Table 1 The possible pathogenic mechanisms of different cytokines in Staphylococcus aureus enterotoxin B-induced CRS with nasal polyposis
From: The role of Staphylococcus aureus enterotoxin B in chronic rhinosinusitis with nasal polyposis
Year, country and reference | Authors | Cell culture (target cytokine) | Outcome |
|---|---|---|---|
2011, Canada [72] | Liu et al | Nasal mucosa (IL-17) | SEB may contribute to converting FoxP3+ Treg to FoxP3+ IL-17+ T cells. These cells may have a role in nasal polyposis by remodeling the nasal airways |
2013, Japan [75] | Okano et al | Dispersed NP cells (IL-18) | Inhibition of IL-18 dramatically decreased the production of SEB-induced IFN-γ, IL-5, and IL-13. Thus, IL-18 may have pathogenic effects in CRS and nasal polyposis by boosting both the Th1 and Th2 responses |
2014, Korea [76] | Jin et al | Human nasal epithelial cells (IL-17C) | Inflammatory conditions and bacterial challenges cause the production of IL-17C in epithelial cells. SEB induced the expression of this cytokine in nasal epithelial cells |
2016, Japan [77] | Noyama et al | Dispersed NP and UT cells (IL-22) | SEB triggers IL-22 production from NP, and this cytokine may play a role in the pathogenesis of CRSwNP via its enhancement of MUC1 |
2016, Belgium [13] | Delemarre et al | PBMCs from healthy control and patients with CRSwNP (IL-9) | Stimulation with SEB and S. aureus leads to a remarkable increase in IL-9 gene expression |
2017, Japan [78] | Haruna et al | Dispersed UT and NP cells from patients with CRSwNP and CRSsNP (IL-10) | SEB leads to the production of impaired IL-10 in NP, and this phenomenon may worsen the pathophysiology of CRS, such as lower airway obstruction and eosinophilia |
2017, Sweden [79] | Calus et al | Nasal tissue of (IL-21) | SEB leads to the increase in IL-21 and IL-21+ CD4+ T cells, so; this enterotoxin may regulate the function of T-follicular helper cells in nasal polyps |