Inhibition of Clostridium difficile growth and adhesion to enterocytes by Bifidobacterium supernatants

Trejo, Fernando Miguel; Minnaard, Jessica; Pérez, Pablo; Antoni, Graciela L. De

doi:10.1016/j.anaerobe.2006.03.004

Cited by 65 publications

(47 citation statements)

References 36 publications

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“…Bifidobacterium strains against C. difficile were dependent on their production of lactic and acetic acids (Trejo et al, 2006). Additionally, Naaber et al (2004) also demonstrated the correlation of hydrogen peroxide and lactic acid production with inhibition of C. difficile by intestinal lactobacilli while Tejero-Sarinena et al (2012) showed that these substances were lactic acid and acetic acid (Naaber et al, 2004;Tejero-Sarinena et al, 2012).…”

Section: Also Reported That the Inhibition Of Isolatedmentioning

confidence: 89%

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In vitro inhibition of Clostridium difficile by commercial probiotics: A microcalorimetric study

Fredua‐Agyeman

Stapleton

Basit

et al. 2017

International Journal of Pharmaceutics

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The aim of the study was to investigate the influence of some commercial probiotics on the growth of Clostridium difficile using the isothermal microcalorimeter, an instrument which can monitor the real time growth of bacteria. Commercial probiotic strains and products, Lactobacillus acidophilus LA-5 ® , Bifidobacterium lactis BB-12 ® , Probio 7 ® and Symprove tm were co-cultured with C. difficile in Brain Heart Infusion (BHI) broth supplemented with 0.1% (w/v) L-cysteine hydrochloride and 0.1% (w/v) sodium taurocholate and monitored in the microcalorimeter. Pseudomonas aeruginosa NCIMB 8628 was also co-cultured with C. difficile and studied. The results indicated inhibition of C. difficile by the probiotics. The inhibition of C. difficile was shown to be pH-dependent using neutralized and unmodified cell free supernatant (CFS) produced by the probiotic strains. However, concentrated CFS of the probiotics also inhibited the intestinal pathogen in a non pH-dependent manner, likely due to specific antimicrobial substances produced. The results also indicated that C. difficile growth was greatly influenced by the presence of sodium taurocholate and by the pH of the medium. A medium pH of between 6.45 and 6.9 demonstrated maximum growth of the organism in the microcalorimeter.

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Section: Also Reported That the Inhibition Of Isolatedmentioning

confidence: 89%

“…For instance, inhibition of C. difficile was reported by Schoster et al (2013) to be only observed when the pH of the supernatants obtained from the probiotic species was not neutralized (Schoster et al, 2013). Trejo et al (2006) …”

Section: Resultsmentioning

confidence: 99%

In vitro inhibition of Clostridium difficile by commercial probiotics: A microcalorimetric study

Fredua‐Agyeman

Stapleton

Basit

et al. 2017

International Journal of Pharmaceutics

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“…2). Given that normal microbiota (46), along with probiotics, have inhibitory activities against pathogenic bacteria (3) and that effective antibiotics should have specific antimicrobial activity against pathogenic but not nonpathogenic microbes, coprisin analogue may be a good candidate for use as a potential therapeutic reagent for C. difficile-associated acute colitis.…”

Section: Discussionmentioning

confidence: 99%

The Insect Peptide Coprisin Prevents Clostridium difficile-Mediated Acute Inflammation and Mucosal Damage through Selective Antimicrobial Activity

Kang

Hwang

Nam

et al. 2011

Antimicrob Agents Chemother

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Clostridium difficile-associated diarrhea and pseudomembranous colitis are typically treated with vancomycin or metronidazole, but recent increases in relapse incidence and the emergence of drug-resistant strains of C. difficile indicate the need for new antibiotics. We previously isolated coprisin, an antibacterial peptide from Copris tripartitus, a Korean dung beetle, and identified a nine-amino-acid peptide in the ␣-helical region of it (LLCIALRKK) that had antimicrobial activity (J. Here, we examined whether treatment with a coprisin analogue (a disulfide dimer of the nine peptides) prevented inflammation and mucosal damage in a mouse model of acute gut inflammation established by administration of antibiotics followed by C. difficile infection. In this model, coprisin treatment significantly ameliorated body weight decreases, improved the survival rate, and decreased mucosal damage and proinflammatory cytokine production. In contrast, the coprisin analogue had no apparent antibiotic activity against commensal bacteria, including Lactobacillus and Bifidobacterium, which are known to inhibit the colonization of C. difficile. The exposure of C. difficile to the coprisin analogue caused a marked increase in nuclear propidium iodide (PI) staining, indicating membrane damage; the staining levels were similar to those seen with bacteria treated with a positive control for membrane disruption (EDTA). In contrast, coprisin analogue treatment did not trigger increases in the nuclear PI staining of Bifidobacterium thermophilum. This observation suggests that the antibiotic activity of the coprisin analogue may occur through specific membrane disruption of C. difficile. Thus, these results indicate that the coprisin analogue may prove useful as a therapeutic agent for C. difficile infection-associated inflammatory diarrhea and pseudomembranous colitis.-

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“…The production of molecules by the gut microbiota that have direct antibacterial activity may also contribute to colonization resistance against C. difficile. Organic acids produced by bacteria have been proposed to inhibit the in vitro growth of C. difficile, with culture supernatants from strains of Lactobacillus, Lactococcus, and Bifidobacterium species demonstrating pH-dependent anti-C. difficile activity (137)(138)(139). Growth of C. difficile is also inhibited by supernatants from Bacillus amyloliquefaciens cultures (140).…”

Section: Mechanisms Of Colonization Resistance Against CDImentioning

confidence: 99%

Gleaning Insights from Fecal Microbiota Transplantation and Probiotic Studies for the Rational Design of Combination Microbial Therapies

et al. 2017

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SUMMARY Beneficial microorganisms hold promise for the treatment of numerous gastrointestinal diseases. The transfer of whole microbiota via fecal transplantation has already been shown to ameliorate the severity of diseases such as Clostridium difficile infection, inflammatory bowel disease, and others. However, the exact mechanisms of fecal microbiota transplant efficacy and the particular strains conferring this benefit are still unclear. Rationally designed combinations of microbial preparations may enable more efficient and effective treatment approaches tailored to particular diseases. Here we use an infectious disease, C. difficile infection, and an inflammatory disorder, the inflammatory bowel disease ulcerative colitis, as examples to facilitate the discussion of how microbial therapy might be rationally designed for specific gastrointestinal diseases. Fecal microbiota transplantation has already shown some efficacy in the treatment of both these disorders; detailed comparisons of studies evaluating commensal and probiotic organisms in the context of these disparate gastrointestinal diseases may shed light on potential protective mechanisms and elucidate how future microbial therapies can be tailored to particular diseases.

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Inhibition of Clostridium difficile growth and adhesion to enterocytes by Bifidobacterium supernatants

Cited by 65 publications

References 36 publications

In vitro inhibition of Clostridium difficile by commercial probiotics: A microcalorimetric study

In vitro inhibition of Clostridium difficile by commercial probiotics: A microcalorimetric study

The Insect Peptide Coprisin Prevents Clostridium difficile-Mediated Acute Inflammation and Mucosal Damage through Selective Antimicrobial Activity

Gleaning Insights from Fecal Microbiota Transplantation and Probiotic Studies for the Rational Design of Combination Microbial Therapies

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