Lichtman S N, Keku J, Schwab J H, Sartor R B
Department of Pediatrics, University of North Carolina, Chapel Hill 27599-7220.
Infect Immun. 1991 Feb;59(2):555-62. doi: 10.1128/iai.59.2.555-562.1991.
Surgical creation of jejunal self-filling blind loops (SFBL) causes small bowel bacterial overgrowth which is associated with hepatobiliary inflammation in the susceptible Lewis and Wistar rat strains. Since hepatic injury occurs when small bowel anaerobic bacterial concentrations are increased 4 to 6 log10 units per ml and hepatic bacterial cultures are negative, we postulate that the inflammation is caused by absorption of phlogistic cell wall polymers originating from bacteria within the loop. To demonstrate absorption of bacterial cell wall polymers, we measured plasma and hepatic levels of immunoreactive peptidoglycan-polysaccharide (PG-PS) following intraluminal injection as well as anti-PG antibodies as an indirect measure of absorption and/or accumulation of endogenous PG. PG-PS purified from group A streptococci was detected in plasma by enzyme-linked immunosorbent assay after intraluminal injection; rats with SFBL showed significantly more uptake into plasma and the liver than sham-operated rats or SFBL rats which were treated with metronidazole (P less than 0.025). Total plasma immunoglobulin A (IgA), IgG, and IgM levels did not differ among sham-operated rats and those with self-emptying blind loops or SFBL, but plasma anti-PG IgA (P less than 0.05), IgG, and IgM (P less than 0.01) levels were increased in rats with SFBL. Metronidazole and tetracycline prevented the elevation of anti-PG antibody, but gentamicin and polymyxin B did not. Anti-lipid A, anti-soy protein, and anti-chow antibodies in plasma were not consistently increased in rats with SFBL indicating the lack of a generalized antibody response to luminal antigens. These data suggest that PG from normal flora bacteria is absorbed from the intestinal lumen and that mucosal injury and/or increased luminal concentrations of PG, such as those induced by small bowel bacterial overgrowth, lead to enhanced absorption of potentially inflammatory bacterial polymers.
通过手术创建空肠自充盈盲袢(SFBL)会导致小肠细菌过度生长,这与易感的Lewis和Wistar大鼠品系中的肝胆炎症相关。由于当小肠厌氧菌浓度每毫升增加4至6个对数10单位且肝脏细菌培养为阴性时会发生肝损伤,我们推测炎症是由源自盲袢内细菌的促炎细胞壁聚合物的吸收引起的。为了证明细菌细胞壁聚合物的吸收,我们在腔内注射后测量了血浆和肝脏中免疫反应性肽聚糖 - 多糖(PG - PS)的水平以及抗PG抗体,作为内源性PG吸收和/或积累的间接测量指标。腔内注射后,通过酶联免疫吸附测定法在血浆中检测到从A组链球菌纯化的PG - PS;与假手术大鼠或用甲硝唑治疗的SFBL大鼠相比,患有SFBL的大鼠在血浆和肝脏中的摄取明显更多(P小于0.025)。假手术大鼠与具有自排空盲袢或SFBL的大鼠之间的血浆总免疫球蛋白A(IgA)、IgG和IgM水平没有差异,但患有SFBL的大鼠的血浆抗PG IgA(P小于0.05)、IgG和IgM(P小于0.01)水平升高。甲硝唑和四环素可防止抗PG抗体升高,但庆大霉素和多粘菌素B则不能。患有SFBL的大鼠血浆中的抗脂质A、抗大豆蛋白和抗食物抗体并未持续增加,表明对腔内抗原缺乏全身性抗体反应。这些数据表明,正常菌群细菌的PG从肠腔中被吸收,并且粘膜损伤和/或PG腔内浓度增加,如小肠细菌过度生长所诱导的那些,会导致潜在炎症性细菌聚合物的吸收增强。