Abstract
BackgroundThe role of chemokines in anaphylaxis is unclear.MethodsWe prospectively recruited 49 patients presenting to the emergency department with an acute episode of anaphylaxis and 28 healthy subjects. We measured serum levels of the chemokines CCL2, CCL5, CCL7, CCL8, CCL11, CCL13, CCL17, CCL21, CCL22, CCL24, and CCL26, tryptase, the absolute number of circulating basophils, monocytes, lymphocytes, and PMNs, and whole blood FCER1A, CPA3 and HDC gene expression at two time points: during the anaphylactic episode and in convalescent samples collected approximately 3 months later. We then investigated the in vitro chemotactic activity of chemokines induced during anaphylaxis for the in vitro migration of the corresponding cells.ResultsOnly CCL2 chemokine levels were significantly increased in anaphylaxis samples (median 514 pg/ml) compared to convalescent samples (284 pg/ml, P < 0.0001) and healthy subjects (279 pg/ml, P < 0.0001); there was no significant difference in any of the other chemokines. There was a significant positive correlation between the rates of increase of serum CCL2 (median [range]: 106.0% [− 44.7% to 557.4%]) and tryptase (133.8% [− 6.6% to 893.4%]; r = 0.68, P < 0.0001) and between the acute concentration of serum CCL2 and the acute concentration of serum tryptase (r = 0.77, P < 0.0001). The number of circulating basophils, but not other blood cells, significantly decreased during anaphylaxis (median 5.0 vs. 19.1 cells/µl in convalescent samples; P < 0.0001); a decrease in whole-blood gene expression of basophil markers (P ≤ 0.0018) confirmed these changes. Anaphylactic serum enhances the in vitro migration of basophils via CCL2-dependent chemotactic activity; in contrast, no CCL2-dependent chemotactic activity was observed for convalescent samples.ConclusionsOur findings imply an important and specific role for CCL2-mediated chemotactic activity in the pathophysiology of human anaphylaxis.
Highlights
The role of chemokines in anaphylaxis is unclear
In a prospective study during and after anaphylaxis caused by Hymenoptera venom, medication, food, or other, we investigated the serum concentration of a large panel of different chemokines (CCL2, CCL5, CCL7, CCL8, CCL11, CCL13, CCL17, CCL21, CCL22, CCL24, and CCL26), which were previously described in allergic diseases [6, 7, 15,16,17,18,19,20,21,22,23,24,25]
The chemokine CCL2, but not other chemokines, is significantly increased during anaphylactic episodes Monocyte chemoattractant protein (MCP) chemokines CCL2/MCP‐1, CCL7/MCP‐3, CCL8/MCP‐2, and CCL13/MCP‐4 CCL2 concentrations measured during the anaphylactic episode were significantly higher than those measured in convalescent serum samples collected later
Summary
The role of chemokines in anaphylaxis is unclear. Anaphylaxis is a potentially life-threatening, rapidly progressing systemic hypersensitivity reaction, often following exposure to a small amount of allergen, includingVantur et al Clin Transl Allergy (2020) 10:63 increase in CCL2 (C-C Motif Chemokine Ligand 2) levels during human anaphylaxis [7], with no changes demonstrated for the chemokines CCL5 [7] and CCL11 [6, 7]. Chemokines that diffuse out from the site of release and form a concentration gradient to which leukocytes respond and migrate might be involved in the recruitment of basophils [4] or other potential effector cells of anaphylaxis, including monocytes/macrophages [11], neutrophils [12, 13], and platelets [14], to the inflamed tissue sites. For monocyte chemoattractant proteins (MCPs), an increase in CCL7 levels in allergic conjunctivitis [15], an increase in CCL8 levels in chronic/eosinophilic atopic dermatitis [16], and an increase in CCL13 levels in allergic rhinitis [17] were demonstrated. CCL5, CCL17, CCL21, and CCL22 were reported to be involved in asthma, atopic dermatitis, allergic rhinitis and drug hypersensitivity syndrome [20,21,22,23,24,25]
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