Muehlstedt Steven G, Lyte Mark, Rodriguez Jorge L
Hennepin County Medical Center, Minneapolis, Minnesota 55415-1829, USA.
Shock. 2002 Jun;17(6):443-50. doi: 10.1097/00024382-200206000-00001.
The incidence of nosocomial pneumonia (NP) among injured patients is substantial. We hypothesize that traumatic injury induces alterations in local organ effector cell function that may predispose the lungs of injured patients to infection. It is the objective of this study to compare the systemic and alveolar effector cell response to injury and assess the relationship these have to the development of NP. Peripheral blood and bronchoalveolar lavage fluid (BAL) were collected from 10 elective surgery patients (controls) and 16 multitrauma patients at 12, 36, and 60 h post-injury. Systemic and alveolar levels of IL-8 and IL-10 were measured. CD11b expression on peripheral blood neutrophils (PBN) and alveolar neutrophils (AN) and HLA-DR expression on peripheral blood monocytes (PBM) and alveolar macrophages (AM) were measured. Alveolar levels of IL-8 and IL-10 were significantly higher than systemic levels after injury. HLA-DR expression was reduced on both PBM and AM after injury but was lowest on the AM. Six of 16 patients (38%) developed NP (NP+). There were no differences in cytokine levels (IL-8 and IL-10) or effector cell phenotype (CD11b and HLA-DR expression) within the systemic circulation of NP+ and NP- patients. In contrast, NP+ and NP- patients differed significantly in alveolar cytokine levels and alveolar effector cell phenotype. IL-8 was significantly higher in BAL form NP+ patients at all time points after injury. Furthermore, alveolar levels of IL-10 decreased in NP- patients but increased in NP+ patients. In all patients, AM HLA-DR expression was significantly reduced from normal controls 12 h post-injury. In NP-patients, AM HLA-DR expression returned to normal 60 h post-injury, whereas in NP+ patients, expression remained suppressed. These findings identify distinct trends in local organ cytokine production and alterations in effector cell phenotype that precede NP. The persistence of reduced HLA-DR expression amidst increasing levels of IL-10 in NP+ patients suggest that cell-mediated immune function is being suppressed. As such, local organ immunosuppression may be responsible for the development of nosocomial pneumonia in injured patients.
创伤患者医院获得性肺炎（NP）的发生率相当高。我们推测，创伤性损伤会导致局部器官效应细胞功能发生改变，这可能使创伤患者的肺部更容易感染。本研究的目的是比较全身和肺泡效应细胞对损伤的反应，并评估这些反应与NP发生之间的关系。在受伤后12、36和60小时，从10名择期手术患者（对照组）和16名多发伤患者中采集外周血和支气管肺泡灌洗液（BAL）。检测IL-8和IL-10的全身和肺泡水平。检测外周血中性粒细胞（PBN）和肺泡中性粒细胞（AN）上的CD11b表达以及外周血单核细胞（PBM）和肺泡巨噬细胞（AM）上的HLA-DR表达。受伤后肺泡中IL-8和IL-10的水平显著高于全身水平。受伤后PBM和AM上的HLA-DR表达均降低，但AM上的最低。16名患者中有6名（38%）发生了NP（NP+）。NP+和NP-患者的全身循环中细胞因子水平（IL-8和IL-10）或效应细胞表型（CD11b和HLA-DR表达）没有差异。相比之下，NP+和NP-患者在肺泡细胞因子水平和肺泡效应细胞表型上有显著差异。受伤后所有时间点，NP+患者BAL中的IL-8均显著更高。此外，NP-患者肺泡中IL-10水平下降，而NP+患者则升高。在所有患者中，受伤后12小时AM上的HLA-DR表达较正常对照组显著降低。在NP-患者中，受伤后60小时AM上的HLA-DR表达恢复正常，而在NP+患者中，表达仍受抑制。这些发现确定了在NP发生之前局部器官细胞因子产生的不同趋势和效应细胞表型的改变。NP+患者中IL-10水平升高的同时HLA-DR表达持续降低，这表明细胞介导的免疫功能受到抑制。因此，局部器官免疫抑制可能是创伤患者医院获得性肺炎发生的原因。
