Role of toll-like receptors and nod-like receptors in acute lung infection.
NOD (nucleotide binding and oligomerization domain) and leucine rich repeat containing receptor (NLR)
Neutrophil
TLR - toll-like receptor
cytokine
lung
Journal
Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960
Informations de publication
Date de publication:
2023
2023
Historique:
received:
28
06
2023
accepted:
28
07
2023
medline:
5
9
2023
pubmed:
4
9
2023
entrez:
4
9
2023
Statut:
epublish
Résumé
The respiratory system exposed to microorganisms continuously, and the pathogenicity of these microbes not only contingent on their virulence factors, but also the host's immunity. A multifaceted innate immune mechanism exists in the respiratory tract to cope with microbial infections and to decrease tissue damage. The key cell types of the innate immune response are macrophages, neutrophils, dendritic cells, epithelial cells, and endothelial cells. Both the myeloid and structural cells of the respiratory system sense invading microorganisms through binding or activation of pathogen-associated molecular patterns (PAMPs) to pattern recognition receptors (PRRs), including Toll-like receptors (TLRs) and NOD-like receptors (NLRs). The recognition of microbes and subsequent activation of PRRs triggers a signaling cascade that leads to the activation of transcription factors, induction of cytokines/5chemokines, upregulation of cell adhesion molecules, recruitment of immune cells, and subsequent microbe clearance. Since numerous microbes resist antimicrobial agents and escape innate immune defenses, in the future, a comprehensive strategy consisting of newer vaccines and novel antimicrobials will be required to control microbial infections. This review summarizes key findings in the area of innate immune defense in response to acute microbial infections in the lung. Understanding the innate immune mechanisms is critical to design host-targeted immunotherapies to mitigate excessive inflammation while controlling microbial burden in tissues following lung infection.
Identifiants
pubmed: 37662905
doi: 10.3389/fimmu.2023.1249098
pmc: PMC10469605
doi:
Substances chimiques
NLR Proteins
0
Toll-Like Receptors
0
Pathogen-Associated Molecular Pattern Molecules
0
Types de publication
Journal Article
Review
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
1249098Subventions
Organisme : NHLBI NIH HHS
ID : F31 HL168986
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI140500
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI157353
Pays : United States
Informations de copyright
Copyright © 2023 Le, Kulatheepan and Jeyaseelan.
Déclaration de conflit d'intérêts
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.
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