Plusa S, Webster N, Primrose J
Academic Unit of Surgery, St James's University Hospital, Leeds.
Gut. 1996 May;38(5):784-7. doi: 10.1136/gut.38.5.784.
Obstructive jaundice is associated with an increased incidence of infection and endotoxaemia, which may result from impaired host immunity. Neutrophil adhesion to vascular endothelium is a key part of the inflammatory response.
To investigate neutrophil adhesion molecule expression and activation in obstructive jaundice.
Nine adult patients with obstructive jaundice and 11 control subjects.
The expression of the neutrophil adhesion receptors L-selectin, CD11a, CD11b, CD11c, and CD15 was determined using flow cytometry. CD11b expression in response to stimulation with fMLP and endotoxin was measured.
The basal expression of L-selectin, CD11a, and CD15 was significantly decreased in jaundiced patients (p < 0.05) and the expression of CD11b in response to stimulation with fMLP and endotoxin was significantly impaired in the jaundiced group. Endotoxin stimulation without plasma did not reverse the impaired response showing that it is not caused by endotoxin inactivation by plasma proteins.
Neutrophils from patients with obstructive jaundice show decreased adhesion receptor expression and an impaired response to stimulation with bacterial products. This cellular dysfunction may be responsible for the high incidence of septic complications in these patients.
梗阻性黄疸与感染和内毒素血症的发生率增加相关，这可能是由于宿主免疫功能受损所致。中性粒细胞与血管内皮的黏附是炎症反应的关键部分。
研究梗阻性黄疸时中性粒细胞黏附分子的表达及活化情况。
9例成年梗阻性黄疸患者和11例对照者。
采用流式细胞术测定中性粒细胞黏附受体L-选择素、CD11a、CD11b、CD11c和CD15的表达。测定用fMLP和内毒素刺激后CD11b的表达。
黄疸患者L-选择素、CD11a和CD15的基础表达显著降低（p < 0.05），黄疸组用fMLP和内毒素刺激后CD11b的表达明显受损。无血浆的内毒素刺激不能逆转受损反应，表明这不是由血浆蛋白对内毒素的灭活所致。
梗阻性黄疸患者的中性粒细胞显示黏附受体表达降低，对细菌产物刺激的反应受损。这种细胞功能障碍可能是这些患者败血症并发症高发的原因。
