Role of the Intestinal Microflora in Host Defense against Infection

Hentges, David J.

doi:10.1016/b978-0-12-341280-5.50020-3

Cited by 87 publications

(52 citation statements)

References 61 publications

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“…As a result, the endogenous gut flora is stimulated and intestinal contents are acidified due to the production of lactic acid and short chain fatty acids. 26 Consequently, the colonisation of foodborne pathogens might be inhibited through enhanced competition for nutrients and mucosal adhesion sites 27 and increased luminal killing of acid sensitive pathogens, like salmonella.…”

Section: Discussionmentioning

confidence: 99%

Dietary fructo-oligosaccharides and lactulose inhibit intestinal colonisation but stimulate translocation of salmonella in rats

Bovee‐Oudenhoven

Bruggencate²,

Lettink-Wissink³

et al. 2003

Gut

128

100

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Background and aims: It is frequently assumed that dietary non-digestible carbohydrates improve host resistance to intestinal infections by stimulating the protective gut microflora. However, compelling scientific evidence from in vivo infection studies is lacking. Therefore, we studied the effect of several nondigestible carbohydrates on the resistance of rats to Salmonella enteritidis infection. Methods: Rats (n = 8 per group) were fed ''humanised'' purified diets containing 4% lactulose, fructooligosaccharides (FOS), resistant starch, wheat fibre, or cellulose. After an adaptation period of 2 weeks the animals were orally infected with S enteritidis. Supplement induced changes in faecal biochemical and microbiological parameters were studied before infection. Colonisation of salmonella was determined by studying the faecal excretion of this pathogen and translocation by analysis of urinary nitric oxide metabolites over time and classical organ cultures. Intestinal mucosal myeloperoxidase activity was determined to quantify intestinal inflammation after infection. Results: Despite stimulation of intestinal lactobacilli and bifidobacteria and inhibition of salmonella colonisation, FOS and lactulose significantly enhanced translocation of this pathogen. These supplements also increased cytotoxicity of faecal water and faecal mucin excretion, which may reflect mucosal irritation. In addition, caecal and colonic, but not ileal, mucosal myeloperoxidase activity was increased in infected rats fed FOS and lactulose. In contrast, cellulose, wheat fibre, and resistant starch did not affect the resistance to salmonella. Conclusions: In contrast to most expectations, FOS and lactulose impair the resistance of rats to intestinal salmonella infection. Obviously, stimulation of the endogenous lactobacilli and bifidobacteria is no guarantee of improved host defence against intestinal infections.

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Section: Discussionmentioning

confidence: 99%

Dietary fructo-oligosaccharides and lactulose inhibit intestinal colonisation but stimulate translocation of salmonella in rats

Bovee‐Oudenhoven

Bruggencate²,

Lettink-Wissink³

et al. 2003

Gut

128

100

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“…Streptomycin treatment alters the microecology of the cecum, decreasing the populations of facultative anaerobes (enterococci, streptococci, and lactobacilli) and strict anaerobes (lactobacilli and bifidobacteria). Accompanying these changes in microflora is a general decrease in the concentration of volatile fatty acids, which may play a role in the natural resistance of the conventional mouse intestine to invading E. coli strains (18,19). Nevertheless, populations of the genera Bacteroides and Eubacterium in cecal contents of streptomycin-treated mice remain largely unchanged (19).…”

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confidence: 99%

Mouse Intestine Selects Nonmotile flhDC Mutants of Escherichia coli MG1655 with Increased Colonizing Ability and Better Utilization of Carbon Sources

et al. 2005

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D-Gluconate which is primarily catabolized via the Entner-Doudoroff (ED) pathway, has been implicated as being important for colonization of the streptomycin-treated mouse large intestine by Escherichia coli MG1655, a human commensal strain. In the present study, we report that an MG1655 ⌬edd mutant defective in the ED pathway grows poorly not only on gluconate as a sole carbon source but on a number of other sugars previously implicated as being important for colonization, including L-fucose, D-gluconate, D-glucuronate, N-acetyl-D-glucosamine, D-mannose, and D-ribose. Furthermore, we show that the mouse intestine selects mutants of MG1655 ⌬edd and wild-type MG1655 that have improved mouse intestinecolonizing ability and grow 15 to 30% faster on the aforementioned sugars. The mutants of MG1655 ⌬edd and wild-type MG1655 selected by the intestine are shown to be nonmotile and to have deletions in the flhDC operon, which encodes the master regulator of flagellar biosynthesis. Finally, we show that ⌬flhDC mutants of wild-type MG1655 and MG1655 ⌬edd constructed in the laboratory act identically to those selected by the intestine; i.e., they grow better than their respective parents on sugars as sole carbon sources and are better colonizers of the mouse intestine.

