Macrophage cytokine responses to commensal Gram-positive Lactobacillus salivarius strains are TLR2-independent and Myd88-dependent.


Journal

Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288

Informations de publication

Date de publication:
15 03 2021
Historique:
received: 16 02 2020
accepted: 26 02 2021
entrez: 16 3 2021
pubmed: 17 3 2021
medline: 15 12 2021
Statut: epublish

Résumé

The mechanisms through which cells of the host innate immune system distinguish commensal bacteria from pathogens are currently unclear. Toll-like receptors (TLRs) are a class of pattern recognition receptors (PRRs) expressed by host cells which recognize microbe-associated molecular patterns (MAMPs) common to both commensal and pathogenic bacteria. Of the different TLRs, TLR2/6 recognize bacterial lipopeptides and trigger cytokines responses, especially to Gram-positive and Gram-negative pathogens. We report here that TLR2 is dispensable for triggering macrophage cytokine responses to different strains of the Gram-positive commensal bacterial species Lactobacillus salivarius. The L. salivarius UCC118 strain strongly upregulated expression of the PRRs, Mincle (Clec4e), TLR1 and TLR2 in macrophages while downregulating other TLR pathways. Cytokine responses triggered by L. salivarius UCC118 were predominantly TLR2-independent but MyD88-dependent. However, macrophage cytokine responses triggered by another Gram-positive commensal bacteria, Bifidobacterium breve UCC2003 were predominantly TLR2-dependent. Thus, we report a differential requirement for TLR2-dependency in triggering macrophage cytokine responses to different commensal Gram-positive bacteria. Furthermore, TNF-α responses to the TLR2 ligand FSL-1 and L. salivarius UCC118 were partially Mincle-dependent suggesting that PRR pathways such as Mincle contribute to the recognition of MAMPs on distinct Gram-positive commensal bacteria. Ultimately, integration of signals from these different PRR pathways and other MyD88-dependent pathways may determine immune responses to commensal bacteria at the host-microbe interface.

Identifiants

pubmed: 33723368
doi: 10.1038/s41598-021-85347-7
pii: 10.1038/s41598-021-85347-7
pmc: PMC7961041
doi:

Substances chimiques

Cytokines 0
Ligands 0
Myeloid Differentiation Factor 88 0
NF-kappa B 0
Receptors, Pattern Recognition 0
Toll-Like Receptor 2 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

5896

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Auteurs

Sreeram Udayan (S)

APC Microbiome Ireland, University College Cork, Cork, Ireland.
School of Biochemistry and Cell Biology, University College Cork, Cork, Ireland.

Ludovica F Buttó (LF)

APC Microbiome Ireland, University College Cork, Cork, Ireland.

Valerio Rossini (V)

APC Microbiome Ireland, University College Cork, Cork, Ireland.

Janaki Velmurugan (J)

APC Microbiome Ireland, University College Cork, Cork, Ireland.

Maria Martinez-Lopez (M)

Immunobiology Laboratory, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain.

David Sancho (D)

Immunobiology Laboratory, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain.

Silvia Melgar (S)

APC Microbiome Ireland, University College Cork, Cork, Ireland.

Paul W O'Toole (PW)

APC Microbiome Ireland, University College Cork, Cork, Ireland.
School of Microbiology, University College Cork, Cork, Ireland.

Ken Nally (K)

APC Microbiome Ireland, University College Cork, Cork, Ireland. k.nally@ucc.ie.
School of Biochemistry and Cell Biology, University College Cork, Cork, Ireland. k.nally@ucc.ie.

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