Study: Cannabinoids May Help Prevent and Treat Peanut Allergies
According to a new study epublished by the National Institute of Health, cannabinoids interfere with peanut sensitization and promotes tolerogenic responses, “which might well pave the way for the development of novel prophylactic and therapeutic strategies for peanut allergy.”
“Cannabinoids are lipid-derived mediators with anti-inflammatory properties in different diseases”, states the study’s abstract. “WIN55212-2, a non-selective synthetic cannabinoid [meant to mimic the effects of marijuana-derived THC], reduces immediate anaphylactic reactions in a mouse model of peanut allergy, but its capacity to prevent peanut allergic sensitization and the underlying mechanisms remains largely unknown.”
With this in mind, the purpose of this study was to “investigate the capacity of WIN55212-2 to immunomodulate peanut-stimulated human dendritic cells (DCs) and peanut allergic sensitization in mice.”
Researchers found that the synthetic cannabinoid “reduced peanut-induced hmoDC activation and promoted the generation of CD4+ CD127– CD25+ FOXP3+ Treg cells, while reducing the induction of IL-5-producing T cells.”
In vivo, the cannabinoid “impaired the peanut-induced migration of DCs to lymph nodes and their maturation.” In addition, it “significantly reduced the induction of peanut-specific IgE and IgG1 antibodies in serum during epicutaneous peanut sensitization, reduced the clinical symptoms score upon peanut challenge and promoted the generation of allergen-specific FOXP3+ Treg cells.”
The study concludes by stating: “The synthetic cannabinoid WIN55212-2 interferes with peanut sensitization and promotes tolerogenic responses, which might well pave the way for the development of novel prophylactic and therapeutic strategies for peanut allergy.”
The study’s full abstract can be found below.
Abstract
Background: Cannabinoids are lipid-derived mediators with anti-inflammatory properties in different diseases. WIN55212-2, a non-selective synthetic cannabinoid, reduces immediate anaphylactic reactions in a mouse model of peanut allergy, but its capacity to prevent peanut allergic sensitization and the underlying mechanisms remains largely unknown.
Objective: To investigate the capacity of WIN55212-2 to immunomodulate peanut-stimulated human dendritic cells (DCs) and peanut allergic sensitization in mice.
Methods: Surface markers and cytokines were quantified by flow cytometry, ELISA and qPCR in human monocyte-derived DCs (hmoDCs) and T cell cocultures after stimulation with peanut alone or in the presence of WIN55212-2. Mice were epicutaneously sensitized with peanut alone or peanut/WIN55212-2. After peanut challenge, drop in body temperature, hematocrit, clinical symptoms, peanut-specific antibodies in serum and FOXP3+ regulatory (Treg) cells in spleen and lymph nodes were quantified. Splenocytes were stimulated in vitro with peanut to analyse allergen-specific T cell responses.
Results: WIN55212-2 reduced peanut-induced hmoDC activation and promoted the generation of CD4+ CD127– CD25+ FOXP3+ Treg cells, while reducing the induction of IL-5-producing T cells. In vivo, WIN55212-2 impaired the peanut-induced migration of DCs to lymph nodes and their maturation. WIN55212-2 significantly reduced the induction of peanut-specific IgE and IgG1 antibodies in serum during epicutaneous peanut sensitization, reduced the clinical symptoms score upon peanut challenge and promoted the generation of allergen-specific FOXP3+ Treg cells.
Conclusions: The synthetic cannabinoid WIN55212-2 interferes with peanut sensitization and promotes tolerogenic responses, which might well pave the way for the development of novel prophylactic and therapeutic strategies for peanut allergy.
