The Relationship between Chemokine Ligand 3 and Allergic Rhinitis

Background Allergic rhinitis (AR) is a chronic and frequent condition characterized by an excessive response of the immune system to innocent substances encountered in the nasal mucosa. These reactions are mediated by many factors, including chemokines. Chemokine ligand 3 (CCL3, a macrophage inflammatory protein 1α) is a chemokine implicated in the activation of mast cells - white cells shown to be highly involved in orchestrating allergic reactions. The present study evaluated the role of CCL3 in AR. Material and methods Thirty-nine participants, including 24 patients with AR and 15 healthy controls, were evaluated for allergies to dust mites, cat and dog danders, cockroaches (Blatella germanica), molds, grasses, weeds, and tree pollen using skin prick tests. Participants were also evaluated for inflammatory conditions by measuring total blood count with differential; concentrations of rheumatoid factor, fibrinogen, and C-reactive protein; and erythrocyte sedimentation rate. CCL3 in blood samples was measured at the Immunology Laboratory, Cantacuzino National Institute for Military Medical Research and Development, Bucharest, Romania, using Human Multianalyte Profiling Base Kits (R&D Systems Inc., Minneapolis, MN). Results Mean serum CCL3 concentration was significantly higher in patients with AR than in controls (15.03 ± 7.11 pg/ml vs. 8.34 ± 4.46 pg/ml, p = 0.001 [t-test] and p = 0.026 [Mann-Whitney test]). CCL3 concentrations correlated with polysensitization, defined as two or more positive prick tests per patient (r = 0.325, p = 0.046) and seasonal AR (r = 0.482, p = 0.002). Conclusions Elevated levels of CCL3 were seen in our patients with AR. We have observed correlations with polysensitization and seasonal allergies. These results suggest that chemokines might play an important role in the pathogenesis of AR. In the future, chemokines might be used in endotype classification of patients with AR and as a possible target in the treatment of AR.