| The role of bifidobacteria in gut barrier function after thermal injury in rats. | |
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MedLine Citation:
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PMID: 16967002 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: Early multiple organ dysfunction syndrome appears to be facilitated with bacterial translocation in severe burn injury, yet the mechanisms of bacterial translocation remain in dispute. The aim of this study was to characterize the potential role of intestinal bifidobacteria in the pathogenesis of gut-derived bacterial translocation after burns and to analyze the effects of bifidobacterial supplement on gut barrier function. METHODS: Wistar rats were randomly divided into burn group (Burn, n = 60), sham burn group (SB, n = 10) in experiment 1, and burn + saline group (BS, n = 30), burn + bifidobacteria group (BB, n = 30), and sham-burn + saline group (SS, n = 30) in experiment 2. Animals in BB group were fed bifidobacterial preparation (5 x 10(9) CFU/mL) after burns, 1.5 mL, twice daily. Animals in BS and SS were fed saline. Samples were taken on postburn days 1, 3, and 5. The incidence of bacterial translocation and counts of Bifidobacterium, fungi and Escherichia coli in gut mucosa, as well as the sIgA levels in mucus of the small intestine were determined. The positive sIgA expression in lamina propria and ileum mucosal injury were evaluated light microscopically by blinded examiners. RESULTS: The incidence of bacterial translocation was increased after burns, which was accompanied by significant decrease in number of bifidobacteria but significant increase in E. coli and fungi in gut mucosa, and elevation of levels of plasma endotoxin and IL-6 (p < 0.001). The incidence of bacterial translocation was markedly reduced after 3- and 5-day supplementation of bifidobacteria compared with control group (p < 0.05). The counts of mucosal bifidobacteria were increased by 4- to 40-fold, whereas E. coli and fungi were decreased by 2- to 30-fold and 10- to 150-fold, respectively, after bifidobacterial supplementation. The damage of mucosa tended to be less pronounced after 3-day bifidobacteria-supplemented formula compared with control group (grade 2 [0-6] versus grade 4 [3-6], p < 0.05). Moreover, the expression and release of sIgA was markedly augmented after 3-days of bifidobacteria-supplementation formula and it returned to normal range on postburn day 5. CONCLUSIONS: The decrease in counts and proportion of bifidobacteria to other flora in gut may play an important role in the development of bacterial translocation after thermal injury. Supplementation of exogenous bifidobacteria could improve gut barrier function, and attenuate bacterial/endotoxin translocation secondary to major burns. |
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Authors:
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Zhongtang Wang; Guangxia Xiao; Yongming Yao; Shuzhong Guo; Kaihua Lu; Zhiyong Sheng |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: The Journal of trauma Volume: 61 ISSN: 0022-5282 ISO Abbreviation: J Trauma Publication Date: 2006 Sep |
Date Detail:
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Created Date: 2006-09-12 Completed Date: 2006-10-18 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 0376373 Medline TA: J Trauma Country: United States |
Other Details:
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Languages: eng Pagination: 650-7 Citation Subset: AIM; IM |
Affiliation:
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Center of Plastic Surgery, Xijing Hospital, Fourth Military Medical University, Xi'an, China. wangkingking@hotmail.com |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animal Feed
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microbiology Animals Bacterial Translocation / physiology* Bifidobacterium / isolation & purification, physiology* Burns / blood, microbiology*, physiopathology Colony Count, Microbial Endotoxins / blood Escherichia coli / isolation & purification Female Fungi / isolation & purification Ileum / microbiology*, physiopathology Immunoglobulin A, Secretory / metabolism Interleukin-6 / blood Intestinal Mucosa / microbiology*, physiopathology Male Rats Rats, Wistar |
| Chemical | |
Reg. No./Substance:
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0/Endotoxins; 0/Immunoglobulin A, Secretory; 0/Interleukin-6 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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