Wunderink Richard G
Pulmonary and Critical Care Division, Department of Medicine, Northwestern University Feinberg School of Medicine, 676 North St Clair, Suite 14-044, Chicago, IL 60611, USA.
Proc Am Thorac Soc. 2005;2(5):440-4. doi: 10.1513/pats.2005080-83JS.
Patients with nosocomial pneumonia have evidence of immunosuppression. The most obvious defect in immunity is the loss of mechanical barriers with an endotracheal tube. Only a third of colonized patients on ventilators develop pneumonia, however, suggesting that altered immunity is more extensive. This subgroup of patients tends to get multiple synchronous and sequential infections. The exact mechanisms of this compromise of immunity remain to be fully elucidated. Both a temporary immunocompromised and a specifically predisposed subpopulation, however, can explain the clinical pattern. A temporary immunoparalysis clearly occurs and is associated with increased risk of infections. An underlying genetic predisposition may lead to a predisposed population. Genetic polymorphisms in pathogen recognition molecules increase the risk of nosocomial infections. Genetic variability in immune mediators increase severity of infections and mortality but have not been demonstrated as consistently to lead to infections. Adequate treatment of an initial infection is required for reversal of the temporary immunoparalysis, whereas specific immunomodulatory therapies can reverse the markers of immunoparalysis and may decrease the risk of infection.
医院获得性肺炎患者存在免疫抑制的证据。免疫方面最明显的缺陷是气管内插管导致机械屏障丧失。然而，使用呼吸机的定植患者中只有三分之一会发生肺炎，这表明免疫改变更为广泛。这一亚组患者往往会发生多重同步和相继感染。免疫功能受损的确切机制仍有待充分阐明。不过，暂时免疫受损和特定的易感亚群都可以解释这种临床模式。明显会出现暂时的免疫麻痹，且与感染风险增加有关。潜在的遗传易感性可能导致易感人群。病原体识别分子的基因多态性会增加医院获得性感染的风险。免疫介质的基因变异性会增加感染的严重程度和死亡率，但尚未被一致证明会导致感染。为了逆转暂时的免疫麻痹，需要对初始感染进行充分治疗，而特定的免疫调节疗法可以逆转免疫麻痹的指标，并可能降低感染风险。
