Lipopolysaccharide Induces Formyl Peptide Receptor 1 Gene Expression in Macrophages and Neutrophils via Transcriptional and Posttranscriptional Mechanisms
Open accessAbstract
Bacterial infection promotes the infiltration of inflammatory leukocytes mediated in part by receptors for formyl-methionine-terminated peptides. In this study, we show that LPS can markedly enhance the expression of the formyl peptide receptor gene (FPR1) in mouse macrophages and neutrophils by enhancing transcription and by stabilization of the mRNA. In untreated cells, FPR1 mRNA exhibits a half-life of ∼90 min and this is markedly increased (to >6 h) following stimulation with LPS. Although FPR1 mRNA levels remained elevated over baseline for >20 h after stimulation, the half-life of the message is prolonged only transiently. LPS-induced FPR1 mRNA expression is mediated in part by the intermediate production of secreted factors. First, the response to LPS is partially blocked by the translational inhibitor cycloheximide. Second, a heat-labile but polymyxin B-insensitive factor present in supernatants from LPS-treated cells stimulates enhanced expression of FPR1 mRNA and, like LPS, promotes stabilization of FPR1 mRNA. Furthermore, supernatants from LPS-treated wild-type macrophages can stimulate FPR1 mRNA expression in LPS-insensitive macrophages from TLR4-mutant mice. Elevated FPR1 mRNA expression is also induced in response to ligands for TLR2 and TLR3. TNF-α but not IL-1, IL-6, IFN-β, and IFN-γ can mimic the effects of LPS although other factors apparently also contribute. Collectively, these findings define a distinct molecular pattern of response to TLR stimulation in inflammatory phagocytes and demonstrate that regulation of FPR1 expression is achieved through both transcriptional and posttranscriptional mechanisms.
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TNF and LPS may prime neutrophils by upregulating FPR1 expression.
“Some of the factors involved in priming these neutrophils could include TNF and LPS, which are known to upregulate the expression of FPR1 on neutrophils181–183.”
From The role of mitochondria in rheumatic diseases (2022) · cites this paper as [182]
The section “LPS induces FPR1 mRNA via transcriptional and posttranscriptional mechanisms” (page not supplied) reports increased FPR1 mRNA in mouse neutrophils after LPS treatment. The cytokine experiments (Fig. 7; page not supplied) show that TNF-α increased FPR1 mRNA in macrophages, not neutrophils. The paper therefore supports the LPS portion but does not establish that TNF upregulates FPR1 in neutrophils or directly demonstrate neutrophil priming. (LLM, conf=0.87)
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Immune Mechanisms in Arterial Homeostasis and Disease
Besla, R. (2019) · TSpace (University of Toronto)
- Authors
- Mandal, P., Novotny, M., & Hamilton, T. A.
- Affiliations
- Cleveland Clinic (US)
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2005-11-01
- Volume
- 175
- Issue
- 9
- Pages
- 6085-6091
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W2145261393
- Cited by
- 45
- References
- 37
- Citations by year
- 2025: 1 · 2024: 1 · 2023: 1 · 2022: 3 · 2021: 1 · 2020: 1 · 2019: 5 · 2018: 2 · 2017: 4 · 2016: 4 · 2015: 5 · 2014: 3 · 2012: 3
- FWCI
- 0.95
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- U.S. Public Health Service (CA39621)
- National Cancer Institute (CA-39621, CA62220, P01CA062220, R01CA039621)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Health Sciences › Medicine › Oncology › Chemokine receptors and signaling
- Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Keywords
- lipopolysaccharide, FPR1, macrophages, neutrophils, mRNA stabilization, post-transcriptional regulation, transcriptional regulation, TLR4, TLR2, TLR3, TNF-α, cycloheximide, heat-labile factor, bacterial infection
- MeSH terms
- Animals, Antigens, Differentiation, Female, Gene Expression Regulation, Lipopolysaccharides, Macrophages, Mice, Inbred C3H, Mice, Inbred C57BL, Receptors, Immunologic, RNA, Messenger, Transcription, Genetic, Receptors, Formyl Peptide, Adaptor Proteins, Signal Transducing, Toll-Like Receptor 4, Mice, Myeloid Differentiation Factor 88
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