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EDITORIAL article

Front. Cell. Infect. Microbiol., 09 March 2023
Sec. Microbiome in Health and Disease
This article is part of the Research Topic Mechanism of Colonization and Persistence of Gut Commensal Microbiota and Pathogens View all 5 articles

Editorial: Mechanism of colonization and persistence of gut commensal microbiota and pathogens

  • 1Center of Interventional Medicine for Precision and Advanced Cellular Therapy (IMPACT), Santiago, Chile
  • 2Laboratory of Nano-Regenerative Medicine, Centro de Investigación e Innovación Biomédica (CIIB), Faculty of Medicine, Universidad de los Andes, Santiago, Chile
  • 3Department of Biology, Texas A&M University, College Station, TX, United States
  • 4Departamento de Biología Molecular y Biotecnología, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, Ciudad de México, Mexico

In the gastrointestinal tract, a diverse microbial community, including eukaryotes, bacteria, archaea, and bacteriophage, plays a role in human health and disease (Fan and Pedersen, 2021). To establish and colonize the human gut, several physiological and biological stressors along the digestive tract, such as bacteriophages (Federici et al., 2021), antimicrobial peptides (Mookherjee et al., 2020), bile acids (Collins et al., 2022), and antibiotic intake (Maier et al., 2021), must be overcome by commensal and gut bacteria. In addition, commensal and pathogenic microorganisms have mechanisms to survive and persist in an unfavorable environment, including sporulation, persister cells, viable non-cultivable cells, the inclusion of specific metabolic routes, specific factors, and genetic changes (Dworkin and Losick, 2001). Furthermore, the microbiota is challenged by the intrinsic and extrinsic factors of their hosts, such as diet, age, communicable and non-communicable diseases, and even vaccination. Consequently, adaptation and survival mechanisms of the microbiota play a critical role in gut microbiota modeling. These mechanisms employed to endure and survive in the colonic tract have been explored mainly in pathogens, especially those contributing to the relapse or recurrence of disease (Colangeli et al., 2020; Castro-Córdova et al., 2021). Their role in gut commensals is about to be dissected.

In this Research Topic, we aimed to cover recent and novel research about mechanisms for colonization and persistence employed by commensal and pathogenic bacteria to help us understand which are the factors that shape gut microbiota organization. In addition, we expect to know why dysbiosis is increased in aging and which could be the factors that promote these changes.

The current Research Topic contains three original articles and one mini-review aiming to understand the host-microbial factors or interactions involved in the establishment and maintenance of a healthy microbiota.

The lifespan of different gut microbiota species is determined by age-related changes. Yan et al. studied gut microbiome changes across age groups, eating habits, and metabolism and observed an increase in a group of bacteria in older Chinese people (Bacteroides fragilis, Bifidobacterium longum, Clostridium bolteae, Escherichia coli, Klebsiella pneumoniae, and Parabacteroides merdae) compared with young individuals, that correlated with an enrichment in metabolic pathway activation related to lipopolysaccharide (LPS) biosynthesis and degradation of short-chain fatty acids (SCFAs). On the other hand, Vidal-Veuthey et al., describe the role of proteins secreted by the gut microbiota and its positive or negative influence on the host. Altogether, these suggest that the metabolic pathways associated with the gut microbiota can be related to the immune status and inflammation of older adults, and the discovery of new microbiota-secreted proteins with a positive impact on the host could have therapeutic potential to be used in certain diseases.

In general, the presence and abundance of a bacteria specie have been linked to the protection or risk of a determinate disease. Here, Vega et al. examine whether the changes in the abundance of a determinate microbiome community have been coined as biomarkers for intestinal inflammatory diseases (IBD). By studying the public data on microbiome of patients with IBD, the authors observed that a group of bacteria (Fusobacterium, Streptococcus, and Escherichia/Shigella) were clearly abundant in IBD microbiome. They discuss the importance of redefine microbiome biomarkers by including the intra-taxa diversity, environmental and genetic factors present in the host to explore new candidates for the next generation of probiotics.

Adeno-associated virus vectors are a promising biomedical technology due that can transduce peripheral, autonomic, and enteric nervous systems. Ma et al., describe the effects of transduction with intraperitoneally administered adeno-associated virus 9 (AAV9) vector in the fecal microbiota in rats, where they observed an efficient transduction in the colon and changes in the microbial diversity, as well as upregulation of anaerobic gut microbiota.

To conclude, the gut microbiota changes constantly and is affected by several factors, including diet, diseases, genetic factors, microbial interaction, and infection/diseases such as inflammatory diseases or AAV infection. However, the influence of the microbiota changes, affecting the metabolism and the secretion of bacterial proteins and its effects in the host, is still to be understood. Indeed, targeting the microbiome and its metabolism is an attractive target for the development of new probiotics for better aging and to combat diseases.

Author contributions

PC-C, MP-G, and AR-R contributed to the conception and design of the manuscript. PC-C wrote the first draft of the manuscript. All authors contributed to the article and approved the submitted version.

Funding

PC-C was founded by ANID Basal funding for Scientific and Technological Center of Excellence, IMPACT, #FB210024 grant. AR-R was funded by UNAM/PAPIIT grant IA206823.

Conflict of interest

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Publisher’s note

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.

References

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Keywords: microbiota, gut colonization, bacterial persistence, gut pathogen, commensal microbiota

Citation: Castro-Córdova P, Pizarro-Guajardo M and Romero-Rodríguez A (2023) Editorial: Mechanism of colonization and persistence of gut commensal microbiota and pathogens. Front. Cell. Infect. Microbiol. 13:1176453. doi: 10.3389/fcimb.2023.1176453

Received: 28 February 2023; Accepted: 02 March 2023;
Published: 09 March 2023.

Edited and Reviewed by:

Benoit Chassaing, Institut National de la Santé et de la Recherche Médicale (INSERM), France

Copyright © 2023 Castro-Córdova, Pizarro-Guajardo and Romero-Rodríguez. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

*Correspondence: Alba Romero-Rodríguez, YWxiYXJvbWVyb0BpaWJpb21lZGljYXMudW5hbS5teA==; Pablo Castro-Córdova, cGFjYXN0cm9AdWFuZGVzLmNs

Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.