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Volume 5, Issue 6

The secretome inhibits the growth of complex mycobacteria Open Access

Abstract

, a commensal intestinal bacterium, was demonstrated to inhibit the growth of some complex (MTC) species that cause tuberculosis in humans and mammals. To further explore this preliminary observation, we cross-investigated five strains and seven MTC strains representative of four MTC species using a standardized quantitative agar well diffusion assay. All five strains, calibrated at 10 MacFarland, inhibited the growth of all strains with various susceptibility profiles, but no inhibition was observed with lower inoculums. Further, eight freeze-dried cell-free culture supernatants (CFCS) inhibited the growth of , and , the most susceptible MTC species (inhibition diameter 25±1 mm), proportionally to CFCS protein concentrations. The data reported here indicate that the secretome inhibited growth of all MTC species of medical interest, which broadens previously reported data. In the gut, the secretome may modulate the expression of tuberculosis, exhibiting an anti-tuberculosis effect, with some protective roles in human and animal health.

  • Received:
  • Accepted:
  • Published Online:
Keyword(s): anti-tuberculosis activity , Enterococcus mundtii , inhibition spectrum , Mycobacterium tuberculosis and tuberculosis
Funding
This study was supported by the:
  • Agence Nationale de la Recherche (Award [ANR-10-IAHU-03])
    • Principal Award Recipient: NotApplicable
  • Aix-Marseille Université
    • Principal Award Recipient: WafaaACHACHE
© 2023 The Authors
  • This is an open-access article distributed under the terms of the Creative Commons Attribution License.

Erratum

A correction has been published for this content:
Corrigendum: The secretome inhibits the growth of complex mycobacteria
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2023-06-23
2026-03-06

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The Enterococcus secretome inhibits the growth of Mycobacterium tuberculosis complex mycobacteria
Access Microbiology 5, 000471.v3 (2023); https://doi.org/10.1099/acmi.0.000471.v3
/content/journal/acmi/10.1099/acmi.0.000471.v3
/content/journal/acmi/10.1099/acmi.0.000471.v3
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