Formation of nasal polyps: The roles of innate type 2 inflammation and deposition of fibrin

Takabayashi, Tetsuji; Schleimer, Robert P.

doi:10.1016/j.jaci.2020.01.027

Cited by 111 publications

(110 citation statements)

References 103 publications

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“…118,119 The pathological feature of NPs is a fibrin deposition accompanied by the dysregulation of coagulation and fibrinolysis cascade. 120,121 Eosinophils in NPs release tissue factor (TF), which is an initiator of extrinsic coagulation cascade. 122,123 The levels of thrombin and factor XIIIA are elevated in NPs and act in the final step of the formation of fibrin mesh.…”

Section: Eosinophilic Chronic Rhinosinusitismentioning

confidence: 99%

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Adult‐onset eosinophilic airway diseases

Asano

Ueki

Tamari

et al. 2020

Allergy

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Allergic diseases in the upper and the lower airways such as allergic rhinitis and atopic asthma are usually accompanied by local eosinophilia and sometimes by peripheral blood eosinophilia. Chronic rhinosinusitis with nasal polyps (CRSwNP) and nonatopic asthma are also characterized by local and systemic eosinophilia; however, there are substantial differences in the age of onset and the presence of atopy. Atopic asthma and allergic rhinitis develop during childhood in most cases and mediated by type 1 hypersensitivity reactions to allergen(s), as are other childhood-onset allergic diseases such as food allergies and eczema. Patients often develop these diseases consecutively as an allergic march (Figure 1), suggesting the presence of common genetic backgrounds and pathophysiology. In contrast to childhood-onset disease, adult-onset asthma frequently presents as a nonatopic and eosinophilic condition, 1-6

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Section: Eosinophilic Chronic Rhinosinusitismentioning

confidence: 99%

“…The pathological feature of NPs is a fibrin deposition accompanied by the dysregulation of coagulation and fibrinolysis cascade 120,121 . Eosinophils in NPs release tissue factor (TF), which is an initiator of extrinsic coagulation cascade 122,123 .…”

Section: Clinical Characteristics and Pathophysiology Of Adult‐onset mentioning

confidence: 99%

Adult‐onset eosinophilic airway diseases

Asano

Ueki

Tamari

et al. 2020

Allergy

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“…Another hallmark of nasal polyps is excessive fibrin deposition that can serve to trap plasma proteins and contribute to the mucosal edema observed in CRSwNP. 43 Fibrin is generated as an end product of the coagulation cascade and there is a significant correlation between fibrin levels and eosinophils in nasal polyps. 44 45 Eosinophils have been reported to express tissue factor which can initiate the extrinsic arm of the coagulation cascade, ultimately leading to fibrin formation.…”

Section: Eosinophils In Crswnpmentioning

confidence: 99%

Biology and Function of Eosinophils in Chronic Rhinosinusitis With or Without Nasal Polyps

Bochner

Stevens

2021

Allergy Asthma Immunol Res

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Chronic rhinosinusitis (CRS) with or without nasal polyposis is a complex medical condition characterized by varying patterns of chronic innate and adaptive mucosal inflammation. Treatment of CRS has been traditionally limited to corticosteroids and sinus surgery; however, novel biologics have more recently been evaluated as steroid- and surgery-sparing options. While it is clear that there are different subtypes or endotypes of CRS, perhaps the most frequent presentation involves the features of type 2 inflammation, including a prominent tissue eosinophilia component. The purpose of this review is to provide an update on eosinophil biology as well as on the potential contribution of eosinophils and their mediators to the pathophysiology of CRS, drawing mechanistic conclusions mainly from studies of human sinus mucosal tissues, nasal secretions, and benefits (or lack thereof) from the use of various pharmacotherapies. The unavoidable conclusion derived from this approach is that eosinophils themselves cannot fully explain the underlying pathophysiology of this complex disorder.

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“…At the basis of CRSwNP, in Western countries, there is the so-called Type 2 inflammation and related cytokines. Type 2 immune responses are defined by the cytokines interleukin-4 (IL-4), IL-5, IL-9 and IL-13, which can be host protective, yet, when dysregulated, have pathogenic activity [24]. Type 2 immunity induces a complex response involving granulocytes (eosinophils, basophils), mastocytes, type 2-innate lymphoid cells (ILC2), IL-4-and/or IL-13conditioned macrophages and T helper 2 (Th2) cells [24].…”

Section: Immunological Mechanismsmentioning

confidence: 99%

“…Type 2 immune responses are defined by the cytokines interleukin-4 (IL-4), IL-5, IL-9 and IL-13, which can be host protective, yet, when dysregulated, have pathogenic activity [24]. Type 2 immunity induces a complex response involving granulocytes (eosinophils, basophils), mastocytes, type 2-innate lymphoid cells (ILC2), IL-4-and/or IL-13conditioned macrophages and T helper 2 (Th2) cells [24]. These cells are crucial to the pathogenesis of CRS and related disorders (asthma [25]), therefore, driving mechanisms that control intensity, maintenance and resolution of type 2 immunity are reasonably important regulators of disease progression and have to be fully understood for therapeutical purposes.…”

Section: Immunological Mechanismsmentioning

confidence: 99%