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目的:探讨严重烫伤后补充双歧杆菌与肠道 sIgA 合成、分泌的关系。方法:Wistar 大鼠70只随机分为烫伤对照组(BC,n=30)、烫伤治疗组(BT,n=30)、假伤组(NC,n=10)。BT 组伤后灌胃双歧杆菌悬液(5×10~9 cfu/ml),1.5ml,2/d。检测大鼠细菌及内毒素移位、膜菌群中双歧杆菌量、肠粘液 sIgA 浓度及肠道浆细胞sIgA 表达情况等。结果:(1)伤后3d,BC 组与 BT 组细菌移位率分别为42%和16%(P=0.004),伤后5d 分别为30%和8%(P=0.002)。(2)伤后大鼠盲肠膜菌群中双歧杆菌减少约10～60倍;灌胃双歧杆菌悬液后肠道双歧杆菌明显增多。(3)BC 组肠粘液 sIgA 平均减少约30%,伤后3d 达最低;BT 组3d 伤后基本恢复正常。伤后回肠粘膜下固有层浆细胞 sIgA 表达减弱,补充双歧杆菌后 sIgA 表达显著增强,5d 接近 NC 组。(4)膜菌群中双歧杆菌量与肠粘液 sIgA 浓度呈显著正相关。结论:严重烫伤后肠道 sIgA 产生明显受抑制,其改变与膜菌群中双歧杆菌减少有关,补充外源性双歧杆菌可促进肠道 sIgA 合成与分泌。
Objective: To investigate the relationship between bifidobacterium supplementation and intestinal sIgA synthesis and secretion after severe scald. Methods: Seventy Wistar rats were randomly divided into burn control group (BC, n = 30), scald treatment group (BT, n = 30) and sham injury group (NC, n = 10). BT group was inoculated with Bifidobacterium suspension (5 × 10 ~ 9 cfu / ml), 1.5ml, 2 / d after injury. Detection of bacterial and endotoxin translocation in rats, the amount of bifidobacteria in the bacterial flora, the concentration of sIgA in intestinal mucus and the expression of sIgA in intestinal plasma cells. Results: (1) After 3 days, the bacterial translocation rates were 42% and 16% in BC group and BT group respectively (P = 0.004) and 30% and 8% (P = 0.002) respectively 5 days after injury. (2) The bifidobacteria in the caecal membrane flora in rats decreased about 10 ~ 60 times after the injury; bifidobacteria in the intestinal tract increased significantly after the bifidobacterium was inoculated. (3) The average sIgA in intestinal mucosa of BC group decreased about 30% on average, reaching the minimum on 3d after injury; the BT group returned to normal after 3d. The expression of sIgA was weakened in ileal submucosal lamina propria after injury. The expression of sIgA was significantly increased after bifidobacteria supplementation, and was close to NC group on the 5th day. (4) There was a significant positive correlation between the amount of bifidobacteria in the bacterial flora and the concentration of sIgA in intestinal mucosa. CONCLUSIONS: The sIgA production in the intestine was significantly inhibited after severe scald. The change was related to the decrease of bifidobacteria in the bacterial flora. Supplementation of exogenous bifidobacteria promoted intestinal sIgA synthesis and secretion.