Toxicity of Intestinal Volatile Fatty Acids for Yeast and Esch. Coli

Bergeim, Olaf

doi:10.1093/infdis/66.3.222

Cited by 45 publications

(21 citation statements)

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“…Numerous in vitro studies have demonstrated that the toxicity was attributable to the nonionized forms of these acids, which exist more prominently at low pH (Baskett & Hentges, 1973; Bergeim, 1940; Hentges, 1967; Weiner & Draskoczy, 1961). These early studies also established the pleiotropic effects of weak organic acids ranging from inhibiting oxidative metabolism (Weiner & Draskoczy, 1961) to eliciting chemotactic responses (Repaske & Adler, 1981).…”

Section: Biological Activities Of Scfamentioning

confidence: 99%

Regulation of Bacterial Pathogenesis by Intestinal Short-Chain Fatty Acids

Sun¹,

O’Riordan²

2013

Advances in Applied Microbiology

266

195

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The human gut microbiota is inextricably linked to health and disease. One important function of the commensal organisms living in the intestine is to provide colonization resistance against invading enteric pathogens. Because of the complex nature of the interaction between the microbiota and its host, multiple mechanisms likely contribute to resistance. In this review, we dissect the biological role of short-chain fatty acids (SCFA), which are fermentation end products of the intestinal microbiota, in host–pathogen interactions. SCFA exert an extensive influence on host physiology through nutritional, regulatory, and immunomodulatory functions and can also affect bacterial fitness as a form of acid stress. Moreover, SCFA act as a signal for virulence gene regulation in common enteric pathogens. Taken together, these studies highlight the importance of the chemical environment where the biology of the host, the microbiota, and the pathogen intersects, which provides a basis for designing effective infection prevention and control.

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Section: Biological Activities Of Scfamentioning

confidence: 99%

Regulation of Bacterial Pathogenesis by Intestinal Short-Chain Fatty Acids

Sun¹,

O’Riordan²

2013

Advances in Applied Microbiology

266

195

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“…The presence of volatile acids at higher pH levels may exert a selective effect upon the plaque microflora at the pH range where pH itself is not inhibiting to mi crobial growth [Bergeim, 1940;Meynell, 1963;F reese et al, 1973].…”

Section: G Eddesmentioning

confidence: 99%

Acids Produced by Human Dental Plaque Metabolism in situ

1975

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The pH of plaque and concentration of lactic and volatile acids present before and after exposure in vivo to sugar has been investigated. Plaque was weighed and the acids quantitatively extracted, volatiles were estimated by GLC and the lactate isomers enzymically. All samples contained acetate, propionate, n-butyrate, L(+) and D(––) lactate. Total acid (mostly volatile) in plaque after overnight fasting and 2.5 h after breakfast was similar (3.0 ×10^––5 mmol/mg wet weight). 5 min after exposure to one sugar lump (= 40% w/w sucrose/saliva), at the pH minimum, the concentration was 5 × 10^––5 mmol/mg wet weight, the major change being an 8-fold rise in L(+), a 5-fold rise in D(––) lactate and a halving of volatiles. Increased sugar exposure (five successive lumps) did not immediately produce more acid than one lump, but, after 30 min, more L(+) lactate was present from the increased sugar and the pH recovery was slower. Plaque before or 60 min after sugar had more total volatiles than lactate. The mean values for total and individual acids produced from glucose and sucrose did not differ significantly (p > 0.5). Although the volatiles are the dominant acid radicals around neutral pH the ‘Stephan curve’ is due to production of L(+) and to a lesser extent D(––) lactic acid.

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“…Such sugars in these regions will be the main cause of the growth and exhibiting usefulness of bifidobacteria: The sugars supply energy and components of the cells, and the fermentation products, acetic acid and lactic acid, are considered to be the substances with which bifidobacteria inhibit the growth of harmful bacteria (1,4).…”

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confidence: 99%

Search for Sugar Sources for Selective Increase of Bifidobacteria

Yazawa

Tamura

1982

Bifidobacteria Microflora

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We searched for sugar sources which agree with the selectivity and efficiency of growth of bifidobacteria. Among the sugars tested, raffinose, stachyose, inulin oligomers (4-to 25-saccharides) and dextran oligomers (3-to 5-saccharides) were found to be used by Bifidobacterium infantis and not by Escherichia coli , Streptococcus faecalis nor Lactobacillus acidophilus. Raffinose, stachyose and inulin oligomers (4-to 25-saccharides) showed almost equal growth activities to B . infantis, and the generation time using each sugar was about 1 .0 hr as short as with use of lactose . Raffinose showed a high rate of consumption by B . infantis or B. adolescentis without dependence on the preculture sugar. However , consumption of stachyose, inulin oligomer and inulin was dependent on the preculture sugar . These results indicate that raffinose is the most suitable sugar source for bifidobacteria among the sugars tested, therefore we administered raffinose to conventional mice along with food and found that B. infantis was predominantly implanted (more than 1010.5 viable cells/g feces) in five mice in ten.

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Toxicity of Intestinal Volatile Fatty Acids for Yeast and Esch. Coli

Cited by 45 publications

References 0 publications

Regulation of Bacterial Pathogenesis by Intestinal Short-Chain Fatty Acids

Regulation of Bacterial Pathogenesis by Intestinal Short-Chain Fatty Acids

Acids Produced by Human Dental Plaque Metabolism in situ

Search for Sugar Sources for Selective Increase of Bifidobacteria

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