Publication: Travmatik beyin hasarında inflamatuvar sitokinlerin rolü
Abstract
Travmatik beyin hasarı dünyada, 45 yaş altı bireylerde mortalite ve morbiditenin başlıca nedenlerinden biridir. Oluşan bu birincil lezyonlardan daha çok, esas olarak, bu direkt etkinin başlattığı ikincil süreç, mortalite ve morbiditeden sorumludur ve teröpatik müdahalelere de duyarlıdır. Birincil ve ikincil patofizyolojik süreçlerin her ikisi de hücresel mediatörlerin (proinflamatuvar sitokinler, prostaglandinler, serbest radikaller ve komplemanlar) salınımına, adezyon moleküllerinin ekspresyonuna, savunma ve glial hücrelerinin kemotaksisine ve transmigrasyonuna neden olmaktadır. Travmatik beyin hasarından sonra proinflamatuvar sitokinlerin üretimi ve sekresyonu hem insan hem de deneysel hayvan modellerinde gösterilmiştir. Beyinde travmadan sonra interlökin 1, interlökin 6, tümör nekroz faktör ve santral sinir sistemi kaynaklı sitokinlerin yüksek konsantrasyonlarda saptanması onların travmayı takiben gelişen patolojik süreçte önemli rol oynadıklarını düşündürmektedir. Bu sitokinlerinlerin hasar sürecinde oynadığı rolü bilmek ve geliştirilecek uygun ajanlar ile kendi kendine ilerleyici bu süreci bir noktada durdurmak yani nöronal hasarı azaltmak, kafa travmasında hayat kurtarıcı olabilir. (Marmara Üniversitesi Tıp Fakültesi Dergisi 2012;25:114-7)
Traumatic brain injury is one of the main causes of mortality and morbidity in <45 years old population in the world. Besides the primary lesions, the secondary process initiated by the direct effect is responsible for mortality and morbidity, and sensitive to the therapy. Both the primary and secondary processes cause the release of cell mediators (proinflammatory cytokines, prostaglandins, free radicals and complement system), expression of adhesion molecules, chemotaxis and transmigration of glial and defence cells. The secretion and production of proinflammatory cytokines after traumatic brain injury has been seen in both human and experimental animal models. The high concentration of interleukin-1, interleukin 6, tumor necrosis factor and central nervous system cytokines show that they play important role in the posttraumatic pathological process. Finding out what roles they have in the damage process, and stoppping this spontaneous progression thereby reducing the neuronal damage, may be life-saving in the head trauma. (Marmara Medical Journal 2012;25:114-7)
Traumatic brain injury is one of the main causes of mortality and morbidity in <45 years old population in the world. Besides the primary lesions, the secondary process initiated by the direct effect is responsible for mortality and morbidity, and sensitive to the therapy. Both the primary and secondary processes cause the release of cell mediators (proinflammatory cytokines, prostaglandins, free radicals and complement system), expression of adhesion molecules, chemotaxis and transmigration of glial and defence cells. The secretion and production of proinflammatory cytokines after traumatic brain injury has been seen in both human and experimental animal models. The high concentration of interleukin-1, interleukin 6, tumor necrosis factor and central nervous system cytokines show that they play important role in the posttraumatic pathological process. Finding out what roles they have in the damage process, and stoppping this spontaneous progression thereby reducing the neuronal damage, may be life-saving in the head trauma. (Marmara Medical Journal 2012;25:114-7)