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热损伤和创伤性损伤后人体自然杀伤细胞功能的抑制

Suppression of natural killer-cell function in humans following thermal and traumatic injury.

作者信息

Blazar B A, Rodrick M L, O'Mahony J B, Wood J J, Bessey P Q, Wilmore D W, Mannick J A

出版信息

J Clin Immunol. 1986 Jan;6(1):26-36. doi: 10.1007/BF00915361.

Abstract

Depressed cell-mediated and humoral immune functions have been reported to occur following severe thermal and traumatic injury. In this study we have questioned whether another immune function, natural killing (NK), is also disturbed in these injured patients. Twenty-two thermally injured patients with burns ranging from 5 to 75% of the total body surface area and 15 traumatically injured patients with injury severity scores ranging from 9 to 56 were followed postinjury and compared to 29 age-matched controls. NK activity was measured as the percentage cytotoxicity in chromium-51 release assays with K562 target cells. The more severely burned patients had significantly depressed NK activity for the 40-day period following injury that remained reduced for the duration of the study. Patients with lesser burns had reduced NK-cell function for the initial 10-day period postburn that returned slowly to the normal range. Traumatically injured patients had depressed NK-cell function during the 3- to 6-day period postinjury. The percentage of cells bearing phenotypic markers for the groups in which NK cells are found was either normal or elevated in these patients. A correlation was found between NK activity and interleukin 2 generation by mononuclear cells from these patients. In order to investigate the mechanism of NK suppression in these patients, NK-cell function was studied following the infusion of cortisol, epinephrine, and glucagon into volunteer subjects in amounts known to reproduce serum levels seen following injury of moderate severity. NK-cell function was reduced an average of 66% following infusion, suggesting that the inhibition of NK-cell function seen in patients may be mediated by the stress response to injury.

摘要

据报道,严重热损伤和创伤后会出现细胞介导免疫和体液免疫功能低下。在本研究中,我们探讨了另一种免疫功能——自然杀伤(NK)功能在这些受伤患者中是否也受到干扰。对22名热烧伤患者(烧伤面积占体表面积的5%至75%)和15名创伤患者(损伤严重度评分9至56分)在受伤后进行随访,并与29名年龄匹配的对照者进行比较。NK活性通过用K562靶细胞进行的铬-51释放试验中的细胞毒性百分比来测定。烧伤较严重的患者在受伤后的40天内NK活性显著降低,且在研究期间一直保持较低水平。烧伤较轻的患者在烧伤后的最初10天内NK细胞功能降低,随后缓慢恢复到正常范围。创伤患者在受伤后的3至6天内NK细胞功能降低。在这些患者中,含有NK细胞的细胞群体中带有表型标记的细胞百分比正常或升高。发现这些患者的NK活性与单核细胞产生白细胞介素2之间存在相关性。为了研究这些患者中NK抑制的机制,对志愿者输注已知能重现中度严重度损伤后血清水平的皮质醇、肾上腺素和胰高血糖素后,研究了NK细胞功能。输注后NK细胞功能平均降低66%,这表明患者中所见的NK细胞功能抑制可能由对损伤的应激反应介导。

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