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“…The normal microbial flora of the alimentary tract is a major factor protecting animals and humans against colonization by pathogenic bacteria (17). Newly hatched chickens without an established flora are particularly susceptible to Salmonella infection and colonization.…”

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confidence: 99%

Influence of genes encoding proton-translocating enzymes on suppression of Salmonella typhimurium growth and colonization

Zhang-Barber¹,

Turner²,

Martin³

et al. 1997

J Bacteriol

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Twenty-four-hour-old, aerobically grown, Luria-Bertani broth cultures of Salmonella typhimurium F98 suppressed the growth of a spectinomycin-resistant (Spc r ) derivative of the same strain inoculated at 10 3 CFU ml ؊1 . This growth suppression is genus specific and RpoS independent, and it is not solely a result of nutrient depletion (P. A. Barrow, M. A. Lovell, and L. Zhang-Barber, J. Bacteriol. 178:3072-3076, 1996). Mutations in three genes are shown here to significantly reduce growth suppression under these conditions. The mutations were located in the nuo, cyd, and unc operons, which code for the NADH dehydrogenase I, cytochrome d oxidase, and F 0 F 1 proton-translocating ATPase complexes, respectively. When cultures were grown under strictly anaerobic conditions, only the unc mutant did not suppress growth. Prior colonization of the alimentary tract of newly hatched chickens with the S. typhimurium F98 wild type or nuo or cyd mutants suppressed colonization by an S. typhimurium F98 Spc r derivative inoculated 24 h later. In contrast, the S. typhimurium unc mutant did not suppress colonization. The nuo and unc mutants showed poorer growth on certain carbon sources. The data support the hypothesis that growth suppression operates because of the absence of a utilizable carbon source or electron acceptor.The normal microbial flora of the alimentary tract is a major factor protecting animals and humans against colonization by pathogenic bacteria (17). Newly hatched chickens without an established flora are particularly susceptible to Salmonella infection and colonization. Colonized young chicks often excrete large numbers of salmonellae into their environment for long periods, thus becoming a potential reservoir of infection (7). When chickens reach several weeks of age, the lower alimentary tract is colonized by large numbers of obligate anaerobes which confer increased resistance to the establishment of Salmonella infection. The resistance of young chicks to infection may be artificially increased by oral administration, immediately after hatching, of a suspension or culture of cecal contents obtained from healthy adult birds (23). This phenomenon has been termed "competitive exclusion," and its discovery has led to a search for individual strains of bacteria which can inhibit colonization by pathogens to the same extent as the normal flora. Oral administration of an avirulent Salmonella typhimurium strain to day-old chicks can confer protection against oral infection by a virulent strain (known as colonization inhibition) (8, 10). Colonization inhibition is normally genus specific, is not caused by bacteriophage or bacteriocin activity, and is not a consequence of immunity induced by the first strain (8). Attempts are currently under way to elucidate the mechanisms responsible for this effect. An analogous phenomenon in vitro has been observed with 24-h-old stationaryphase nutrient broth cultures of S. typhimurium (6,8,11). When such cultures are inoculated with small numbers of genetically tagged (antibiot...

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Role of the Intestinal Microflora in Host Defense against Infection

Cited by 87 publications

References 61 publications

Dietary fructo-oligosaccharides and lactulose inhibit intestinal colonisation but stimulate translocation of salmonella in rats

Dietary fructo-oligosaccharides and lactulose inhibit intestinal colonisation but stimulate translocation of salmonella in rats

Mouse Intestine Selects Nonmotile flhDC Mutants of Escherichia coli MG1655 with Increased Colonizing Ability and Better Utilization of Carbon Sources

Influence of genes encoding proton-translocating enzymes on suppression of Salmonella typhimurium growth and colonization

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