Studies have identified a central role for IgE/FcεRI/mast cells in promoting the clinical manifestations of anaphylaxis, however evidence suggests involvement of platelets in anaphylaxis. Herein, we examined platelet activation and involvement in the symptoms of IgE-mediated anaphylaxis in mice.
Platelet activation was measured by flow cytometry analyses (anti-CD41a and anti-CD62p). Passive IgE-mediated anaphylaxis [i.v. injection of anti-IgE (EM95, 20μg)], passive oral antigen-induced IgE anaphylaxis [i.v. anti-trinitrophenyl (TNP)-IgE (20μg), followed by oral gavage with TNP-ovalbumin (TNP-OVA, 50mg)], and active oral antigen-induced anaphylaxis [i.p. 50μg OVA / 1mg alum followed by repeated oral gavage challenge of OVA (50mg)] were induced in BALB/c mice.
I.v. administration of anti-IgE induced shock (Temperature Change (oC) anti-IgE vs control respectively: -2.83 ± 1.43 vs -0.00 ± 0.42, p < 0.001; mean ± SD) and platelet activation as compared with control Ig (% positive CD62p ± SD; 43.8 ± 10.0 vs 18.7 ± 5.3, p < 0.0001). In contrast, passive and active IgE-mediated oral antigen-induced shock (Temperature Change (oC) -2.98 ± 0.76 and -2.63 ± 0.47), were not associated with increased platelet activation compared to control groups (% positive CD62p ± SD; active oral: 33.4 ± 13.8 vs 17.2 ± 3.6, p = 0.1; passive oral: 12.8 ± 0.8 vs 15.1 ± 0.4, p = 0.017). In vitro stimulation of platelets with adenosine diphosphate induced a significant increase in platelet activation in all groups, confirming platelet functionality.
Systemic anaphylaxis and not oral antigen-induced IgE-mediated anaphylaxis in mice is associated with increased platelet activation.