Research Topic

Role of Corynebacterium spp. in Regulation of Staphylococcus aureus Virulence

About this Research Topic

Microbial competition exists in the general environment, such as soil or aquatic habitats, upon or within unicellular or multicellular eukaryotic life forms. Interspecific competition has been reported in several human-associated bacterial communities. On human skin and mucosal surfaces, the outcome of microbial competition determines our normal flora, which are essential for health and immune homeostasis. Staphylococcus aureus is a clinically relevant human pathogen causing an array of serious hospital- or community-acquired infections worldwide. S. aureus asymptomatically colonize about 25% of humans as a member of the nostril and skin microbiota, where it resides with other bacteria including commensal Corynebacterium species. Microbial ecological studies of the anterior naris have revealed the dominance of Corynebacterium, Staphylococcus and Propionibacterium species. Commensal bacteria can play a role in maintaining health by influencing S. aureus gene expression toward a commensal lifestyle or by limiting its expansion, both of which would limit the risk of acute infection.

The molecular mechanisms that regulate microbial competition, leading to niche establishment and microbial monopolization, remain undetermined. A cute hypothesis suggests that microbes regulate and optimize their production of such compounds to kill, limit the growth of or modulate the metabolism of potential niche competitors for maximal advantage. Different factors contribute to the outcome of microbial competition, such as the collection of molecules exchanged between the competing organisms, their respective cell densities and the initial spatial configuration or direction of the microbe–microbe interaction. S. aureus-Corynebacterium interactions limit S. aureus virulence. The molecules facilitating these specific interactions probably are unknown but probably located at the interface between S. aureus and the respective Corynebacterium species, and might be amenable to characterization by means of imaging mass spectrometry.

This Research Topic will accept articles of the type Hypothesis and Theory, Methods, Mini Review, Opinion, Original Research and Perspective that contribute to elucidate the molecular mechanisms involved in the interaction of S. aureus with Corynebacterium spp. and help identify the interactive molecules that act regulating S. aureus virulence and their action mechanism.


Keywords: Staphylococcus aureus, Corynebacterium, microbial competition, virulence regulation


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

Microbial competition exists in the general environment, such as soil or aquatic habitats, upon or within unicellular or multicellular eukaryotic life forms. Interspecific competition has been reported in several human-associated bacterial communities. On human skin and mucosal surfaces, the outcome of microbial competition determines our normal flora, which are essential for health and immune homeostasis. Staphylococcus aureus is a clinically relevant human pathogen causing an array of serious hospital- or community-acquired infections worldwide. S. aureus asymptomatically colonize about 25% of humans as a member of the nostril and skin microbiota, where it resides with other bacteria including commensal Corynebacterium species. Microbial ecological studies of the anterior naris have revealed the dominance of Corynebacterium, Staphylococcus and Propionibacterium species. Commensal bacteria can play a role in maintaining health by influencing S. aureus gene expression toward a commensal lifestyle or by limiting its expansion, both of which would limit the risk of acute infection.

The molecular mechanisms that regulate microbial competition, leading to niche establishment and microbial monopolization, remain undetermined. A cute hypothesis suggests that microbes regulate and optimize their production of such compounds to kill, limit the growth of or modulate the metabolism of potential niche competitors for maximal advantage. Different factors contribute to the outcome of microbial competition, such as the collection of molecules exchanged between the competing organisms, their respective cell densities and the initial spatial configuration or direction of the microbe–microbe interaction. S. aureus-Corynebacterium interactions limit S. aureus virulence. The molecules facilitating these specific interactions probably are unknown but probably located at the interface between S. aureus and the respective Corynebacterium species, and might be amenable to characterization by means of imaging mass spectrometry.

This Research Topic will accept articles of the type Hypothesis and Theory, Methods, Mini Review, Opinion, Original Research and Perspective that contribute to elucidate the molecular mechanisms involved in the interaction of S. aureus with Corynebacterium spp. and help identify the interactive molecules that act regulating S. aureus virulence and their action mechanism.


Keywords: Staphylococcus aureus, Corynebacterium, microbial competition, virulence regulation


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

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Submission Deadlines

17 October 2020 Abstract
14 February 2021 Manuscript

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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Topic Editors

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Submission Deadlines

17 October 2020 Abstract
14 February 2021 Manuscript

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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