CCL22 Antibody (Center) Blocking Peptide
- Known as:
- CCL22 Antibody (Center) Blocking Peptide
- Catalog number:
- BP16351c
- Product Quantity:
- 2
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- CCL22 Antibody (Center) Blocking Peptide
Related genes to: CCL22 Antibody (Center) Blocking Peptide
- Gene:
- CCL22 NIH gene
- Name:
- C-C motif chemokine ligand 22
- Previous symbol:
- SCYA22
- Synonyms:
- MDC, STCP-1, ABCD-1, DC/B-CK, A-152E5.1, MGC34554
- Chromosome:
- 16q21
- Locus Type:
- gene with protein product
- Date approved:
- 1997-08-22
- Date modifiied:
- 2016-10-05
Related products to: CCL22 Antibody (Center) Blocking Peptide
Related articles to: CCL22 Antibody (Center) Blocking Peptide
- Although most upper respiratory tract infections (URTIs) have a viral etiology, antibiotics are widely prescribed, thus contributing substantially to antimicrobial resistance. This study investigated the potential beneficial effects of a novel strain, LMG P-27481, against major URT pathobionts (, , , , and ) with the aim of reducing or delaying antibiotic use. Antibacterial and immunomodulatory activities were evaluated using alone or combined with resveratrol, a natural compound with antiviral and anti-inflammatory properties. Both agents inhibited pathogen growth, while their combination showed additive antibacterial activity, particularly against Gram-negative bacteria. Antioxidant assays demonstrated significant antioxidant capacity for both agents, with enhanced effects in combination in NBT and ABTS assays but antagonistic in ORAC. Immune mediators (IL-6, IL-8, IL-1β, TNF-α, IL-25, IL-33, CCL17, CCL22) were assessed in epidermal, epithelial, and macrophage cell lines, together with epidermal integrity markers (Filaggrin, Loricrin, Involucrin) in a 3D reconstructed human skin model (EpiDermFT). , resveratrol, and their combination exerted cell-specific effects in the different models, modulating cytokine expression and production, and barrier integrity. Our findings support the potential efficacy of oral LMG P-27481 plus resveratrol in URTIs. - Source: PubMed
Publication date: 2026/08/12
Mattioli RobertoDi Risola DanielSivori FrancescaFranzese OrnellaGenovese IlariaMastromarino PaolaMosca Luciana - : Mesenchymal stromal cells from the amniotic membrane (hAMSCs) counteract fibrosis progression, primarily via anti-inflammatory effects like promoting macrophage polarization toward an anti-inflammatory, pro-regenerative phenotype. : We investigated hAMSCs' ability to prevent and halt lung fibrosis in a bleomycin-induced fibrosis murine model. We focused on their impact on recruitment and polarization of different macrophage populations, including SPARC- and CD169-expressing macrophages, implicated in resolving pulmonary inflammation and fibrosis. : hAMSCs, administered early (concomitant with bleomycin, during acute inflammation), or late (at day 7 post-bleomycin, during established fibrosis), showed anti-fibrotic activity, preserving alveolar area, reducing the extent of lung fibrosis, and decreasing α-SMA levels. These preventive and late anti-fibrotic effects of hAMSCs are associated with a context-dependent presence of distinct macrophage signatures. Early treatment reduced macrophage recruitment and increased levels of Arg1/iNOS macrophages, curbing injury-induced inflammation. Late treatment uniquely increased the lung levels of CD169 macrophages, suggesting their contribution to hAMSCs' anti-fibrotic effect. We hypothesized a potential involvement of lung CD169 macrophages in promoting recruitment of regulatory T cells (Tregs) to the lungs. Although these macrophages can establish a CCL22-CCR4 axis with Tregs, and treatment effectively boosted Treg lung levels, the Treg increase is not directly attributable to higher CD169 macrophage numbers, implying other potentially IL-10-driven mechanisms. : hAMSC treatment effectively prevents and blocks lung fibrosis. These effects are associated with distinct lung macrophage marker profiles, suggesting a potential involvement of different macrophage populations in a time-dependent manner; thus highlighting administration timing's role in optimizing therapeutic synergy. - Source: PubMed
Publication date: 2026/08/20
