甲型H1N1流感正在一些國(guó)家肆虐,，但一些患者的病情明顯比其他患者嚴(yán)重,。美國(guó)研究人員推測(cè),，其原因之一可能是流感病毒會(huì)使某些患者的免疫系統(tǒng)在較長(zhǎng)時(shí)間內(nèi)功能失常,，從而容易感染其他細(xì)菌,，使這些人患上肺炎等更嚴(yán)重的疾病,。
這項(xiàng)研究由費(fèi)城兒童醫(yī)院過敏和免疫學(xué)部主任凱瑟琳·沙利文領(lǐng)導(dǎo)完成,，研究成果5月4日發(fā)表在《白細(xì)胞生物學(xué)雜志》網(wǎng)絡(luò)版上。
研究人員調(diào)查了一些患有重度流感的兒科患者血漿中的細(xì)胞因子水平。細(xì)胞因子是一類能在細(xì)胞間傳遞信息,、具有免疫調(diào)節(jié)功能的蛋白質(zhì)或小分子多肽,。
結(jié)果發(fā)現(xiàn)，雖然上述患者血漿中的細(xì)胞因子水平有所升高,，但他們體內(nèi)toll樣受體的反應(yīng)卻有所減少,。toll樣受體是先天性免疫系統(tǒng)的重要受體，可識(shí)別不同病原體,，并在細(xì)菌入侵時(shí)激活快速先天免疫反應(yīng),。此外，它還可以調(diào)節(jié)獲得性免疫,，是連接先天性免疫與獲得性免疫的橋梁,。
研究人員推測(cè)，toll樣受體活性降低導(dǎo)致部分流感患者免疫系統(tǒng)功能失常,，這增加了二次感染的機(jī)會(huì),。沙利文表示，這項(xiàng)研究有助于解釋為何一些流感患者僅僅是感冒而已,，另一些患者卻病情嚴(yán)重甚至因此喪命,；也可以解釋為何在因?yàn)榱鞲卸劳龅膬和校姆种坏娜似鋵?shí)死于細(xì)菌感染,。
《白細(xì)胞生物學(xué)雜志》副主編約翰·惠里評(píng)價(jià)說,，盡管近幾十年來人類在醫(yī)學(xué)上取得了巨大進(jìn)展，但流感病毒一直是個(gè)巨大威脅,。這項(xiàng)新研究使人們更進(jìn)一步了解流感,，將有助于采取有效的治療措施,。（生物谷Bioon.com）
生物谷推薦原始出處：
Journal of Leukocyte Biology, doi:10.1189/jlb.1108710
Immune dysregulation in severe influenza
Meredith L. Heltzer *, Susan E. Coffin , Kelly Maurer *, Asen Bagashev *, Zhe Zhang , Jordan S. Orange *, and Kathleen E. Sullivan *
Divisions of *Allergy and Immunology and Infectious Diseases and Center for Biomedical Informatics, Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania, USA
Among previously healthy children with severe influenza, the mechanisms leading to increased pathology are not understood. We hypothesized that children with severe influenza would have high levels of circulating cytokines. To examine this, we recruited patients with severe influenza and examined plasma cytokine levels as well as the ability of peripheral blood cells to respond to stimuli. Ten patients with severe influenza were enrolled during the 2005–2007 influenza seasons. We evaluated plasma cytokine levels, circulating NK cells, and responses to TLR ligands during the illness. We compared these patients with five patients with moderate influenza, six patients with respiratory syncytial virus (RSV), and 24 noninfected controls. Patients with influenza showed depressed responses to TLR ligands when compared with RSV patients and healthy controls (P<0.05). These normalized when retested during a convalescent phase. Plasma levels of IL-6, IL-12, and IFN- were elevated in influenza patients compared with controls (P<0.05). A compromised ability to produce TNF- was reproduced by in vitro infection, and the magnitude of the effect correlated with the multiplicity of infection and induction of IFN regulatory factor 4 expression. Aberrant, systemic, innate responses to TLR ligands during influenza infection may be a consequence of specific viral attributes such as a high inoculum or rapid replication and may underlie the known susceptibility of influenza-infected patients to secondary bacterial infections.
