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Published on: December 20, 2017
Variable responses of formyl peptide receptor haplotypes toward bacterial peptides
Jeannie M Gripentrog1, John S Mills, George J Saari
1Department of Microbiology, Montana State University, MT 59717, USA.
Abstract:
The chemoattractant neutrophil formyl peptide receptor (FPR) binds bacterial and mitochondrial N-formylated peptides, which allows the neutrophils to find the bacterial source and/or site of tissue damage. Certain inflammatory disorders may be due in part to an impaired innate immune system that does not respond to acute bacterial damage in a timely fashion. Because the human FPR is encoded by a large number of different haplotypes arising from ten single-nucleotide polymorphisms, we examined the possibility that some of these haplotypes are functionally distinct. We analyzed the response of three common FPR haplotypes to peptides from Escherichia coli, Mycobacterium avium ssp. paratuberculosis, and human mitochondria. All three haplotypes responded similarly to the E. coli and mitochondrial peptides, whereas one required a higher concentration of the M. avium peptide fMFEDAVAWF for receptor downregulation, receptor signaling, and chemotaxis. This raises the possibility of additional bacterial species differences in functional responses among FPR variants and establishes a precedent with potentially important implications for our innate immune response against bacterial infections. We also investigated whether certain FPR haplotypes are associated with rheumatoid arthritis (RA) by sequencing FPR1 from 148 Caucasian individuals. The results suggested that FPR haplotypes do not significantly contribute toward RA.
Insights
Investigating neutrophil formyl peptide receptor (FPR) function revealed distinct responses to bacterial peptides among FPR variants. This suggests potential impacts on innate immunity and bacterial infection responses.
Area of Science:
- Immunology
- Genetics
- Microbiology
Background:
- The neutrophil formyl peptide receptor (FPR) is crucial for innate immunity, detecting bacterial and mitochondrial peptides to guide neutrophils to sites of infection or damage.
- Functional variations in FPR, influenced by numerous haplotypes from single-nucleotide polymorphisms, may underlie differential immune responses.
- Impaired innate immune responses to bacterial damage can contribute to inflammatory disorders.
Purpose of the Study:
- To determine if different human FPR haplotypes exhibit distinct functional responses to bacterial and mitochondrial peptides.
- To investigate the potential association between FPR haplotypes and rheumatoid arthritis (RA).
Main Methods:
- Analysis of three common FPR haplotypes' responses to peptides from Escherichia coli, Mycobacterium avium ssp. paratuberculosis, and human mitochondria.
- Assessment of receptor downregulation, signaling, and chemotaxis.
- Sequencing of FPR1 in 148 Caucasian individuals to evaluate association with RA.
Main Results:
- All tested FPR haplotypes responded similarly to E. coli and mitochondrial peptides.
- One FPR haplotype exhibited a reduced response, requiring higher concentrations of the M. avium peptide fMFEDAVAWF for key functions.
- No significant association was found between FPR haplotypes and rheumatoid arthritis.
Conclusions:
- Functional differences exist among FPR haplotypes in response to specific bacterial peptides, with implications for innate immunity and bacterial infection outcomes.
- FPR haplotypes do not appear to be a significant genetic factor contributing to rheumatoid arthritis development.
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