Monkey Lipoxin A4,LXA4 ELISA Kit
- Known as:
- Monkey Lipoxin A4,LXA4 Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- ML004
- Product Quantity:
- 96T
- Category:
- -
- Supplier:
- Meretciel
- Gene target:
- Monkey Lipoxin A4 LXA4 ELISA Kit
Related genes to: Monkey Lipoxin A4,LXA4 ELISA Kit
- Gene:
- FPR2 NIH gene
- Name:
- formyl peptide receptor 2
- Previous symbol:
- FPRL1
- Synonyms:
- LXA4R, HM63, FPRH2, FMLPX, FPR2A, FMLP-R-II, ALXR
- Chromosome:
- 19q13.41
- Locus Type:
- gene with protein product
- Date approved:
- 1991-06-05
- Date modifiied:
- 2016-01-15
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- Although the extracellular matrix (ECM) is a highly dynamic partner of the immune system, its immunoregulatory role during the early phase of sepsis-induced acute lung injury (ALI) remains poorly defined. Using a murine cecal ligation and puncture (CLP) model, we observed dynamic ECM remodeling characterized by rapid collagen loss within 24 h, followed by a pathological fibroproliferation phase. Proteomic profiling of the degraded ECM demonstrated its immunoregulatory potential. In vitro studies revealed that annexin A1 (ANXA1), an upregulated ECM component, promoted anti-inflammatory macrophage polarization via the formyl-peptide receptor 2/lipoxin A4 (FPR2/ALX)-dependent 5'-adenosine monophosphate-activated protein kinase (AMPK)-mammalian target of rapamycin (mTOR) pathway. However, under pathological conditions, collagen loss markedly reduces the number of key binding sites for integrin β1 (Itgb1), thereby disrupting macrophage-ECM adhesion and resulting in macrophage detachment; upon entering the inflammatory microenvironment, these cells acquire a proinflammatory phenotype, exacerbating pulmonary inflammation. Capitalizing on the collagen biosynthetic function of ascorbic acid (AA), we investigated its capacity to restore macrophage-ECM adhesion therapeutically. In vitro, treatment of fibroblasts with AA on decellularized CLP-ECM increased collagen deposition and improved macrophage adhesion. In vivo, intratracheal instillation of AA (20 mg/kg) enhanced collagen biosynthesis, which promoted ECM restoration, sustained interstitial macrophage retention, suppressed proinflammatory cytokine production, and ultimately resolved lung injury. Our study reveals that ECM degradation is an early immunoregulatory event and suggests a therapeutic approach for ECM repair via airway-targeted AA delivery in ALI. - Source: PubMed
Publication date: 2026/05/22
Xie FeiyanSun YuhengWei XinyanZhang WeiLuo WeiHuang JieFang ShencunZhang XinxinQiu HaiboChao Jie - Annexin A1 (AnxA1) is a key anti-inflammatory mediator that regulates both innate and adaptive immunity, promoting resolution of inflammation and tissue repair. It is highly expressed in neutrophils, macrophages, dendritic cells, and select lymphocyte subsets, where it limits excessive immune activation and maintains immune homeostasis. Through binding to the G protein-coupled receptor formyl peptide receptor 2 (FPR2/ALX), AnxA1 induces neutrophil apoptosis and promotes macrophage polarization toward an anti-inflammatory M2 phenotype. In adaptive immunity, AnxA1 regulates CD4 T-cell differentiation in a lineage-specific manner, promoting Th1 and Th17 responses while suppressing Th2 polarization; its deficiency skews T cells toward a Th2 phenotype with increased IL-4/IL-13 and reduced IL-17, highlighting its role in maintaining T-cell balance. In autoimmune and inflammatory disorders such as rheumatoid arthritis, lupus, type-1 diabetes, and multiple sclerosis, hyperactivation of toll-like receptor-4 (TLR4) and epidermal growth factor receptor (EGFR) drives STAT1-dependent signaling, sustaining cytokine production and tissue injury. The Annexin A2 (AnxA2)-EGFR complex further amplifies this response by downregulating AnxA1 and reinforcing pro-inflammatory signaling pathways. In contrast, AnxA1 engagement with EGFR and FPR2 redirects signaling toward STAT3, enhancing IL-10 and TGF-β production while suppressing STAT1-driven pathways. This STAT1-STAT3 balance is critical for immune resolution, inflammation control, and tissue homeostasis. Therapeutically, AnxA1-based strategies suppress STAT1 signaling and promote a regulated STAT3/SOCS3 axis associated with immune resolution, while limiting pathogenic Th17-associated STAT3 activity. Overall, AnxA1 acts as a molecular switch integrating receptor-mediated signals to fine-tune immune responses and mitigate tissue damage in chronic inflammatory and autoimmune diseases. - Source: PubMed
Publication date: 2026/05/19
