Next Article in Journal
The Relationship Between Contrast Associated Nephropathy and Coronary Collateral Circulation in very Old Patients
Previous Article in Journal
Iranian Medicinal Plants: From Ethnomedicine to Actual Studies
Open AccessArticle

Inhibition of Virus-Induced Cytokine Production from Airway Epithelial Cells by the Late Addition of Budesonide

Department of Medicine, Division of Allergology and Respiratory Medicine, Showa University School of Medicine, Tokyo 142-8555, Japan
Author to whom correspondence should be addressed.
Medicina 2020, 56(3), 98;
Received: 10 January 2020 / Revised: 16 February 2020 / Accepted: 21 February 2020 / Published: 27 February 2020
(This article belongs to the Section Translational Medicine)
Background and objectives: Viral infection is the main cause of asthma and COPD (chronic obstructive pulmonary disease) exacerbation and accumulate inflammatory cells to airway tissue. We have reported poly I:C, a mimic product of the virus and ligand of toll-like receptor 3 (TLR3), induced inflammatory chemokines from airway epithelial cells and found prior incubation with corticosteroids diminishes the effect of TLR3 activation. In clinical practice, mild asthma is recommended as-needed budesonide (BUD) when symptoms occur following a viral infection, etc. However, many questions still surround BUD’s usefulness if taken after a virus has already infected airway tissue. The aim of this study was to investigate the inhibitory effects of BUD on inflammatory cytokines induced by viral infection. Materials and Methods: Normal human bronchial epithelial (NHBE) cells were stimulated with poly I:C or infected with human rhinovirus-16 (HRV16) and BUD was added after the initial stimulation. Expression of both thymic stromal lymphopoietin (TSLP) and CCL26/eotaxin-3 was quantified by real-time RT-PCR and enzyme-linked immunosorbent assay (ELISA), respectively. Knockdown study was performed. Results: Pre-or post-incubation with BUD inhibited both poly I:C- and HRV16-induced mRNAs and proteins of both thymic stromal lymphopoietin (TSLP) and CCL26 with significance. Knockdown of the glucocorticoid receptor diminished these effects of BUD. Under the same conditions of BUD’s experiment, post-incubation with neither fluticasone propionate nor dexamethasone suppressed expression of both TSLP and CCL26, which induced by poly I:C. Conclusion: Post-addition of BUD inhibited the virus-induced TSLP and CCL26 from the airway epithelial cells. These results suggest that inhalation of BUD after viral infection has beneficial effects on asthma. Conclusion: Late addition of BUD may benefit among patient with viral infection and type 2 allergic airway disease such as asthma. View Full-Text
Keywords: budesonide; thymic stromal lymphopoietin (TSLP); rhinovirus; epithelial cells budesonide; thymic stromal lymphopoietin (TSLP); rhinovirus; epithelial cells
Show Figures

Figure 1

MDPI and ACS Style

Homma, T.; Fukuda, Y.; Uchida, Y.; Uno, T.; Jinno, M.; Kishino, Y.; Yamamoto, M.; Sato, H.; Akimoto, K.; Kaneko, K.; Fujiwara, A.; Sato, H.; Hirai, K.; Miyata, Y.; Inoue, H.; Ohta, S.; Watanabe, Y.; Kusumoto, S.; Ando, K.; Suzuki, S.; Yamaoka, T.; Tanaka, A.; Ohmori, T.; Sagara, H. Inhibition of Virus-Induced Cytokine Production from Airway Epithelial Cells by the Late Addition of Budesonide. Medicina 2020, 56, 98.

Show more citation formats Show less citations formats
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

Back to TopTop