Nakae H, Endo S, Inada K, Takakuwa T, Kasai T
Critical Care and Emergency Center, Iwate Medical University, Morioka, Japan.
Res Commun Mol Pathol Pharmacol. 1996 Mar;91(3):329-38.
We measured the levels of soluble intercellular adhesion molecule-1 (sICAM-1), CD11a, CD11b, CD18, endotoxin, and various inflammatory cytokines to clarify the relationship between adhesive molecules and cytokines in sepsis. We studied 21 patients with sepsis (sepsis group) and 13 patients with trauma not complicated by infection (trauma group). The mean sICAM-1 level was significantly higher in the sepsis group than in the trauma group. No significant difference was observed in the CD11a, CD11b, and CD18 levels between the two groups. The sICAM-1 levels significantly correlated with the levels of endotoxin, tumor necrosis factor alpha (TNF-alpha), and IL-8, but CD11a, CD11b, and CD18 levels did not correlate with endotoxin or cytokine levels. These findings suggest that ICAM-1 production is induced by endotoxins and cytokines produced in excess by inflammatory reactions and that endotoxins and cytokines are involved in qualitative, but not quantitative changes in LFA-1 (CD11a/CD18) and Mac-1 (CD11b/CD18).
我们检测了可溶性细胞间黏附分子-1（sICAM-1）、CD11a、CD11b、CD18、内毒素及多种炎性细胞因子的水平，以阐明脓毒症中黏附分子与细胞因子之间的关系。我们研究了21例脓毒症患者（脓毒症组）和13例未并发感染的创伤患者（创伤组）。脓毒症组的平均sICAM-1水平显著高于创伤组。两组间CD11a、CD11b和CD18水平未观察到显著差异。sICAM-1水平与内毒素、肿瘤坏死因子α（TNF-α）及IL-8水平显著相关，但CD11a、CD11b和CD18水平与内毒素或细胞因子水平无关。这些发现提示，ICAM-1的产生是由炎性反应中过量产生的内毒素和细胞因子所诱导，且内毒素和细胞因子参与了淋巴细胞功能相关抗原-1（LFA-1，CD11a/CD18）和巨噬细胞-1（Mac-1，CD11b/CD18）的定性而非定量变化。
