Source: International Congress 2014 – New mechanisms in the pathogenesis of asthma and other lung diseases
Disease area: Airway diseases

Abstract

Expression of fractalkine (CX3CL1) is elevated in asthma and may be involved in controlling the inflammatory response in lungs by regulating influx of leukocytes, cell survival and function of fractalkine receptor (CX3CR1) expressing cells. In this study, the cellular distribution of CX3CR1 and CX3CL1 in lungs from asthmatics was determined by immunohistochemistry using validated antibodies. CX3CR1 is expressed in bronchial epithelial cells, endothelial cells, CD3⁺ cells, CD4⁺ cells, CD207⁺ cells, CD68⁺ cells, and mast cells. Interestingly, very few of the CD8⁺ cells that were located to lamina propria and submucosa expressed CX3CR1 whereas within the bronchial epithelium in asthmatics, numerous CD8⁺ cells were co-expressing CX3CR1. Overall, no difference in expression intensity was observed comparing lung biopsies from healthy volunteers and asthmatics, independent of disease severity (GINA). CX3CL1 was expressed in airway epithelia with highest intensity at the apical side facing the airway lumen, inflammatory cells in lamina propria and smooth muscle cells. Steroid treatment did not affect the expression pattern, nor the intensity in staining.The changed expression pattern of CX3CR1 expressing cells in asthmatics suggest that CX3CR1 signaling could be of importance for cellular redistribution in inflamed airways. A potent and highly selective small molecule CX3CR1 antagonist was therefore used to study the role of CX3CL1 to mediate cell survival in CX3CR1 expressing leukocytes. The data suggest that CX3CR1 signaling does enhance cell survival and that pharmacological inhibition of CX3CR1 signaling may be efficacious in reducing chronic airway inflammation and hyper responsiveness.

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Citations should be made in the following way:
D. Cunoosamy, X. H. Zhou, M. Rehnberg, K. Svensson, K. Sandberg (Mölndal, Sweden). Expression of CX3CL1 and CX3CR1 in human asthmatic lung in relation to cell survival. Eur Respir J 2014; 44: Suppl. 58, 3863

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