芝加哥Loyola大學(xué)Stritch醫(yī)學(xué)院的一項(xiàng)研究結(jié)果中包含了一些有關(guān)煙霧吸入性損傷患者免疫系統(tǒng)的令人意想不到的發(fā)現(xiàn)。
與預(yù)想的相反,跟那些存活的患者相比,因煙霧吸入性損傷致死患者其肺部有較低水平的炎癥反應(yīng).
"或許,更好地了解這一早期肺免疫功能低下能夠引發(fā)一些更好的療法,以進(jìn)一步提高燒傷護(hù)理的成果."
研究結(jié)果發(fā)表于1-2月刊的《燒傷護(hù)理研究》（JBCR）上,。第一作者為Loyola燒傷及休克創(chuàng)傷研究所Christopher S.Davis醫(yī)師,，通訊作者為燒傷及休克創(chuàng)傷研究所主任Elizabeth J.Kovacs博士,。
研究人員對Loyola燒傷中心的60位燒傷患者進(jìn)行了追蹤調(diào)查,。正如所料,，在重癥病房及醫(yī)院中,，燒傷結(jié)合煙霧吸入性損傷（一種最嚴(yán)重的情況）的患者需要更長時(shí)間的使用呼吸機(jī),。這些患者也更容易死亡,，盡管這項(xiàng)結(jié)果差一點(diǎn)點(diǎn)就達(dá)到顯著的統(tǒng)計(jì)學(xué)意義。
也如其所料,，與存活下來的人相比,，那些死去的患者年齡都較大并有更大的損傷。
但免疫系統(tǒng)的結(jié)果卻出乎意料,。研究者收集了燒傷和煙霧吸入性損傷14小時(shí)內(nèi)的患者肺部液體,，檢測了其中28種免疫系統(tǒng)調(diào)節(jié)因子的水平。
這些調(diào)節(jié)因子是由白細(xì)胞和其他一些沿著呼吸道排列的細(xì)胞生產(chǎn)的蛋白質(zhì),。一些調(diào)節(jié)因子招募白細(xì)胞至組織損傷區(qū)域或激活白細(xì)胞開始進(jìn)行組織損傷修復(fù),。
基于Loyola和其他中心開展的研究，研究者們期待在死亡患者的肺部發(fā)現(xiàn)較高水平的調(diào)節(jié)因子，因?yàn)椴∏樵街氐幕颊邇A向于有更積極的炎癥反應(yīng),。但研究者的發(fā)現(xiàn)卻恰恰相反,，死亡患者的肺部中這些調(diào)節(jié)因子的水平都較低。
為什么有些患者肺部有強(qiáng)大的免疫反應(yīng)而其他患者卻沒有,？這可能與年齡,、遺傳、健康狀況差異或其他有可能破壞炎癥反應(yīng)平衡的因素有關(guān),，David說。
燒傷患者的存活率自1950年起就有了顯著的增加,，這歸因于燒傷護(hù)理及預(yù)防和治療感染方面的進(jìn)步,，但在過去10年中進(jìn)展有所停滯。
"損傷的免疫反應(yīng)依然未完全了解,，還需要做更多的努力來進(jìn)一步提高燒傷患者的存活率,，"研究人員寫道。
這項(xiàng)研究由國家衛(wèi)生研究院,、美國國防部,、國際消防員協(xié)會(huì)及Ralph & Marian C.Falk醫(yī)學(xué)研究信托資助。（生物谷bioon.com）
doi:10.1097/BCR.0b013e318234d903
PMC:
PMID:
Early Pulmonary Immune Hyporesponsiveness Is Associated With Mortality After Burn and Smoke Inhalation Injury
Davis, Christopher S.; Albright, Joslyn M.; Carter, Stewart R.; Ramirez, Luis; Kim, Hajwa; Gamelli, Richard L.; Kovacs, Elizabeth J.
Abstract： This prospective study aims to address mortality in the context of the early pulmonary immune response to burn and inhalation injury. The authors collected bronchoalveolar lavage fluid from 60 burn patients within 14 hours of their injury when smoke inhalation was suspected. Clinical and laboratory parameters and immune mediator profiles were compared with patient outcomes. Patients who succumbed to their injuries were older (P = .005), had a larger % TBSA burn (P < .001), and required greater 24-hour resuscitative fluids (P = .002). Nonsurvivors had lower bronchoalveolar lavage fluid concentrations of numerous immunomodulators, including C5a, interleukin (IL)-1β, IL-1RA, IL-8, IL-10, and IL-13 (P < .05 for all). Comparing only those with the highest Baux scores to account for the effects of age and % TBSA burn on mortality, nonsurvivors also had reduced levels of IL-2, IL-4, granulocyte colony-stimulating factor, interferon-γ, macrophage inflammatory protein-1β, and tumor necrosis factor-α (P < .05 for all). The apparent pulmonary immune hyporesponsiveness in those who died was confirmed by in vitro culture, which revealed that pulmonary leukocytes from nonsurvivors had a blunted production of numerous immune mediators. This study demonstrates that the early pulmonary immune response to burn and smoke inhalation may be attenuated in patients who succumb to their injuries.
