The Role of Infection and Autoimmunity in Urticaria and Angioedema as a Common Entity

EMJ Allergy & Immunology ◽

10.33590/emjallergyimmunol/20-00148 ◽

2021 ◽

pp. 79-85

Author(s):

Michael Rudenko

Keyword(s):

Mast Cell ◽

Chronic Urticaria ◽

Bacterial Infections ◽

Cell Activation ◽

Keyword Search ◽

Epidemiological Data ◽

Chronic Spontaneous Urticaria ◽

Mast Cell Activation ◽

Practice Parameters

Chronic spontaneous urticaria with angioedema is prevalent, affecting approximately 1% of the general population, and has a significant impact on quality of life, according to epidemiological data. This article aims to broaden the view on the mechanisms of urticaria and the role of infection in the current environment. It is not easy to identify the cause of urticaria but appropriate steps to treat an underlying infection can, in some cases, improve the symptoms of urticaria and angioedema, reduce severity and duration, or lead to remission. Although chronic spontaneous urticaria with angioedema is a multifactorial condition involving inflammation, autoimmunity, and coagulation, IgE-mediated autoimmunity, or autoallergy, is thought to play a major role. Every year, more is learnt about the role of cells releasing mediators, underlying autoimmune processes that lead to the development of mast cell activation and urticaria. It has become increasingly clear that mast cell roles in immune system responses are not limited to an allergic role; they are key players in protective immune responses, both innate and adaptive, to various pathogens and in defence of some infections. Several guidelines, consensus papers, and practice parameters have been developed for the management of chronic urticaria. The Dermatology Section of the European Academy of Allergology and Clinical Immunology (EAACI), the Global Allergy and Asthma European Network (GA2LEN), the European Dermatology Forum (EDF), and the World Allergy Organization (WAO) produce a guideline, which is revised every 4 years by a global panel of experts in the field. Infections may be a cause, aggravating factor, or unassociated bystander in chronic urticaria. The author looked at evidence, using a keyword search, for the role of viral and bacterial infections in acute, acute recurrent, and chronic urticaria and angioedema, including COVID-19, herpes, viral hepatitis, and Helicobacter pylori.

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The Role of Coagulation and Complement Factors for Mast Cell Activation in the Pathogenesis of Chronic Spontaneous Urticaria

Cells ◽

10.3390/cells10071759 ◽

2021 ◽

Vol 10 (7) ◽

pp. 1759

Author(s):

Yuhki Yanase ◽

Shunsuke Takahagi ◽

Koichiro Ozawa ◽

Michihiro Hide

Keyword(s):

Mast Cells ◽

Cell Activation ◽

Coagulation Factors ◽

Chronic Spontaneous Urticaria ◽

Mast Cell Activation ◽

Coagulation Cascade ◽

Edema Formation ◽

Complement Components ◽

Complement Factors

Chronic spontaneous urticaria (CSU) is a common skin disorder characterized by an almost daily recurrence of wheal and flare with itch for more than 6 weeks, in association with the release of stored inflammatory mediators, such as histamine, from skin mast cells and/or peripheral basophils. The involvement of the extrinsic coagulation cascade triggered by tissue factor (TF) and complement factors, such as C3a and C5a, has been implied in the pathogenesis of CSU. However, it has been unclear how the TF-triggered coagulation pathway and complement factors induce the activation of skin mast cells and peripheral basophils in patients with CSU. In this review, we focus on the role of vascular endothelial cells, leukocytes, extrinsic coagulation factors and complement components on TF-induced activation of skin mast cells and peripheral basophils followed by the edema formation clinically recognized as urticaria. These findings suggest that medications targeting activated coagulation factors and/or complement components may represent new and effective treatments for patients with severe and refractory CSU.

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