Journal ArticleDOI
The inflammatory response in interleukin-1 beta-deficient mice: comparison with other cytokine-related knock-out mice.
TLDR
Although IL‐1β‐deficient mice respond normally to the systemic administration of lipopolysaccharide (LPS), they do not develop an acute‐phase response in the localized tissue damage model of turpentine injection.Abstract:
Interleukin-1 (IL-1) plays a crucial role in the development of the pathophysiological responses to infection and inflammation. However, the relative contributions of IL-1 alpha and IL-1 beta remain to be clarified. IL-1 beta-deficient mice are a powerful tool to investigate the specific role of IL-1 beta in various experimental conditions. In this report, we summarize the response of IL-1 beta deficient mice to two different inflammatory stimuli, turpentine and endotoxin. Although IL-1 beta-deficient mice respond normally to the systemic administration of lipopolysaccharide (LPS), they do not develop an acute-phase response in the localized tissue damage model of turpentine injection. The results obtained using the IL-1 beta-deficient mice are compared here with those observed in the IL-1 beta-converting enzyme-deficient, IL-6-deficient, tumour necrosis factor-receptor p55-deficient, and interferon-gamma-receptor-deficient mice.read more
Citations
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Journal ArticleDOI
Regulation of the Hypothalamic-Pituitary-Adrenal Axis by Cytokines: Actions and Mechanisms of Action
TL;DR: Findings are reviewed that have documented which cytokines have been shown to influence hormone secretion from the HPA axis, determined under what physiological/pathophysiological circumstances endogenous cytokines regulate HPAaxis activity, established the possible sites of cytokine action on HPA Axis hormone secretion, and identified the potential neuroanatomic and pharmacological mechanisms by which cytokine signal the neuroendocrine hypothalamus.
Journal ArticleDOI
Role of IL-6 and Its Soluble Receptor in Induction of Chemokines and Leukocyte Recruitment
Maria Romano,Marina Sironi,Carlo Toniatti,Nadia Polentarutti,Paolo Fruscella,Pietro Ghezzi,Raffaella Faggioni,Walter Luini,Victor W.M. van Hinsbergh,Silvano Sozzani,Federico Bussolino,Valeria Poli,Gennaro Ciliberto,Alberto Mantovani,Alberto Mantovani +14 more
TL;DR: In vivo and in vitro evidence supports the concept that the IL-6 system plays an unexpected positive role in local inflammatory reactions by amplifying leukocyte recruitment.
Journal ArticleDOI
Production of Mice Deficient in Genes for Interleukin (IL)-1α, IL-1β, IL-1α/β, and IL-1 Receptor Antagonist Shows that IL-1β Is Crucial in Turpentine-induced Fever Development and Glucocorticoid Secretion
Reiko Horai,Masahide Asano,Katsuko Sudo,Hirotaka Kanuka,Masatoshi Suzuki,Masugi Nishihara,Michio Takahashi,Yoichiro Iwakura +7 more
TL;DR: IL-1β but not IL-1α is crucial in febrile and neuro-immuno-endocrine responses, and that this is because IL- 1α expression in the brain is dependent on IL-2β, as well as in peritoneal macrophages stimulated with lipopolysaccharide in vitro.
Journal ArticleDOI
Regulation of Cytochromes P450 During Inflammation and Infection
TL;DR: In contrast to the down-regulation of P450s in the liver, the induction of several forms in this and other tissues suggests a more specific homeostatic role of these effects, e.g., in generation or catabolism of bioactive metabolites.
Journal ArticleDOI
Exposure to acute stress induces brain interleukin-1beta protein in the rat
Kien T. Nguyen,Terrence Deak,Stephanie M. Owens,Tadahiko Kohno,Monika Fleshner,Linda R. Watkins,Steven F. Maier +6 more
TL;DR: Elimination of the stress-induced rise in corticosterone unmasked a robust and widespread increase in brain IL-1β, possibly suppressed by the rapid and prolonged high levels of glucocorticoids produced by IS.
References
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Journal ArticleDOI
Impaired immune and acute-phase responses in interleukin-6-deficient mice
Manfred Kopf,Heinz Baumann,Giulia Freer,Marina A. Freudenberg,Marinus C. Lamers,Tadamitsu Kishimoto,Rolf M. Zinkernagel,Horst Bluethmann,Georges Köhler +8 more
TL;DR: It is concluded that IL-6 production induced by injury or infection is an important in vivo SOS signal which coordinates activities of liver cells, macrophages and lymphocytes.
Journal ArticleDOI
Mice deficient for the 55 kd tumor necrosis factor receptor are resistant to endotoxic shock, yet succumb to L. monocytogenes infection.
Klaus Pfeffer,Toshifumi Matsuyama,Thomas M. Kündig,Andrew Wakeham,Kenji Kishihara,Arda Shahinian,Katja Wiegmann,Pamela S. Ohashi,Martin Krönke,Tak W. Mak +9 more
TL;DR: The TNFRp55 function renders mice resistant to lethal dosages of either lipopolysaccharides or S. aureus enterotoxin B, and the 55 kd TNFR plays a decisive role in the host's defense against microorganisms and their pathogenic factors.
Journal ArticleDOI
Immunoregulatory feedback between interleukin-1 and glucocorticoid hormones
TL;DR: The results strongly support the existence of an immunoregulatory feedback circuit in which IL-1 acts as an afferent and glucocorticoid as an efferent hormonal signal in which the pituitary-adrenal axis is stimulated.
Journal ArticleDOI
Tumor necrosis factor (cachectin) is an endogenous pyrogen and induces production of interleukin 1
Charles A. Dinarello,Joseph G. Cannon,Sheldon M. Wolff,H A Bernheim,Bruce Beutler,Anthony Cerami,Irene S. Figari,Michael A. Palladino,O'connor John +8 more
TL;DR: These studies show that TNF (cachectin) is another endogenous pyrogen which, like IL-1 and IFN-alpha, directly stimulate hypothalamic PGE2 synthesis and is an endogenous inducer ofIL-1.
Journal ArticleDOI
Mice deficient in IL-1β-converting enzyme are defective in production of mature IL-1β and resistant to endotoxic shock
Ping Li,Hamish Allen,Subhashis Banerjee,Simon Franklin,Linda Herzog,Cynthia Johnston,Jack McDowell,Michael Paskind,Laura Rodman,Jochen G. Salfeld,Elizabeth Towne,Daniel E. Tracey,Scott Wardwell,Feng-Yi Wei,Winnie W. Wong,Robert Kamen,Tara Seshadri +16 more
TL;DR: IL-1β-converting enzyme (ICE) plays a dominant role in the generation of mature IL- 1β, a previously unsuspected role in production of IL-1α, but has no autonomous function in apoptosis.