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Respir Med. 2010 Oct;104(10):1404-9. doi: 10.1016/j.rmed.2010.04.017. Epub 2010 May 10.

Mediators of inflammation in nasal lavage from aspirin intolerant patients after aspirin challenge.

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  • 1Department of Internal Medicine, Asthma and Allergy, Medical University of Łódź, Kopcinskiego 22, Łódź, Poland. matiska@wp.pl


The pathogenetic mechanisms underlying development of persistent inflammation in aspirin (ASA) intolerance are not fully understood. The aim of this study was to determine levels of MCP-3, RANTES, eotaxin, Il-5 and Il-3 in aspirin intolerant asthmatics (AIA) after nasal lysine-aspirin (Lys-ASA) challenge. Twenty AIA and 10 aspirin tolerant controls (ATC) were challenged with saline or 14.4mg of Lys-ASA. Lys-ASA challenge induced clinical symptoms and influx of eosinophils and basophils only in AIA group. Statistically significant higher levels of MCP-3 and RANTES were found in lavages from AIA as compared with ATC (p<0.05 in all time points). Before challenge the average level of MCP-3 was 86.95pg/ml in AIA and 47.61pg/ml in ATC, RANTES levels were 34.20pg/ml in AIA and 17.21pg/ml in ATC and did not change after the challenge in both group. The mean eotaxin's level was 11.01pg/ml in AIA and 8.03pg/ml in ATC before and increased to 20.06, 26.22pg/ml (4 and 24h in AIA) as compared to 10.51, 14.76pg/ml (4 and 24h in ATC) after the challenge (p<0.05). Interleukin-3 and Il-5 were not detectable. The highest inhibition of eosinophils' chemotaxis was induced by anti-eotaxin (47% of inhibition), followed by anti-RANTES (29%), anti-MCP-3 (19%) and anti-Il-5 (9%). In summary, we found that persistent inflammation in AIA patients is characterized by overproduction of MCP-3 and RANTES. Lack of increase in MCP-3 and RANTES levels after Lys-ASA challenge suggest that those mediators are involved in chronic rather than acute phase of ASA induced inflammation.

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