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      Corticosterone Changes in Response to Stressors, Acute and Protracted Actions of Tumor Necrosis Factor-α, and Lipopolysaccharide Treatments in Mice Lacking the Tumor Necrosis Factor-α p55 Receptor Gene

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          Systemic administration of the proinflammatory cytokine, tumor necrosis factor-α (TNF-α), has acute as well as sensitizing effects on behavioral and neurochemical functioning. Objectives: As many of the central consequences of TNF-α are mediated by its p55 receptor, the present investigation determined the role of this receptor on the plasma corticosterone increase associated with the acute TNF-α treatment and the sensitized response evident upon reexposure to the cytokine. Moreover, the role of p55 in the provocation of corticosterone release engendered by lipopolysaccharide (LPS) and psychogenic stressors (noise or restraint) was also determined. Methods: Plasma corticosterone levels were determined in wild-type and p55-deficient mice that received systemic treatments with TNF-α and LPS, as well as exposure to auditory and restraint stressors. Results: Mice deficient for p55 displayed a greatly attenuated plasma corticosterone response to TNF-α irrespective of whether they had been previously exposed to the cytokine. In contrast, p55 deletion did not affect corticosterone responses elicited by LPS and by stressors. Conclusions: It appears that although p55 modulates the corticosterone-inducing effects of TNF-α, the receptor does not play a critical role in the activation of the HPA axis by ‘traditional’ psychogenic stressors (noise, restraint) or systemic endotoxin challenge.

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          Most cited references 13

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          Effects of circulating tumor necrosis factor on the neuronal activity and expression of the genes encoding the tumor necrosis factor receptors (p55 and p75) in the rat brain: a view from the blood–brain barrier

           S Rivest,  S Nadeau (1999)
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            Cytokines and antibody responses during Trypanosoma congolense infections in two inbred mouse strains that differ in resistance.

            We studied IL-4, IL-10 and IFN-gamma secretion by splenocytes and the plasma levels of different isotypes of antibodies against various antigens of Trypanosoma congolense in highly susceptible BALB/c and relatively resistant C57BL/6 mice during the early course of infection with T. congolense. The patterns of appearance of cytokine spotforming cells in the spleens were essentially similar in the two mouse strains although higher numbers were detected in the spleens of BALB/c than C57BL/6 mice on some days post-infection. However, the amount of IL-4, IL-10 and IFN-gamma secreted into the culture fluids was dramatically different. From day 4 forward, splenocytes from BALB/c mice secreted very high levels of these cytokines. In contrast, splenocytes from infected C57BL/6 mice did not secrete detectable levels of IL-4 throughout the period tested. The secretion of IL-10 and IFN-gamma by C57BL/6 splenocytes only became appreciable on day 6 and was down-regulated by day 8, when the first wave of parasitaemia was being controlled. At days 6-8, splenocytes from infected C57BL/6 mice secreted two-fold higher amounts of IL-12 p40 than those from BALB/c mice. Infected BALB/c mice mounted an earlier IgM antibody response to variant surface glycoprotein (VSG), formalin-fixed T. congolense and whole T. congolense lysates than did infected C57BL/6 mice. However, they failed to make any detectable IgG3 and IgG2a antibody responses to these antigens whereas infected C57BL/6 mice made strong IgG3 and IgG2a responses. We speculate that enhanced resistance against T. congolense infections in mice may be mediated by IL-12 dependent synthesis of IgG2 antibodies to VSG and possibly also common trypanosomal antigens.
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              The role of interleukin-1 and tumor necrosis factor α in the neurochemical and neuroendocrine responses to endotoxin

               Adrian Dunn (1992)

                Author and article information

                S. Karger AG
                July 2004
                09 July 2004
                : 11
                : 4
                : 241-246
                aInstitute of Neuroscience, Carleton University, bNeuroscience Research Institute, University of Ottawa, Ottawa, Ont., Canada
                78442 Neuroimmunomodulation 2004;11:241–246
                © 2004 S. Karger AG, Basel

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                Figures: 3, References: 31, Pages: 6
                Original Paper


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