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ABSTRACT: New Clues on Cathelicidin-Related Antimicrobial Peptide Alleviates Acute

PROVIDER: PRJNA1037277 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26771208_1.fastq.gz	Fastqsanger.gz
	SRR26771208_2.fastq.gz	Fastqsanger.gz
	SRR26771209_1.fastq.gz	Fastqsanger.gz
	SRR26771209_2.fastq.gz	Fastqsanger.gz
	SRR26771210_1.fastq.gz	Fastqsanger.gz

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Project description:Alterations in Metabolome and Microbiome: New Clues on Cathelicidin-Related Antimicrobial Peptide Alleviates Acute Ulcerative Colitis

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Investigation into the effect of cathelicidin on autoimmune CD4+ T cells

Project description:We have shown that, in acute models of vaccination, the antimicrobial peptide cathelicidin potentiates Th17 cell differentiation. TO examine this in long-term, chronic inflammation, here we studied T cells in the mouse model of Multiple Sclerosis. We examined T cells from wildtype mice and those lacking cathelicidin.

2021-11-14 | GSE188655 | GEO

Human cathelicidin antimicrobial peptide LL37 effect on human neonatal epidermal keratinocytes (NHEKs).

Project description:Analysis of undifferentiated keratinocytes or differentiated keratinocytes stimulated with or without human cathelicidin antimicrobial peptide (CAMP) LL37. Results provide insight into the biological effects of CAMP on human keratinocytes. NHEKs were divided into two groups; low calcium (0.05 mM) and high calcium condition (1.6 mM). Then keratinocytes were stimulated with human cathelicidin antimicrobial peptide LL37 at 0, 2.56, and 7.68 M-NM-<M for 12 h to 24 h.

2014-08-01 | E-GEOD-49472 | biostudies-arrayexpress

Human cathelicidin antimicrobial peptide LL37 effect on human neonatal epidermal keratinocytes (NHEKs).

2014-08-01 | GSE49472 | GEO

Toll-like receptor triggering of a vitamin D-mediated human antimicrobial response

Project description:In innate immune responses, activation of Toll-like receptors (TLRs) triggers direct antimicrobial activity against intracellular bacteria, which in murine, but not human, monocytes and macrophages is mediated principally by nitric oxide. We report here that TLR activation of human macrophages up-regulated expression of the vitamin D receptor and the vitamin D-1-hydroxylase genes, leading to induction of the antimicrobial peptide cathelicidin and killing of intracellular Mycobacterium tuberculosis. We also observed that sera from African-American individuals, known to have increased susceptibility to tuberculosis, had low 25-hydroxyvitamin D and were inefficient in supporting cathelicidin messenger RNA induction. These data support a link between TLRs and vitamin D-mediated innate immunity and suggest that differences in ability of human populations to produce vitamin D may contribute to susceptibility to microbial infection. Keywords: timecourse, cell type comparison

2007-09-01 | GSE8921 | GEO

Antimicrobial production by perifollicular dermal preadipocytes is essential to the pathophysiology of acne

Project description:Innate immune defense against deep tissue infection by Staphylococcus aureus is orchestrated by fibroblasts that become antimicrobial when triggered to differentiate into adipocytes. However, the role of this process in non-infectious human diseases is unknown. To investigate the potential role of adipogenesis by dermal fibroblasts in acne, a disorder triggered by Cutibacterium acnes (C. acnes), single-cell RNA-sequencing was performed on human acne lesions and mouse skin challenged by C. acnes. A transcriptome consistent with adipogenesis was observed within specific fibroblast subsets from human acne and mouse skin lesions infected with C. acnes. Perifollicular dermal preadipocytes in human acne and mouse skin lesions showed colocalization of PREF1, an early marker of adipogenesis, and cathelicidin (Camp), an antimicrobial peptide. This capacity of C. acnes to trigger production of cathelicidin in preadipocytes was dependent on TLR2. Treatment of wild-type mice with retinoic acid (RA) suppressed the capacity of C. acnes to form acne-like lesions, inhibited adipogenesis and enhanced cathelicidin expression in preadipocytes, but lesions were unresponsive in Camp-/- mice, despite the anti-adipogenic action of RA. Analysis of inflamed skin of acne patients after retinoid treatment also showed enhanced induction of cathelicidin, a previously unknown beneficial effect of retinoids in difficult-to-treat acne. Overall, these data provide evidence that adipogenic fibroblasts are a critical component of the pathogenesis of acne and represent a potential target for future therapy.

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Project description:Dermal fibroblasts (dFB) resist infection by locally differentiating into adipocytes and producing the antimicrobial peptide cathelicidin in response to S. aureus. We found that neonatal dFB were highly adipogenic whereas this adipogenic function was lost during adulthood. To better understand the molecular nature of the change in antimicrobial and adipogenic function of dFB, we profiled the transcriptomes of primary dFB isolated at different ages by RNA-seq. RNA-seq identified the pro-adipogenic to pro-fibrotic gene signature switch in dFB during aging, and identified TGF-beta as the top up-regulated pathway that was activated in 2M dFB compared to neonatal P1 dFB.

2018-10-18 | GSE121460 | GEO

Homo sapiens

Project description:Human cathelicidin antimicrobial peptide LL37 effect on human neonatal epidermal keratinocytes (NHEKs).

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The effect of mouse cathelicidin (mCRAMP) on gene expression in CD4+ T cells cultured under Th17-driving conditions

Project description:We have shown that cathelicidin amplifies Th17 differentiation. To determine the mechanism through which this host defence peptide acts, we performed multiplex gene expression analysis (NanoString) to identify the effects of mouse cathelicidin (mCRAMP) on murine CD4+ T cells cultured under Th17-driving conditions.

2020-11-04 | GSE160757 | GEO

Cathelicidin-deficient mice exhibit increased survival and upregulation of key inflammatory response genes following cecal ligation and puncture

Project description:Antimicrobial peptides possess a myriad of molecular properties including bacterial killing and the regulation of many aspects of innate immunity. Cathelicidins are a group of antimicrobial peptides widely investigated by the scientific community. Many studies have focused on the bactericidal and pro-inflammatory roles of cathelicidins. Because the role of endogenous cathelicidin expression remains obscure in deep-seated systemic infections, we induced sepsis in cathelicidin knockout and wild-type (WT) mice by cecal ligation and puncture, performing transcriptome screening by DNA microarray in conjunction with other immunologic assays. Cathelicidin-deficient mice showed increased survival compared to WT mice in this established experimental model of polymicrobial sepsis, in association with upregulation of certain key inflammatory response genes. Therefore, cathelicidins can exert both pro- and anti-inflammatory activities depending on the disease and cellular context.

2017-06-20 | GSE90727 | GEO

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