[Various aspects of IL-1 biological activity. II. IL-1 beta in diseases and the Central Nervous System].
Precise understanding of the mechanisms of reciprocal relations between the nervous and the immune systems, has been the subject of numerous studies for the recent two decades. These mechanisms are significant, particularly at the stage of early response to bacterial, parasite, or viral infections. They are also essential from the medical point of view, as they may help in the development of the new methods of treatment of infectious diseases, and also may provide better methods to neutralize possible side effects of the therapy. As it is commonly understood, both forms of IL-1 (alpha and beta), play an important role as a signaling molecules in these mechanisms. Regardless of the route of administration, they cause to the activation of the brain neurotransmitters, and the hypothalamo-pituitary-adrenal-axis (HPA). The HPA response induced by activity of the immune system is a normal, physiological phenomenon with essential meaning. It gives the negative feedback where glucocorticoids, released from the adrenal cortex, inhibit activity of the immune system, and by this reduce the probability of the over-stimulation of this system and its self-aggression. Therefore, precise recognition of the mechanism which is the indicator of influence of cytokines on the brain and also leads to initiate that response has a significant scientific and practical meaning. Also, the two mechanisms are probably the most important, and under appropriate conditions could complement each other. These are enzymatic and neural ways by which immune system influences the brain. The former predicts, that Il-1 influences the tissue, stimulating them to the synthesis, via the cyclooxygenases (COX) activation, and release molecules such as prostaglandines (especially PGE2), which have the ability to penetrate the brain barrier. The latter assumes that IL-1, directly or indirectly, can influence the peripheral nerves (the most important is probably the vagus nerve), which afferent sensory endings subsequently send signals to the brain. The results of many experiments (including the authors' own) indicate that both mentioned above ways take part in the mechanism of the communication between the immune and the nervous systems. These point out that signaling via the vagus nerve and via COX may contribute to the effects of IL-1 administration on animals behavior, and the activation of HPA axis and brain neurochemistry. However, the vagal pathway and the COX-system appear to substitute each other during infections or pathogens invasion. The experimantal data also suggest that these two mechanisms by which IL-1 can affect the brain are probably the most important ones, by which the immune system influences the nervous system.
Wieczorek
Marek
M
Zakład Neurofizjologii, Uniwersytet Łódzki, ul. Rewolucji 1905 r 66, 90-222 Łódź. marek@biol.uni.lodz.pl
D000818:Animals; D001921:Brain / Q000378:metabolism*; D016207:Cytokines / Q000378:metabolism; D015232:Dinoprostone / Q000378:metabolism; D006801:Humans; D007030:Hypothalamo-Hypophyseal System / Q000378:metabolism; D007239:Infections / Q000276:immunology*; D007375:Interleukin-1 / Q000378:metabolism*; D053583:Interleukin-1beta / Q000378:metabolism*; D007376:Interleukin-2 / Q000378:metabolism*; D010913:Pituitary-Adrenal System / Q000378:metabolism; D015398:Signal Transduction / Q000276:immunology*; D014630:Vagus Nerve / Q000378:metabolism
D016207:Cytokines; D007375:Interleukin-1; D053583:Interleukin-1beta; D007376:Interleukin-2; D015232:Dinoprostone