title: Mediators of inflammation in nasal lavage from aspirin intolerant patients after aspirin challenge.
abstract: 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.
authors.affiliation: Department of Internal Medicine, Asthma and Allergy, Medical University of Łódź, Kopcinskiego 22, Łódź, Poland. matiska@wp.pl
authors.forename: Maciej
authors.initials: M
authors.lastname: Kupczyk
authors.forename: Zofia
authors.initials: Z
authors.lastname: Kurmanowska
authors.forename: Izabela
authors.initials: I
authors.lastname: Kupryś-Lipińska
authors.forename: Małgorzata
authors.initials: M
authors.lastname: Bocheńska-Marciniak
authors.forename: Piotr
authors.initials: P
authors.lastname: Kuna
mesh_terms: D000328:Adult; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects*; D001241:Aspirin / Q000009:adverse effects*; D001249:Asthma / Q000188:drug therapy / Q000378:metabolism*; D016022:Case-Control Studies; D054413:Chemokine CCL11 / Q000032:analysis; D018946:Chemokine CCL5 / Q000032:analysis; D054410:Chemokine CCL7 / Q000032:analysis; D004342:Drug Hypersensitivity / Q000378:metabolism*; D005260:Female; D005541:Forced Expiratory Volume; D006801:Humans; D018836:Inflammation Mediators / Q000032:analysis*; D007377:Interleukin-3 / Q000032:analysis; D015848:Interleukin-5 / Q000032:analysis; D008297:Male; D055556:Nasal Lavage; D009297:Nasal Mucosa / Q000378:metabolism*; D009299:Nasal Provocation Tests
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; C515450:CCL7 protein, human; D054413:Chemokine CCL11; D018946:Chemokine CCL5; D054410:Chemokine CCL7; D018836:Inflammation Mediators; D007377:Interleukin-3; D015848:Interleukin-5; D001241:Aspirin