Cargnoni AnnaFarigu SerafinaRomele PietroPapait AndreaMagatti MartaSilini AntoniettaParolini Ornella - : Atopic dermatitis (AD) is a persistent and recurring skin disease characterized by epidermal barrier dysfunction, immune dysregulation, and elevated expression of proinflammatory mediators. We investigated the anti-inflammatory potential of polynucleotides (PN), highly purified DNA biopolymers isolated from salmonid gonads, in keratinocyte and macrophage activation models. : RAW 264.7 macrophages were stimulated with lipopolysaccharide (LPS), whereas HaCaT keratinocytes were stimulated with tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ). The effects of PN treatment on the production or expression of inflammatory mediators, cytokines, and chemokines were evaluated. Changes in the phosphorylation of mitogen-activated protein kinases (MAPKs) and Janus kinase 1/signal transducer and activator of transcription 3 (JAK1/STAT3) and in the nuclear localization of nuclear factor-κB (NF-κB) were also assessed. : In LPS-activated RAW 264.7 macrophages, PN treatment significantly suppressed nitric oxide production and downregulated the expression of inducible nitric oxide synthase (iNOS), TNF-α, IL-1β, and IL-8, accompanied by reduced NF-κB nuclear translocation. In TNF-α/IFN-γ-stimulated HaCaT keratinocytes, PN treatment markedly decreased the secretion levels of IL-6, IL-1β, and thymic stromal lymphopoietin. Moreover, PN treatment markedly reduced T-cell-recruiting chemokines, including MDC/CCL22, TARC/CCL17, RANTES/CCL5, and IL-8. Signaling analyses demonstrated that PN treatment attenuated the phosphorylation of key MAPKs (ERK, JNK, and p38) and the JAK1/STAT3 axis. Furthermore, PN treatment markedly reduced NF-κB nuclear translocation. : These in vitro findings indicate that the anti-inflammatory effects of PN are associated with reduced activation of multiple core signaling pathways governing cytokine and chemokine responses, supporting further investigation of PN in AD and other chronic inflammatory skin diseases. - Source: PubMed
Publication date: 2026/08/13
Ha Ye JinTak Ka HeeLee Jong LyulKim Chan WookMoon Ik JunYoon Yong Sik - Asthma is a chronic inflammatory disease affecting over 300 million people worldwide. This disease has multiple underlying etiologies, and a major endotype of asthma is characterized by cellular and molecular signatures of type 2 (allergic) inflammation. In this study we conducted bronchoscopies with airway segmental allergen challenge in allergic asthmatics to dissect airway responses to allergen. Using mass cytometry and single-cell RNA sequencing, we characterized with high resolution the airway immune landscape before and after allergen challenge and the heterogeneity present between subjects. This heterogeneity generally falls along a type 1/ type 2 axis. In type 2 high individuals, we identified allergen-reactive Th2 cells by using TCR sequences to barcode clonal T cell populations in single-cell genomic and activation-induced marker expression assays. These potentially pathogenic Th2 cell clones were present systemically and expanded following allergen challenge, connecting local lung inflammation to systemic clonal Th2 cell dynamics. Th2 cell airway ingress was coordinated with myeloid cell expression of T cell chemoattractants including CCL17 and CCL22. This study provides insight into the molecular and cellular components of allergen-induced tissue inflammation in asthma. Deeper resolution of the T cell response to aeroallergens may inform novel diagnostic and therapeutic strategies for asthma and other allergic airway diseases. - Source: PubMed
Publication date: 2026/08/06
Wheeler Benjamin DWang JingmingNerella SrilaxmiJohansson KristinaGarudadri SureshMuñoz-Sandoval PriscilaMazumder ThomasChristenson Stephanie ABhakta Nirav RErle David JAnsel K MarkWoodruff Prescott G - CSF inflammatory biomarkers in Huntington disease (HD), a neurodegenerative CAG-triplet expansion disorder, usually increase with disease progression. CSF leukocytes as an inflammatory marker have not been explored in HD. We explored high-precision CSF-leukocyte counts across different HD stages in the multicenter prospective biosample HD study HDClarity and their association with CSF neurofilament light chain (NFL) and cytokine and chemokine patterns. - Source: PubMed
Publication date: 2026/08/17
Gao YuÁsbjörnsdóttir BirnaVinther-Jensen TuaVon Essen Marina RodeHellem Marie Nathalie NickelsenHjermind Lena EEjlerskov PatrickLandwehrmeyer G BernhardSellebjerg FinnNielsen Joergen ErikLewerenz Jan