymphotoxin-alpha / Q000097:blood*; D051379:Mice; D011247:Pregnancy; D018124:Receptors, Tumor Necrosis Factor; D047888:Receptors, Tumor Necrosis Factor, Type I; D018805:Sepsis / Q000097:blood* / Q000276:immunology
D015703:Antigens, CD; D008233:Lymphotoxin-alpha; D018124:Receptors, Tumor Necrosis Factor; D047888:Receptors, Tumor Necrosis Factor, Type I