Effects of venom immunotherapy on serum level of CCL5/RANTES in patients withHymenopteravenom allergy

Abstract

Hymenoptera venoms are known to cause life-threatening IgE-mediated anaphylactic reactions in allergic individuals. Venom immunotherapy is a recommended treatment of insect allergy with still the mechanism not being completely understood. We decided to assess the serum CCL5/RANTES level in patients who experienced severe anaphylactic reaction to Hymenoptera venom and to find out changes in the course of immunotherapy. Twenty patients (9 men, 11 women, mean age: 31.91 ± 7.63 years) with history of anaphylactic reaction after insect sting were included into the study. Diagnosis was made according to sIgE and skin tests. All of them were enrolled into rush venom immunotherapy with bee or wasp venom extracts (Pharmalgen, ALK-Abello, Horsholm, Denmark). Serum levels of CCL5/RANTES were measured using a commercially available ELISA kit (R&D Systems, Minneapolis, MN). CCL5/RANTES serum concentration are higher in insect venom allergic patients than in healthy controls (887.5 ± 322.77 versus 387.27 ± 85.11 pg/ml). Serum concentration of CCL5/RANTES in insect venom allergic patient was significantly reduced in the course of allergen immunotherapy already after 6 days of vaccination (887.5 ± 322.77 versus 567.32 ± 92.16 pg/ml). CCL5/RANTES serum doesn't correlate with specific IgE. Chemokine CCL5/RANTES participates in allergic inflammation induced by Hymenoptera venom allergens. Specific immunotherapy reduces chemokine CCL5/RANTES serum level already after initial days of venom immunotherapy.

High-dose bee venom exposure induces similar tolerogenic B-cell responses in allergic patients and healthy beekeepers

“…The natural ligands for CCR5 are macrophage inflammatory protein 1α (MIP1α/CCL3), MIP1β/CCL4, and regulated upon activation, normal T‐cell expressed, and secreted (RANTES/CCL5). CCL5/RANTES serum concentration is elevated in insect venom‐allergic patients compared to healthy individuals and decreases significantly during the course of AIT . CCR5 is involved in chemotaxis of immune cells to inflammatory sites in the periphery .…”

Allergen‐specific immunotherapy induces the suppressive secretoglobin 1A1 in cells of the lower airways

“…27 Two AITinduced chemokines, CCL-5 (RANTES), and CCL-23 (MIP3), which are known to be involved in macrophage chemotaxis and were reported to be elevated in serum samples of patients receiving (insect venom) immunotherapy, were also detected in-and off-season. 28 CCL-5 is a major regulator of suppressive immune programs 29 and may contribute to antagonize pro-allergic type-2 immunity by recruiting Th1 cells as well as regulatory T cells. 30 The atypical chemokine receptor ACKR2, 30 the major CCL-5 scavenger receptor, is decreased through AIT and further increases the biological activity of CCL5.…”

Expression of eosinophils, RANTES and IL-25 in the first phase of Hymenoptera venom immunotherapy

“…In considering the increase of eosinophils in the circulation during the initial phase of VIT we assume that CCL5/RANTES and DCs' cytokines may result in the eosinophil response. It has been reported by Gawlik et al [32] that the chemokine level was significantly reduced after 6 days of rush venom immunotherapy. Our observations have shown that in patients treated with bee venom the CCL5/RANTES concentration increased after venom administration (p = 0.39).…”

“…It has been reported by Gawlik et al . [ 32 ] that the chemokine level was significantly reduced after 6 days of rush venom immunotherapy. Our observations have shown that in patients treated with bee venom the CCL5/RANTES concentration increased after venom administration ( p = 0.39).…”