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Pharmacological Targeting of IL17/neutrophil axis to Treat Calciphylaxis

ABSTRACT: Pharmacological Targeting of IL17/neutrophil axis to Treat Calciphylaxis

PROVIDER: PRJNA1287493 | ENA |

REPOSITORIES: ENA

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Pharmacological Targeting of IL17/neutrophil axis to Treat Calciphylaxis

Project description:Calciphylaxis is a rare but life-threatening disorder characterized by ectopic calcification affecting the subcutaneous tissues and blood vessels of the skin. Calciphylaxis affects individuals with end stage renal disease but increasingly recognized to occur in individuals with normal kidney function. Once diagnosed, survival rates are less than a year and yet despite the severity of the condition, the pathobiology of calciphylaxis is ill understood. Here, we create animal models of calciphylaxis that recapitulate many characteristics of the human phenotype. We demonstrate that calcific deposits in the skin are preceded by recruitment of inflammatory cells. We show that increased local inflammation of the skin, regardless of the inciting cause, in the presence of hypercalcemia and hyperphosphatemia contributes to cutaneous ectopic calcification. Using multiple models of genetically modified rodents that have deficits in immune activation of T and B cells or NK cells, we demonstrate that such immunocompromised rodents are resistant to developing cutaneous calcification. Consistent with this observation, administration of the immunosuppressive cyclophosphamide rescued calcific deposits as did T cell suppression with cyclosporine. We demonstrate IL17 is upregulated in calcific skin and neutrophils are the predominant cell types expressing IL 17 and tissue alkaline phosphatase that is necessary for ectopic calcification. Targeting IL17 with a monoclonal antibody or use of a myeloperoxidase inhibitor to blunt neutrophil activation significantly attenuated calcific deposits in vivo. Taken together, these observations provide fresh insight into the role of the immune system and the IL17/neutrophil axis in mediating ectopic calcification in rodent models of calciphylaxis.

2025-07-08 | GSE301731 | GEO

Characterization of the IL23-IL17 immune axis in IBD patients

Project description:The aim of this study is to investigate the molecular mechanisms of IL23-IL17 immune axis in IBD, with particular attention to its role in maintaining mucosal barrier integrity under both physiological and pathological conditions

2021-11-26 | GSE165512 | GEO

Characterization of the IL23-IL17 immune axis in IBD patients

Project description:Characterization of the IL23-IL17 immune axis in IBD patients

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Paraventricular nucleus CRH neurons regulate acute lung injury via sympathetic nerve–neutrophil axis [neutrophil]

Project description:Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are severe conditions with high morbidity and mortality, and effective treatments are limited. Neuroimmune interactions play a critical role in lung homeostasis, but it remains unclear if specific brain regions regulate lung inflammation. Here, we unveil the critical role of neuroimmune signaling in ALI, focusing on the regulatory function of corticotropin-releasing hormone (CRH) neurons in the paraventricular nucleus (PVN) of the hypothalamus. Using viral tracing, chemogenetic modulation, and pharmacological interventions in mouse models of ALI induced by intranasal lipopolysaccharide and cecal ligation and puncture (CLP), we found that lung injury activated CRHPVN neurons that projected to the lung. Activation of these neurons protected mice from ALI and death, reducing neutrophil infiltration and effector functions in the lung. In contrast, inhibiting CRHPVN neurons exacerbated ALI. Notably, the beneficial impact of CRHPVN neuron activation is compromised by the pulmonary chemical sympathectomy or inhibition of the β2-adrenergic receptor. These protective effects were dependent on sympathetic nerves, with norepinephrine released locally to modulate neutrophil functions via β2-AR–β-arrestin2 signaling, inhibiting the NF-κB pathway. Our findings reveal a brain-lung axis that regulates immune responses in ALI, suggesting novel therapeutic targets for ALI and ARDS.

2025-02-07 | GSE288911 | GEO

Paraventricular nucleus CRH neurons regulate acute lung injury via sympathetic nerve–neutrophil axis [neutrophil]

Project description:Paraventricular nucleus CRH neurons regulate acute lung injury via sympathetic nerve–neutrophil axis [neutrophil]

| PRJNA1219998 | ENA

Analysis of the function of IL17 in C.elegans

Project description:RNAseq of C.elegans mutants of varying IL17 loss and gain of function mutants

2022-07-08 | E-MTAB-11701 | biostudies-arrayexpress

Paraventricular nucleus CRH neurons regulate acute lung injury via sympathetic nerve–neutrophil axis

2025-02-06 | GSE288588 | GEO

The neutrophil–osteogenic cell axis promotes bone destruction in periodontitis

Project description:The neutrophil–osteogenic cell axis promotes bone destruction in periodontitis

| PRJNA1071651 | ENA

Transcriptome profile of NON CF (normal) bronchial epithelial cells treated with TNFalpha, IL17 and TNFalpha+IL17

Project description:To analyse gene expression differences between differentiated bronchial epithelial cells kept under control conditions or treated for 72 hours with cytokines (TNFalpha10 ng/ml; IL17 20ng/ml)

2022-10-19 | GSE182957 | GEO

Transcription profiling of human T84 colonic epithelial cell line response to IL17 and IL22 stimulation

Project description:The effects of stimulating intestinal epithelial cells with Th17 cytokines, IL17 and IL22, was investigated Experiment Overall Design: The human colonic epithelial cell line, T84 was grown to confluency in standard transwell plates and either mock treated, or treated with cytokines IL17 and IL22

2008-06-20 | E-GEOD-11345 | biostudies-arrayexpress

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