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Tumor necrosis factor‐α‐induced inflammatory responses in cattle
Author(s) -
KUSHIBIKI Shiro
Publication year - 2011
Publication title -
animal science journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.606
H-Index - 38
eISSN - 1740-0929
pISSN - 1344-3941
DOI - 10.1111/j.1740-0929.2011.00931.x
Subject(s) - tumor necrosis factor alpha , immune system , cytokine , inflammation , immunology , proinflammatory cytokine , lipopolysaccharide , biology , lactoferrin , genetics
Tumor necrosis factor‐alpha (TNF‐α) is recognized as a cytokine because of its involvement in inflammation‐mediated biological defense functions. Although TNF‐α is primarily produced by macrophages, it is also produced by other cells, including lymphocytes, Kupffer cells, natural killer cells and adipocytes. While TNF‐α has diverse immune system functions, including antitumor activity, antimicrobial activity and mediation of inflammation, it also regulates a number of physiological functions, including appetite, fever, energy metabolism and endocrine activity. Factors such as viruses, parasites, other cytokines, and endotoxins induce TNF‐α production. In combination with other cytokines, TNF‐α plays a clinically important role in cattle by mediating immune inflammatory responses such as mastitis and endotoxic shock. It has been reported that cytokines such as TNF‐α are involved in metabolic disease such as acidosis. On the other hand, several data suggest that lactoferrin (LF) acts to prevent the release of a number of inflammatory mediators from various activated cells, and further suggest that the prophylactic effect of LF involves inhibition of cytokine production, including TNF‐α, that are principal mediators of the inflammatory response leading to death from toxic shock. This review discusses the role of TNF‐α in pathological conditions in cattle, including infections and metabolic diseases caused by perturbation of metabolism and endocrine functions.