The role of Staphylococcus aureus enterotoxin B in chronic rhinosinusitis with nasal polyposis

CRS with nasal polyps (CRSwNP) is a multifactorial disease, and various etiological factors like bacterial superantigens are known to develop this disease. Recent studies reported that Staphylococcus aureus nasal colonization was detected in 67% of the patients with CRSwNP. Moreover, it was reported that specific IgE against S. aureus enterotoxins are discovered in almost half of the nasal tissue homogenates from nasal polyps. Thus, investigations have highlighted the role of staphylococcal enterotoxins, especially enterotoxin B (SEB), in pathogenesis of CRSwNP. The destruction of mucosal integrity was reported as a main SEB-related pathogenic mechanisms in CRSwNP. SEB activates Toll Like Receptor 2 and triggers the production of pro-inflammatory cytokines; furthermore, it induces reactive oxygen species and endoplasmic reticulum stress-induced inflammation that may cause epithelial cell integrity disruption and enhance their permeability. SEB-induced Type 2/Th2 pathway results in degranulation of eosinophils, cationic proteins production, and localized eosinophilic inflammation. Furthermore, SEB may be involved in the expression of RORC and HIF-1 alpha in Tregs and by maintaining the inflammation in sinonasal mucosa that could have a main role in the pathogenesis of nasal polyposis. Different in vitro findings were confirmed in animal studies; however, in vivo analysis of SEB-induced nasal polyps and CRS remains unfulfilled due to the lack of appropriate animal models. Finally, after elucidating different aspects of SEB pathogenesis in CRSwNP, therapeutic agents have been tested in recent studies with some encouraging results. The purpose of this article is to summarize the most important findings regarding SEB-induced CRS and nasal polyposis.

Automated summary

Chronic Rhinosinusitis with Nasal Polyps (CRSwNP) is a multifactorial disease, and bacterial superantigens such as Staphylococcus aureus are known to play a role in its development. Specifically, Staphylococcus aureus nasal colonization and IgE response to Staphylococcus aureus enterotoxins have been found in CRSwNP patients. Among the enterotoxins, enterotoxin B (SEB) has been identified as a key player in the pathogenesis of CRSwNP by disrupting mucosal integrity and triggering inflammatory responses. SEB activates Toll Like Receptor 2, leading to the production of pro-inflammatory cytokines, and induces cellular stress and oxidative damage. It also promotes eosinophil degranulation and localized eosinophilic inflammation. Furthermore, SEB may be involved in the regulation of immune cells and maintenance of sinonasal mucosal inflammation. While in vitro and animal studies have provided valuable insights, further research is needed to fully understand the role of SEB in CRSwNP.