Neuroimmunomodulation
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Neuroimmunomodulation · Jan 2007
ReviewNeuroimmunomodulation during exercise: role of catecholamines as 'stress mediator' and/or 'danger signal' for the innate immune response.
Exercise-induced neuroimmunomodulation is clearly accepted today. The present article reviews the main literature concerning the immunomodulatory capacity of catecholamines on the innate immune response during physical exercise, and presents our laboratory's latest results on this topic. ⋯ The exercise-induced stimulation of the phagocytic response in particular and the innate responses in general have been considered as a prevention strategy of the athlete's organism in order to prevent the entry and/or maintenance of antigens in a situation where the adaptive immune response seems to be depressed, and thus it has been suggested that catecholamines participate as a 'stress mediator' of these effects. Given this hypothesis, it is also suggested here that catecholamines may be the first 'danger signal' to the immune system during exercise-induced stress.
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Neuroimmunomodulation · Jan 2007
Role of histamine H3 and H4 receptors in mechanical hyperalgesia following peripheral nerve injury.
Histamine is a chemical mediator that acts at four known types of histamine receptors and has been widely implicated in the development of nociception and neuropathic pain. Blocking histamine H(1) and H(2) receptors has been shown to reduce hyperalgesia following nerve injury, but the role of histamine H(3) and H(4) receptors in neuropathic pain has not been studied. Here, we used blockers of histamine H(3) and H(4) receptors to assess their effects on neuropathic pain behavior and mast cell numbers following peripheral nerve injury. In addition, we assessed the effect of activating H(4) receptors on neuropathic pain behavior. ⋯ We propose that the increase in mechanical hyperalgesia produced by thioperamide and JNJ 7777120 and the decrease in mechanical hyperalgesia produced by VUF 8430 may represent a direct effect of these agents on mechanospecific primary afferents, or an indirect effect of these agents via injury-induced inflammation.