Fungal-induced inflammation and nasal polyps

Eugene B. Kern; David A. Sherris; Hirohito Kita; Jens U. Ponikau

doi:10.1007/978-3-642-11412-0_11

Fungal-induced inflammation and nasal polyps

Eugene B. Kern, David A. Sherris, Hirohito Kita, Jens U. Ponikau

Allergic Diseases

Research output: Chapter in Book/Report/Conference proceeding › Chapter

1 Scopus citations

Abstract

Fungi are present in the mucus of chronic rhinosinusitis (CRS) patients and normal healthy controls. Fungi (especially Alternaria) induce the production of cytokines (IL-13 and IL-5) crucial for the eosinophilic inflammation. This immune response occurred only in CRS patients but not in healthy controls. Fungi induce an eosinophilic tissue airway inflammation in mammals (mice), which is in contrast to a neutrophilic response to bacteria. Fungi can induce an eosinophilic airway inflammation and congestion in patients. Eosinophils, in vivo, target fungi in the mucus with CRS and nasal polyps. Fungal antigens with a molecular weight of 61 kilodaltons (kDa) cause activation and degranulation of human eosinophils via the beta-2 integrin on the CD11b receptor. Clinically, antifungal drugs can reduce nasal polyps, improve computed tomography (CT) scans, and decrease levels of interleukin-5 (IL-5) and markers of eosinophilic inflammation. However, data between different antifungal applications and different outcome measures are conflicting.

Original language	English (US)
Title of host publication	Nasal Polyposis: Pathogenesis, Medical and Surgical Treatment
Publisher	Springer Berlin Heidelberg
Pages	95-101
Number of pages	7
ISBN (Print)	9783642114113
DOIs	https://doi.org/10.1007/978-3-642-11412-0_11
State	Published - 2010

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ASJC Scopus subject areas

Medicine(all)

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Kern, E. B., Sherris, D. A., Kita, H., & Ponikau, J. U. (2010). Fungal-induced inflammation and nasal polyps. In Nasal Polyposis: Pathogenesis, Medical and Surgical Treatment (pp. 95-101). Springer Berlin Heidelberg. https://doi.org/10.1007/978-3-642-11412-0_11

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N2 - Fungi are present in the mucus of chronic rhinosinusitis (CRS) patients and normal healthy controls. Fungi (especially Alternaria) induce the production of cytokines (IL-13 and IL-5) crucial for the eosinophilic inflammation. This immune response occurred only in CRS patients but not in healthy controls. Fungi induce an eosinophilic tissue airway inflammation in mammals (mice), which is in contrast to a neutrophilic response to bacteria. Fungi can induce an eosinophilic airway inflammation and congestion in patients. Eosinophils, in vivo, target fungi in the mucus with CRS and nasal polyps. Fungal antigens with a molecular weight of 61 kilodaltons (kDa) cause activation and degranulation of human eosinophils via the beta-2 integrin on the CD11b receptor. Clinically, antifungal drugs can reduce nasal polyps, improve computed tomography (CT) scans, and decrease levels of interleukin-5 (IL-5) and markers of eosinophilic inflammation. However, data between different antifungal applications and different outcome measures are conflicting.

AB - Fungi are present in the mucus of chronic rhinosinusitis (CRS) patients and normal healthy controls. Fungi (especially Alternaria) induce the production of cytokines (IL-13 and IL-5) crucial for the eosinophilic inflammation. This immune response occurred only in CRS patients but not in healthy controls. Fungi induce an eosinophilic tissue airway inflammation in mammals (mice), which is in contrast to a neutrophilic response to bacteria. Fungi can induce an eosinophilic airway inflammation and congestion in patients. Eosinophils, in vivo, target fungi in the mucus with CRS and nasal polyps. Fungal antigens with a molecular weight of 61 kilodaltons (kDa) cause activation and degranulation of human eosinophils via the beta-2 integrin on the CD11b receptor. Clinically, antifungal drugs can reduce nasal polyps, improve computed tomography (CT) scans, and decrease levels of interleukin-5 (IL-5) and markers of eosinophilic inflammation. However, data between different antifungal applications and different outcome measures are conflicting.

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Access to Document

10.1007/978-3-642-11412-0_11