Proinflammatory impact of Staphylococcus aureus enterotoxin B on human nasal epithelial cells and inhibition by dexamethasone.
BACKGROUND
The pathophysiology and etiology of chronic rhinosinusitis with nasal polyps (CRSwNP) are poorly understood. Although a potential role of staphylococcal enterotoxins (SE) in the pathogenesis of CRSwNP has been detected, additional studies are needed on the impact of SE on nasal epithelial cells. The purpose of this study was to evaluate the impact of Staphylococcus aureus enterotoxin B (SEB) on proinflammatory cytokine/chemokine releases in primary human nasal epithelial cells (HNEC) of subjects with and without CRSwNP and the inhibitory effect of glucocorticoid on it.


METHODS
Epithelial cells of NP and inferior turbinate (IT) were cultured serum free under stimulus of SEB, and interleukin (IL)-1beta, respectively. Furthermore, the inhibitory effect of glucocorticoid on the proinflammatory response was investigated by addition of dexamethasone. In situ hybridization and Western immunoblot assays were used to investigate the proinflammatory impact of SEB on IL-5 and granulocyte macrophage colony-stimulating factor (GM-CSF) mRNA levels and protein production in HNEC.


RESULTS
Results indicate (1) stimulation of HNEC with SEB resulted in increased IL-5 and GM-CSF expression, which could be suppressed by dexamethasone (p < 0.05), and SEB at concentrations of 1-100 ng/mL effectively promoted IL-5 and GM-CSF release by HNEC (p < 0.05); (2) patients with CRSwNP showed a significantly increased expression of IL-5 and GM-CSF in HNEC than patients without CRSwNP (p < 0.05); and (3) the expression of IL-5 and GM-CSF was significantly up-regulated under the stimulus of SEB compared with IL-1beta (p < 0.05).


CONCLUSIONS
SEB acts as a superantigen and exhibits a dramatic proinflammatory impact on HNEC, which can be inhibited by the addition of glucocorticoid.
Yu
Rui-Li
RL
Department of Otorhinolaryngology Head and Neck Surgery, China-Japan Union Hospital of Jilin University, Changchun, China.
Dong
Zhen
Z
D015153:Blotting, Western; D002908:Chronic Disease; D003907:Dexamethasone / Q000494:pharmacology*; D004768:Enterotoxins / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D004847:Epithelial Cells / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D015870:Gene Expression; D005938:Glucocorticoids / Q000494:pharmacology*; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000037:antagonists & inhibitors / Q000096:biosynthesis / Q000235:genetics; D006801:Humans; D017403:In Situ Hybridization; D015848:Interleukin-5 / Q000037:antagonists & inhibitors / Q000096:biosynthesis / Q000235:genetics; D009297:Nasal Mucosa / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D009298:Nasal Polyps / Q000188:drug therapy / Q000209:etiology / Q000473:pathology; D012333:RNA, Messenger / Q000235:genetics; D012220:Rhinitis / Q000188:drug therapy / Q000209:etiology / Q000473:pathology*; D012852:Sinusitis / Q000188:drug therapy / Q000209:etiology / Q000473:pathology*; D013211:Staphylococcus aureus / Q000276:immunology
D004768:Enterotoxins; D005938:Glucocorticoids; D015848:Interleukin-5; D012333:RNA, Messenger; C031818:enterotoxin B, staphylococcal; D003907:Dexamethasone; D016178:Granulocyte-Macrophage Colony-Stimulating Factor