The ambiguous role of FPR1 in immunity and inflammation

No impact of cancer and plague-relevant FPR1 polymorphisms on COVID-19

“…5 Formyl peptide receptor 1 (FPR1) is a patternrecognition receptor (PRR) 10 that is mostly expressed by myeloid cells including granulocytes, macrophages, and dendritic cells. 11 Like other PRRs, FPR1 recognizes pathogen-associated molecular patterns (PAMPs), which are microbial structures, and danger-associated molecular patterns (DAMPs), which are host molecules displayed on, or released by, stressed and dying cells. [12][13][14][15] As its name indicates, FPR1 recognizes formylated peptides, mostly peptides from bacteria that have undergone a prokaryote-specific post-translation protein modification called formylation.…”

“…24 The roles of FPR1 in the response to infectious pathogens can be either positive or negative. 11,22 Thus, FPR1-deficient mice are more susceptible to lethal infection by Escherichia coli and Listeria monocytogenes 25,26 but resistant against Yersinia pestis, the agent causing plague. 27 Similarly, FPR1 has an ambiguous role in the context of noninfectious diseases.…”

A major genetic accelerator of cancer diagnosis: rs867228 in FPR1

“…Although it is tempting to speculate that this effect might result from compromised immunosurveillance, it might also involve reduced inflammatory reactions, knowing that FPR1 tends to stimulate tissue inflammation. 15 Moreover, at this point, it cannot be excluded that FPR1 would influence other general cancer-predisposing phenotypes including diabetes and overweight. Future adjusted analyses must clarify this issue.…”

“…FPR1 has multiple functions, not only in immunosurveillance but also in the acute response to inflammatory signals and the resolution of inflammation. 14,15 It is possible, yet remains to be demonstrated, that rs867228 affects both anticancer immunosurveillance and procarcinogenic inflammation, likely in an opposite fashion, thus explaining its capacity to accelerate the age of cancer diagnosis without affecting the incidence of malignant disease nor the prognosis of tumor patients. Irrespective of this speculation, it appears that the diagnosis-accelerating effect of rs867228 is demographically relevant.…”

An independent predictor of poor prognosis in locally advanced rectal cancer: rs867228 in formyl peptide receptor 1 (FPR1)

“…For example, FPR1 mediates neutrophil activation and migration in innate immunity, DC positioning, and maturation in adaptive immunity and antitumor immunity. 7 Several single nucleotide polymorphisms (SNPs) were reported to influence the functions of FPR1. Among these SNPs, E346A (rs867228, c. 1037 A > C) is a loss-of-function SNP that affects the extreme C-terminus of FPR1, thus altering the interaction with Gi-proteins and causing defective signal transduction.…”