Mast cell degranulation and bradykinin-induced angioedema - searching for the missing link

被引:1
|
作者
Porebski, Grzegorz [1 ]
Dziadowiec, Alicja [1 ,2 ]
Rybka, Hubert [3 ,4 ]
Kitel, Radoslaw [4 ]
Kwitniewski, Mateusz [2 ]
机构
[1] Jagiellonian Univ, Med Coll, Dept Clin & Environm Allergol, Krakow, Poland
[2] Jagiellonian Univ, Dept Immunol, Fac Biochem Biophys & Biotechnol, Krakow, Poland
[3] Jagiellonian Univ, Doctoral Sch Exact & Nat Sci, Krakow, Poland
[4] Jagiellonian Univ, Fac Chem, Dept Organ Chem, Krakow, Poland
来源
FRONTIERS IN IMMUNOLOGY | 2024年 / 15卷
关键词
bradykinin; C1 inhibitor deficiency; HAE; hereditary angioedema; mast cell; MRGPRX2; PSEUDO-ALLERGIC REACTION; FACTOR-XII; CONTACT SYSTEM; CHRONIC URTICARIA; ADVERSE-REACTIONS; C1; INHIBITOR; AMINO-ACID; IN-VITRO; HEPARIN; ACTIVATION;
D O I
10.3389/fimmu.2024.1399459
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Initiation of the bradykinin generation cascade is responsible for the occurrence of attacks in some types of angioedema without wheals. Hereditary angioedema due to C1 inhibitor deficiency (HAE-C1-INH) is one such clinical entity. In this paper, we explore the existing evidence that mast cells (MCs) degranulation may contribute to the activation of the kallikrein-kinin system cascade, followed by bradykinin formation and angioedema. We present the multidirectional effects of MC-derived heparin and other polyanions on the major components of the kinin-kallikrein system, particularly on the factor XII activation. Although, bradykinin- and histamine-mediated symptoms are distinct clinical phenomena, they share some common features, such as some similar triggers and a predilection to occur at sites where mast cells reside, namely the skin and mucous membranes. In addition, recent observations indicate a high incidence of hypersensitivity reactions associated with MC degranulation in the HAE-C1-INH patient population. However, not all of these can be explained by IgE-dependent mechanisms. Mast cell-related G protein-coupled receptor-X2 (MRGPRX2), which has recently attracted scientific interest, may be involved in the activation of MCs through a different pathway. Therefore, we reviewed MRGPRX2 ligands that HAE-C1-INH patients may be exposed to in their daily lives and that may affect MCs degranulation. We also discussed the known inter- and intra-individual variability in the course of HAE-C1-INH in relation to factors responsible for possible variability in the strength of the response to MRGPRX2 receptor stimulation. The above issues raise several questions for future research. It is not known to what extent a prophylactic or therapeutic intervention targeting the pathways of one mechanism (mast cell degranulation) may affect the other (bradykinin production), or whether the number of mast cells at a specific body site and their reactivity to triggers such as pressure, allergens or MRGPRX2 agonists may influence the occurrence of HAE-C1-INH attacks at that site.
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页数:11
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