IL-4 Down-Regulates Lipopolysaccharide-Induced Formyl Peptide Receptor 2 in Murine Microglial Cells by Inhibiting the Activation of Mitogen-Activated Protein Kinases

Iribarren, Pablo; Cui, Yinghui; Le, Yingying; Guo, Ying; Zhang, Xia; Gong, Wanghua; Wang, Ji Ming

doi:10.4049/jimmunol.171.10.5482

Cited by 26 publications

(21 citation statements)

References 36 publications

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“…1C). This is consistent with previous studies showing that LPS treatment can increase the chemotactic response of macrophages to formylated peptides (10,11).…”

Section: Lps Induces Fpr1 Mrna Via Transcriptional and Posttranscriptsupporting

confidence: 82%

Lipopolysaccharide Induces Formyl Peptide Receptor 1 Gene Expression in Macrophages and Neutrophils via Transcriptional and Posttranscriptional Mechanisms

Mandal

Novotny

Hamilton

2005

The Journal of Immunology

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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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“…1C). This is consistent with previous studies showing that LPS treatment can increase the chemotactic response of macrophages to formylated peptides (10,11).…”

Section: Lps Induces Fpr1 Mrna Via Transcriptional and Posttranscriptsupporting

confidence: 82%

Lipopolysaccharide Induces Formyl Peptide Receptor 1 Gene Expression in Macrophages and Neutrophils via Transcriptional and Posttranscriptional Mechanisms

Mandal

Novotny

Hamilton

2005

The Journal of Immunology

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“…Another interesting finding is that LPS similarly to A␤ impairs CD11c expression by microglia (unpublished observation), and both induce similar patterns of mitogen-activated protein kinase activation in microglia (32). IL-4 can attenuate a mitogenactivated protein kinase pathway activated by LPS, an effect evidently associated with serine͞threonine phosphatase activity (33). The latter phenomenon might indeed serve as a molecular mechanism underlying the present finding that IL-4 attenuates the detrimental effect of A␤-activated microglia.…”

Section: Discussionmentioning

confidence: 60%

Glatiramer acetate fights against Alzheimer’s disease by inducing dendritic-like microglia expressing insulin-like growth factor 1

Butovsky

Koronyo‐Hamaoui

Kunis

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

369

348

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Alzheimer's disease (AD) is characterized by plaque formation, neuronal loss, and cognitive decline. The functions of the local and systemic immune response in this disease are still controversial. Using AD double-transgenic (APP͞PS1) mice, we show that a T cell-based vaccination with glatiramer acetate, given according to a specific regimen, resulted in decreased plaque formation and induction of neurogenesis. It also reduced cognitive decline, assessed by performance in a Morris water maze. The vaccination apparently exerted its effect by causing a phenotype switch in brain microglia to dendritic-like (CD11c) cells producing insulin-like growth factor 1. In vitro findings showed that microglia activated by aggregated ␤-amyloid, and characterized as CD11b ؉ ͞CD11c ؊ ͞ MHC class II ؊ ͞TNF-␣ ؉ cells, impeded neurogenesis from adult neural stem͞progenitor cells, whereas CD11b ؉ ͞CD11c ؉ ͞MHC class II ؉ ͞TNF-␣ ؊ microglia, a phenotype induced by IL-4, counteracted the adverse ␤-amyloid-induced effect. These results suggest that dendritic-like microglia, by facilitating the necessary adjustment, might contribute significantly to the brain's resistance to AD and argue against the use of antiinflammatory drugs.␤-amyloid ͉ CD11c ͉ T cell vaccination ͉ immunomodulation ͉ neurodegeneration

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“…Immune cells possess high sensitivity to LPS with the activation of various intracellular cascades that induce the expression of defense systems. Interestingly, LPS-induced increased expression has also been observed for Fpr1 and Fpr2 in microglial cells (48,49) and for Fpr1 in neutrophils (50). We now show that Fpr3 belongs to the group of genes that are up-regulated after LPS exposure in immune cells and thus likely contributes to immune defense against bacteria.…”

Section: Discussionmentioning

confidence: 68%

Strain-specific Loss of Formyl Peptide Receptor 3 in the Murine Vomeronasal and Immune Systems

Stempel¹,

Jung

Pérez-Gómez³

et al. 2016

Journal of Biological Chemistry

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Social animals benefit from sharing information that promotes fitness and survival (1-3). In rodents, there is extensive evidence that the detection of chemosensory cues emitted by other individuals is a fundamental feature of social recognition and a prerequisite for a wide range of social behaviors (4 -6).For example, rodents use such chemical signals to distinguish between parasitized individuals, recognize infected conspecifics, and avoid and display aversive responses to infected individuals (7-9). Defining the cellular and molecular mechanisms and neural circuits underlying the detection of infection-and illness-associated states is not only crucial for understanding the sensing of health status in animals but also for advancing our knowledge of disease-related odors and diagnostic olfactory biomarkers in humans (10, 11).The vomeronasal organ (VNO) 4 is an olfactory substructure of the mammalian nose that is essential for social recognition and chemical communication (12). The VNO houses vomeronasal sensory neurons (VSNs), specialized nerve cells that detect a wide range of volatile and non-volatile molecular cues, including pheromones and predator odors (13-15). Among these cues are major histocompatibility complex class I binding peptides (antigens) and other small urinary peptides (16 -18) thus providing initial support for an evolutionary link between recognition mechanisms in immune cells and subsets of VSNs (14, 19). More recently, clear evidence has emerged that the VNO plays an important role in mediating sick conspecific avoidance and thus seems to function as a sensor of infection (20), but the underlying cellular and molecular basis for this function remains unclear. VSNs are characterized by the expression of large families of G protein-coupled receptors, vomeronasal type 1 receptors (Vmn1r) expressed in the apical vomeronasal layer and vomeronasal type 2 receptor (Vmn2r) that function together with non-classical class I major histocompatibility complex receptors of the H2-Mv subtype in the basal layer (21, 22). An important development has been the identification of a third family of G protein-coupled receptors expressed in subsets of VSNs as follows: the formyl peptide receptors (Fprs) (23,24). Fprs are primarily known from the innate immune system where they are involved in chemoattraction of phagocytic immune cells to sites of infection mediating host defense against invading microorganisms (25-28). Fprs detect a wide range of inflammation markers as well as bacterial and mitochondrial peptides (25-28), and consistent with the results from immune cells, some of these ligands have also been shown to activate specific VSNs (23,29). Hence, members of the Fpr family are currently prime candidates for mediating VNO pathogen sensing, although it cannot be ruled out that

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IL-4 Down-Regulates Lipopolysaccharide-Induced Formyl Peptide Receptor 2 in Murine Microglial Cells by Inhibiting the Activation of Mitogen-Activated Protein Kinases

Cited by 26 publications

References 36 publications

Lipopolysaccharide Induces Formyl Peptide Receptor 1 Gene Expression in Macrophages and Neutrophils via Transcriptional and Posttranscriptional Mechanisms

Lipopolysaccharide Induces Formyl Peptide Receptor 1 Gene Expression in Macrophages and Neutrophils via Transcriptional and Posttranscriptional Mechanisms

Glatiramer acetate fights against Alzheimer’s disease by inducing dendritic-like microglia expressing insulin-like growth factor 1

Strain-specific Loss of Formyl Peptide Receptor 3 in the Murine Vomeronasal and Immune Systems

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