Phospholipase A2-dependent Release of Inflammatory Cytokines by Superantigen-Stimulated Nasal Polyps of Patients with Chronic Rhinosinusitis

Abstract

This study further supports the key role of secretory PLA2 in the pathophysiology of respiratory disorders and presents secretory PLA2 inhibition as a therapeutic strategy for the treatment of CRS and airway pathologies in general.

Role of Superantigens in Allergic Inflammation: Their Relationship to Allergic Rhinitis, Chronic Rhinosinusitis, Asthma, and Atopic Dermatitis

“…Basophils can become activated in 2 ways: as usual, through antigen binding to CDRs; but also in superantigenic fashion by binding to the framework region of anti-SEE IgE, thus producing complexes of IgE targeting SEE and FceRI. Mruwat et al 84 6 Discusses what part PLA2 plays in respiratory diseases. Argues for blockade of secretion of PLA2 as a way to treat CRS among other airway diseases.…”

Understanding the Role of Biofilms and Superantigens in Chronic Rhinosinusitis

“…More recently, eicosanoids such as leukotrienes and pro-inflammatory leukotrienes have been known to be downstream of superantigens in the setting of Th2 upper airway disease [93–95]. Furthermore, Murawat et al demonstrated that SAEs cause cytokine secretion in nasal polyps via phospholipase A2, the first and key regulatory enzyme in metabolizing eicosanoids [96]. Further investigation will hopefully shed increasing light on how these molecules are contributing.…”

Editorial: Inflammatory and Allergic Diseases of the Upper Airways

“…2 CRS has been linked to imbalances in the production of eicosanoids (arachidonic acid metabolites), which results from phospholipid hydrolysis by phospholipase A2 (PLA2). Mruwat et al 3 investigated the expression of PLA2s and multiple cytokines in super-antigen Staphylococcus aureus enterotoxin stimulated human nasal polyps from patients with CRSwNP. Stimulation of nasal polyp cells by S. aureus enterotoxin induced cytokine secretion and enhanced expression of several secretory PLA2 and calciumindependent PLA2, while suppressing cytoplasmic PLA2 expression.…”

“…This supports a role for secretory PLA2s in the pathophysiology of CRS. 3 Wang et al 4 evaluated the ethmoid bone tissue samples from a group of patients with CRS by histologic examination and quantitative real-time reverse transcription polymerase chain reaction and showed an increased infiltration of eosinophils in the periosteum, along with neo-osteogenesis in CRS. The investigators found increased expression of TGF-␤1, TGF-␤ receptor I, and p-Smad3 in patients with CRSwNP compared with CRSsNP at the mRNA and protein levels.…”