Abstract
Angioedema is a life-threatening emergency event that is associated with bradykinin and histamine-mediated cascades. Although bradykinin-mediated angioedema currently has specific therapeutic options, angioedema is sometimes intractable with current treatments, especially histamine-mediated angioedema, suggesting that some other mediators might contribute to the development of angioedema. Fatty acids are an essential fuel and cell component, and act as a mediator in physiological and pathological human diseases. Recent updates of studies revealed that these fatty acids are involved in vascular permeability and vasodilation, in addition to bradykinin and histamine-mediated reactions. This review summarizes each fatty acid’s function and the specific receptor signaling responses in blood vessels, and focuses on the possible pathogenetic role of fatty acids in angioedema.
Highlights
The human body is surrounded by various external environments and is continually exposed to various harmful substances [1,2,3]
There is no evidence that bradykinin itself enhances the release of (ACE), histamine from has a unique protein complex with angiotensin-converting enzymes suggestmast cells and forms wheal, indicating that bradykinin-mediated hereditary angioedema ing that this complex protein formation plays an important role in the interplay mechabasically does not cause urticaria, which is a helpful objective symptom to distinguish nism between the renin–angiotensin and kinin–kallikrein systems
The antihistamine agent suppresses the potent IgE-mediated production of histamine and PGD2 [56]. These findings suggest that PGD2 boosts histaminemediated cutaneous reaction, and antihistamine agents are expected to regulate PGD2mediated reaction in angioedema
Summary
The human body is surrounded by various external environments and is continually exposed to various harmful substances [1,2,3]. As a protective function of the human body against these environmental stimuli, the epithelial immune reaction attempts to remove these dangerous factors. A representative host immune protective reaction is edema, which plays a cleansing function in the epithelial host defense after the entry of external environmental factors [4]. The localized edematous reaction is a biological defense mechanism that dilutes external toxins and pushes them to the outermost layer of the human body. C1-inhibitor supplementation and icatibant obtain a therapeutic clinical effect for hereditary angioedema [5,6]. Receptor-specific action is helpful to obtain a better understanding of fatty-acid-mediated physiological and pathological responses. Since cyclo-oxygenase inhibitors are the trigger for angioedema [8], it is assumed that fatty acids might have a bifunctional action in both beneficial and unbeneficial effects on angioedema. We focus on the role of prostanoids in the pathogenesis of angioedema, and on an update of the knowledge gained from current research
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