PATHOGENESIS OF SALMONELLOSIS - STUDIES OF FLUID SECRETION, MUCOSAL INVASION, AND MORPHOLOGIC REACTION IN RABBIT ILEUM
PATHOGENESIS OF SALMONELLOSIS - STUDIES OF FLUID SECRETION, MUCOSAL INVASION, AND MORPHOLOGIC REACTION IN RABBIT ILEUM
复制标题
DOI：
10.1172/jci107201
复制
发表时间：
1973-01-01
影响因子：
15.9
通讯作者：
COLLINS, H
中科院分区：
文献类型：
--
作者：
GIANNELLA, RA;FORMAL, SB;COLLINS, H
在兔回肠结扎模型上对鼠伤寒沙门氏菌菌株进行了研究，以了解侵入胃肠道粘膜的细菌引起液体吸收的机制。所使用的微生物在不同的生物学属性上有所不同，包括侵袭回肠上皮、在粘膜内繁殖、引发急性炎症反应和跨肠壁传播的能力。一些菌株可引起小肠液吸收，但这些菌株并未详细说明肠毒素。只有那些侵入粘膜的菌株才伴有粘膜炎症或液体吸收。非侵袭性菌株既没有产生组织学异常，也没有产生液体分泌。虽然侵入粘膜的菌株会引起急性炎症反应，但并不是所有这些菌株都能引起液体分泌。此外，入侵生物引起液体分泌的能力、粘膜炎症的强度、粘膜内沙门氏菌的数量或从兔回肠传播的能力之间没有相关性。这些观察表明，就像志贺氏菌病一样，粘膜侵袭可能是沙门氏菌病肠道液体丢失的一个必要因素。细菌的性质或因素，除了对胃肠道粘膜的侵袭外，似乎也是液体吸收的原因。然而，沙门氏菌肠毒素不太可能与沙门氏菌的液体分泌有关，这与霍乱弧菌、产毒大肠杆菌或志贺氏菌痢疾1的阐述类似。
Strains ofSalmonella typhimuriumwere studied in the ligated rabbit ileal loop model to gain insight into the mechanisms whereby bacteria which invade the gastrointestinal mucosa evoke fluid exsorption. The organisms employed differed in various biologic attributes including the ability to invade the ileal epithelium, multiply within the mucosa, elicit an acute inflammatory reaction, and disseminate across the intestinal wall. Some strains provoked small intestinal fluid exsorption although these did not elaborate enterotoxin. Only those strains which invaded the mucosa were accompanied by either mucosal inflammation or fluid exsorption. Noninvasive strains produced neither histologic abnormalities nor fluid secretion. While strains which invaded the mucosa caused an acute inflammatory reaction, not all such strains evoked fluid secretion. Furthermore, there was no correlation in ability of invasive organisms to evoke fluid secretion or in the intensity of mucosal inflammation, number of intramucosal salmonellae, or in ability to disseminate from the rabbit ileum.These observations suggest that, as is the case in shigellosis, mucosal invasion may be a necessary factor for the intestinal fluid loss in salmonellosis. A bacterial property or factor, in addition to invasion of the gastrointestinal mucosa, seems to be responsible for fluid exsorptin. However, it is unlikely that a salmonella enterotoxin comparable to that elaborated byVibrio cholerae, toxigenicEscherichia coli, orShigella dysenteriae1 is related to fluid secretion in salmonellosis.Images