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Abstract Background Staphylococcus aureus releases virulence factors (VF) that may impair the innate protective functions of airway cells. The aim of this study was to determine whether a long-acting β2 adrenergic receptor agonist (salmeterol hydroxynaphthoate, Sal) combined with a corticosteroid (fluticasone propionate, FP) was able to regulate ion content and cytokine expression by airway glandular cells after exposure to S. aureus supernatant. Methods A human airway glandular cell line was incubated with S. aureus supernatant for 1 h and then treated with the combination Sal/FP for 4 h. The expression of actin and CFTR proteins was analyzed by immunofluorescence. Videomicroscopy was used to evaluate chloride secretion and X-ray microanalysis to measure the intracellular ion and water content. The pro-inflammatory cytokine expression was assessed by RT-PCR and ELISA. Results When the cells were incubated with S. aureus supernatant and then with Sal/FP, the cellular localisation of CFTR was apical compared to the cytoplasmic localisation in cells incubated with S. aureus supernatant alone. The incubation of airway epithelial cells with S. aureus supernatant reduced by 66% the chloride efflux that was fully restored by Sal/FP treatment. We also observed that Sal/FP treatment induced the restoration of ion (Cl and S) and water content within the intracellular secretory granules of airway glandular cells and reduced the bacterial supernatant-dependent increase of pro-inflammatory cytokines IL8 and TNFα. Conclusions Our results demonstrate that treatment with the combination of a corticosteroid and a long-acting β2 adrenergic receptor agonist after bacterial infection restores the airway glandular cell function. Abnormal mucus induced by defective ion transport during pulmonary infection could benefit from treatment with a combination of β2 adrenergic receptor agonist and glucocorticoid.

Web‐based studies of human dimensions are increasing across environmental and socio‐ecological disciplines. However, the prevalence of fraud threatens research quality. Increased fraud rates should be expected as surveys move progressively more online, motivated by expanding reach, cost savings and/or in response to COVID‐19. Web‐based research must better account for fraud to maintain confidence in findings. Practical diagnostic tools and data quality protocols are required to detect fraud and ensure results quality.Drawing on our experience using an online participatory mapping case study, we discuss methods to detect potentially fraudulent responses—and identify some limitations. We begin by reviewing the current state of knowledge on fraudulent responses or 'fraudsters' and its relative absence in environmental and socio‐ecological disciplines. We then describe our research approach, the indicators and variables we used to detect and assess fraud and our decision‐making process to eliminate suspicious responses without jeopardizing research integrity.We found that despite several preventative measures, many fraudulent respondents could provide survey responses and effectively mimicked legitimate respondents at first glance. By assuming each response to be 'potentially fraudulent', we determined that the complete screening of each respondent, while time‐consuming, can limit the prevalence of fraud. We also determined that the most common data consistency checks (e.g. duration, trap questions and straight‐liner checks) are unlikely to guarantee valid respondents.If not acknowledged and addressed, fraud has the potential to undermine data integrity, discredit research findings and limit the utility of results for policy. This study contributes to environmental and socio‐ecological research by reviewing existing fraudster literature and using our experience with fraud to provide recommendations for researchers to address this problem. We encourage researchers implementing online qualitative research methods to thoroughly assess and report fraud, when possible, to ensure widespread knowledge of this growing threat. Read the free Plain Language Summary for this article on the Journal blog. Read the free Plain Language Summary for this article on the Journal blog. [ABSTRACT FROM AUTHOR]

Although Staphylococcus aureus is a major cause of pulmonary infection, the role played by this bacterium in the induction of inflammation of human airway epithelial cells (HAEC) is poorly understood. In this study, we investigated the inflammatory response of HAEC to S. aureus soluble virulence factors and demonstrate that the combination of a long-acting [[beta].sub.2]-adrenergic receptor agonist (salmeterol) with a glucocorticoid (fluticasone propionate) has an anti-inflammatory effect on HAEC. First, we demonstrate increased expression at both the mRNA and protein levels of interleukin (IL)-8, IL-6, and tumor necrosis factor (TNF)-[alpha] following incubation of HAEC in the presence of S. aureus soluble virulence factors and the increase of 1) the tree nuclear factor-[kappa]B (NF-[kappa]B) and activator protein-1 (AP-1) activities and 2) the phosphorylated (P-) extracellular signal-regulated kinases 1 and 2 (ERK1/ERK2), the P-c-Jun [NH.sub.2]-terminal kinase (JNK), and the P-isoform-[alpha] of the NF-[kappa]B inhibitor (I[kappa]B[alpha]). Next, when HAEC were preincubated with the combination of salmeterol and fluticasone propionate, the inflammatory response of HAEC was markedly attenuated in that levels of IL-8, IL-6, TNF-[alpha], NF-[kappa]B, AP-1, P-ERK1/ERK2, P-JNK, and P-I[kappa]B[alpha] decreased significantly. These data emphasize the deleterious effect of S. aureus soluble virulence factors and suggest that the combination of a [[beta].sub.2]-adrenergic receptor agonist with a glucocorticoid may attenuate the associated airway epithelial inflammation. airway inflammation; proinflammatory cytokines; nuclear fator-[kappa]B and activator protein-1 activation; glucocorticoid; bacterial virulence factors