Differential inhibition of lipopolysaccharide-induced phenomena by anti-tumor necrosis factor alpha antibody.
Tumor necrosis factor alpha (TNF alpha) has been implicated as a major mediator of lipopolysaccharide (LPS)-induced phenomena. Administration to mice of a polyclonal, monospecific antibody prepared against recombinant murine TNF alpha abolished detection of LPS-induced TNF alpha activity and significantly reduced levels of LPS-induced colony-stimulating factor but failed to reduce the production of LPS-induced interferon, corticosterone, or LPS-induced hypoglycemia.
Department of Microbiology, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814.
S N
SN
Vogel
E A
EA
Havell
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D003115:Colony-Stimulating Factors / Q000097:blood; D003345:Corticosterone / Q000097:blood; D005260:Female; D007074:Immunoglobulin G / Q000502:physiology; D007372:Interferons / Q000097:blood; D008070:Lipopolysaccharides / Q000502:physiology*; D051379:Mice; D008810:Mice, Inbred C57BL; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis / Q000502:physiology*
D001786:Blood Glucose; D003115:Colony-Stimulating Factors; D007074:Immunoglobulin G; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D007372:Interferons; D003345:Corticosterone