Journal
INTERNATIONAL IMMUNOPHARMACOLOGY
Volume 103, Issue -, Pages -Publisher
ELSEVIER
DOI: 10.1016/j.intimp.2021.108449
Keywords
Anaphylaxis; ALA; Mast cells; IgE; Lyn kinase; FceRI
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Funding
- Natural National foundation of science [81872837]
- Institutional Science Foundation of The First Affiliated Hospital of Xi'an Jiaotong University [2020ZYTS-12]
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The findings suggest that alpha-linolenic acid (ALA) could serve as a therapeutic drug candidate for preventing IgE-mediated anaphylaxis by regulating immune reactions and attenuating inflammation caused by allergies.
Excessive reactions to allergens can induce systemic, life-threatening physiological dysfunction (anaphylaxis) in humans. The surface of mast cells expresses high-affinity IgE receptors that play a vital role during anaphylaxis. Alpha-linolenic acid (ALA) is an essential non-toxic fatty acid in humans. Since it has been reported having potential to regulate pro-inflammatory reactions, we postulated that ALA could inhibit anaphylaxis by down-regulating Lyn kinase phosphorylation. We found that local and systematic inflammation induced by albumin from chicken egg white (OVA) were attenuated by ALA in vivo. Furthermore, ALA inhibited IgE-mediated Ca2+ mobilization, degranulation, and cytokine release in Laboratory of Allergic Disease 2 (LAD2) cells. The western blot results showed that ALA down-regulate the FceRI/Lyn/Syk signaling pathway by suppressing Lyn kinase activity. Therefore, ALA could serve as a therapeutic drug candidate for preventing IgE-mediated anaphylaxis.
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