Ambrish ThrupthiJayaswamy Pavan KHaridas VikramKellarai AdithiShetty SukanyaShetty Praveenkumar - Neutrophils, the most abundant leukocyte population, play a central role in host defense against (GBS), an encapsulated bacterium that frequently causes severe infections in humans, including sepsis and meningitis. However, the molecular pathways by which human neutrophils detect and respond to GBS remain incompletely defined. - Source: PubMed
Publication date: 2026/05/04
Fiore LuigiDe Gaetano Giuseppe ValerioGrasso FedericaCoppolino FrancescoFamà AgataStifano MariachiaraPetrungaro AnnamariaVita FedericaQuartarone EugeniaCipollina ChiaraLentini GermanaBeninati Concetta - Patients with advanced high-grade serous ovarian carcinoma (HGSOC) often experience extremely poor prognoses due to extensive peritoneal metastases, yet the underlying driving mechanisms remain unclear. This study reveals that serum amyloid A1 (SAA1) is markedly upregulated in late-stage HGSOC and is closely associated with poor prognosis and distant metastasis. These findings were validated through both single-cell RNA sequencing and clinical specimen analyses. Surprisingly, SAA1 does not directly promote tumour cell proliferation or migration. Instead, it reshapes the immunosuppressive tumour microenvironment by activating FPR2 tumour-associated macrophages (TAMs). Mechanistically, the SAA1-FPR2 signalling axis triggers the JAK2/STAT3 pathway in macrophages, enhancing the transcription and secretion of CXCL1. This, in turn, induces epithelial-mesenchymal transition (EMT) in tumour cells and endows them with greater metastatic potential. Animal models further confirmed that SAA1 knockdown, macrophage depletion, or CXCL1 blockade all significantly suppressed peritoneal dissemination. Collectively, this study identifies a novel SAA1-TAM-CXCL1 immune-inflammatory signalling axis, elucidates its critical role in ovarian cancer metastasis, and provides a robust theoretical foundation for the development of innovative anti-metastatic therapeutic strategies. KEY POINTS: A distinct SAA1-enriched tumour cell subset with metastasis-associated features is identified in ovarian cancer. Tumour-derived SAA1 reprograms TAM through FPR2-mediated JAK2-STAT3 signalling to induce an immunosuppressive phenotype. The SAA1-TAM-CXCL1 axis facilitates metastatic progression in ovarian cancer. - Source: PubMed
Zhou XuanMeng HuangyangChang QianjingRen JingjingWen MeichenZhang LinCheng Wenjun - Oxidative stress and inflammation are two closely related pathogenesis processes during ischemic injury. The current study investigated the neuroprotective effects of resolvin D1 (RvD1, a pro-resolving mediator) and its corresponding receptor formyl peptide receptor 2 (FPR2) in a rat model of middle cerebral artery occlusion (MCAO). Dynamic expressions of endogenous RvD1 and FPR2 in ischemic hemisphere were firstly examined by ELISA and western blot respectively. To explore the therapeutic effects of RvD1/FPR2 on ischemic injury, exogenous RvD1 were given at 0.4 µg/kg after MCAO (i.p.). Boc-2 (specific FPR2 antagonist to inhibit effects of RvD1/FPR2) were administered at 0.4 mg/kg (i.p.) 30 min before MCAO to inhibit the binding of RvD1 to FPR2. For evaluating ischemic injury, neurological performances were determined by deficit score and grip strength, and infarction volume were assayed by TTC. Neuronal damage was further observed by stainings of H&E, Fluoro-Jade C (FJC), and TUNEL. Inflammation markers were assayed by MPO immunostaining and mRNA dectection. Oxidative stress was determined by related kits (MDA, NO, GSH and SOD) and MitoSOX staining. Our results showed that endogenous cerebral levels of RvD1 were decreased after focal ischemia, but expression of FPR2 was increased. Exogenous RvD1 treatment alleviated neurological deficits, reduced infarct volume and attenuated neuronal apoptosis, however, inhibition of FPR2 by Boc-2 inhibited these effects. Furthermore, RvD1 reduced MPO positive cells and mRNA levels of pro-inflammatory mediators (TNF-α, IL-1β, and iNOS), but increased mRNA levels of anti-inflammatory mediators (TGF-β1 and IL-10). Concurrently, RvD1 inhibited oxidative stress, evidenced by down-regulated pro-oxidative mediators (such as MDA and NO) and up-regulated anti-oxidative mediators (SOD and GSH). Boc-2 alleviated the anti-inflammatory and anti-oxidant effects of RvD1. Mechanistically, RvD1 decreased expression of NOX2 in microglia and astrocytes, while co-administration of Boc-2 reversed these effects. These finding demonstrate that RvD1/FPR2 alleviated cerebral ischemic injury by attenuating inflammation and oxidative stress, which is beneficial to break the vicious cycle between inflammation and oxidative stress, thus highlighting its potential role in treatment for ischemic stroke. - Source: PubMed
Publication date: 2026/05/11
Wu FanghuaQiu WentingLi JieyuanZhou YafanDai JiayingZhang YaxingZhou YaqiXu JieanLiu YulianGao YurongLiu Wei