Human Lipoxin A4,LXA4 ELISA Kit
- Known as:
- Human Lipoxin A4,LXA4 Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- 201-12-0613
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Sunredbio SunBT Sun red bio
- Gene target:
- Human Lipoxin A4 LXA4 ELISA Kit
Related genes to: Human 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
Related products to: Human Lipoxin A4,LXA4 ELISA Kit
Related articles to: Human Lipoxin A4,LXA4 ELISA Kit
- Metabolic dysregulation is increasingly recognized as a critical contributor to asthma pathogenesis. Emerging clinical and metabolomic evidence has implicated histidine metabolism in asthma; however, whether histidine metabolic reprogramming contributes to severe asthma pathogenesis and the underlying mechanisms remain unclear. Here, we integrated clinical cohort analyses, multi-omics profiling, primary human airway epithelial cell experiments, and both toluene diisocyanate (TDI)- and house dust mite/lipopolysaccharide (HDM/LPS)-induced severe asthma murine models to systematically delineate this relationship. Histidine levels were markedly elevated in induced sputum from asthma patients and were strongly associated with disease severity, airflow limitation, and inflammatory indices. Integrated metabolomic and transcriptomic analyses revealed a pathogenic reprogramming of histidine metabolism, characterized by enhanced histamine biosynthesis and depletion of the cytoprotective carnosine, thereby amplifying airway inflammatory responses. Pharmacological blockade of histidine metabolism significantly alleviated airway hyperresponsiveness, inflammation, and structural remodeling in both TDI- and HDM/LPS-induced severe asthma models. Mechanistically, histidine metabolic dysregulation drives oxidative stress mediated mitochondrial dysfunction, leading to mtDNA release and subsequent activation of mt-ND6/FPR2 signaling, ultimately triggering necroptotic epithelial cell death. Collectively, these findings define a histidine-driven oxidative stress-mtDNA-necroptosis axis as a central mechanism of airway inflammation in severe asthma, offering new therapeutic opportunities through metabolic targeting. - Source: PubMed
Publication date: 2026/06/27
Chen YingHuang JunwenGong ZhaoqianLi YuemaoChen YaoxinFan KekeZhu BangMa YanyanHu DapengHuang ShuyuYang JiePeng XiaoqianZhao WenquZhao Haijin - Ulcerative colitis (UC) is a chronic inflammatory bowel disease (IBD). Neutrophil extracellular traps (NETs) have been recognized as contributing to UC progression. This study aimed to identify key genes driving NET formation in UC and evaluate their potential as biomarkers. - Source: PubMed
Publication date: 2026/06/01
Al-Jamali Hawra Zia HosseinSheikhesmaili FarshadMoradzad MohammadAhmadi AmjadJalili AliNikkhoo BahramRahmani Mohammad RezaFakhari Shohreh - ERK1/2 are core components of the MAPK signaling pathway and play a central role in the regulation of inflammation. Although ERK1/2 activation is well established for driving pro-inflammatory responses, accumulating evidence systematically summarized in this review demonstrates that ERK1/2 activation can also exert potent anti-inflammatory and pro-resolving effects. At the cellular level, ERK1/2 activation mediates anti-inflammatory regulation through multiple coordinated mechanisms: It promotes activation-induced cell death in T cells, drives macrophages and microglia toward anti-inflammatory phenotypes while fine-tuning their phagocytic activity, enhances efferocytosis of apoptotic cells by myeloid cells to drive inflammation resolution, inhibits dendritic cell maturation, and induces production of the key anti-inflammatory cytokine IL-10. At the molecular signaling pathway level, ERK1/2 suppresses pro-inflammatory NF-κB activity by stabilizing IκBα, directly interacting with NF-κB p65 subunit, or activating PPARγ in both immune cells and tissue-resident cells. In addition, ERK1/2 exerts anti-inflammatory effects through the Nrf2/HO-1 axis, which negatively regulates NF-κB. Further anti-inflammatory axes include the ERK1/2/CREB pathway and the FPR2/ERK1/2 pro-resolving signaling cascade. Other anti-inflammatory mechanisms include the ERK1/2/sCD14 axis that neutralizes LPS, ERK1/2-induced autophagy, and anti-inflammatory signaling triggered by diverse upstream regulators of ERK1/2. - Source: PubMed
Publication date: 2026/06/20
Tao KaiwenXu LinCheng ChaoYuan FukangYu YichengZhang LidanLi RunminXia RuiDong HaibeiWang Xingqi - Periodontitis is a chronic inflammatory disease driven by immune dysregulation, in which neutrophils play a central but functionally heterogeneous role. The contributions of specific neutrophil subsets to disease pathogenesis remain poorly defined. - Source: PubMed
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Sun YuqiangShen ZiHanZhen WenyuXu FeiLu YutongPan YufeiMi DaweiMa ShouzhengLi WeiSun WansuYu JintaoZhang Hengguo - The egg-derived tripeptides IRW and IQW have been widely reported to possess anti-inflammatory and -antioxidant effects. This study aims to investigate their mechanistic roles in modulating the LPS-induced acute intestinal immune stress. The findings indicated that IRW and IQW significantly alleviated the LPS-induced intestinal and mitochondrial damage. Notably, IRW and IQW significantly reduced the release of mitochondrial -formyl peptides (mtNFPs) caused by mitochondrial damage, which could activate FPR2. Consistently, FPR2 expression in the intestinal tissue was suppressed following peptide treatment. In addition, IRW and IQW inhibited ERK1/2 phosphorylation, which is potentially linked to improved mitochondrial function and reduced FPR2 expression. Metabolic analysis revealed elevated aspartate and glutamine levels while decreasing l-serine levels, which favored mitochondrial function recovery, suggesting that IRW and IQW can regulate mitochondrial function through amino acid metabolism. Overall, these findings indicate that the alleviating effects of IRW and IQW on LPS-induced intestinal immune stress are associated with the FPR2-mitochondrial axis. - Source: PubMed
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