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Creatine activates airway epithelium in asthma.

Authors: Ferreira, SC  Toledo, AC  Hage, M  Santos, AB  Medeiros, MC  Martins, MA  Carvalho, CR  Dolhnikoff, M  Vieira, RP 
Citation: Ferreira SC, etal., Int J Sports Med. 2010 Dec;31(12):906-12. Epub 2010 Nov 11.
Pubmed: (View Article at PubMed) PMID:21072743
DOI: Full-text: DOI:10.1055/s-0030-1267160

Airway epithelium plays important roles in the pathophysiology of asthma. Creatine supplementation (Cr) was shown to increase asthma features in a murine model of allergic asthma; however, the role of the airway epithelium in this inflammatory response is not known. BALB/c mice were divided into control, creatine supplementation, ovalbumin-sensitized (OVA) and OVA plus creatine supplementation groups. OVA sensitization occurred on days 0, 14, 28 and 42, and ovalbumin challenge from days 21-53. Cr was also given on days 21-53. Total and differential cells counts in BALF were evaluated. Quantitative epithelial expression of interleukin (IL)-4, IL-5, IL-13, CCL11, CCL5, CCL2, iNOS, VCAM-1, ICAM-1, NF-kappaB, VEGF, TGF-beta, IGF-1, EGFR, TIMP-1, TIMP-2, MMP-9, MMP-12 and arginase II were performed. Cr increased the number of total cells and eosinophils in BALF, the epithelial content of goblet cells and the epithelial expression of IL-5, CCL2, iNOS, ICAM-1, NF-kappaB, TGF-beta, TIMP-1 and MMP-9 when compared to the control group (p<0.05). Creatine supplementation also exacerbated goblet cell proliferation, and IL-5 and iNOS expression by epithelial cells compared to the OVA group (p<0.01). Creatine up-regulates the pro-inflammatory cascade and remodelling process in this asthma model by modulating the expression of inflammatory mediators by epithelial cells.

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CRRD Object Information
CRRD ID: 5131642
Created: 2011-05-09
Species: All species
Last Modified: 2011-05-09
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.