RESUMEN
OBJECTIVE: This study's purpose was to better understand the dynamics of trust attitude and behavior in human-agent interaction. BACKGROUND: Whereas past research provided evidence for a perfect automation schema, more recent research has provided contradictory evidence. METHOD: To disentangle these conflicting findings, we conducted an online experiment using a simulated medical X-ray task. We manipulated the framing of support agents (i.e., artificial intelligence (AI) versus expert versus novice) between-subjects and failure experience (i.e., perfect support, imperfect support, back-to-perfect support) within subjects. Trust attitude and behavior as well as perceived reliability served as dependent variables. RESULTS: Trust attitude and perceived reliability were higher for the human expert than for the AI than for the human novice. Moreover, the results showed the typical pattern of trust formation, dissolution, and restoration for trust attitude and behavior as well as perceived reliability. Forgiveness after failure experience did not differ between agents. CONCLUSION: The results strongly imply the existence of an imperfect automation schema. This illustrates the need to consider agent expertise for human-agent interaction. APPLICATION: When replacing human experts with AI as support agents, the challenge of lower trust attitude towards the novel agent might arise.
RESUMEN
SARS-CoV-2 has evolved to enter the host via the ACE2 receptor which is part of the kinin-kallikrein pathway. This complex pathway is only poorly understood in context of immune regulation but critical to control infection. This study examines SARS-CoV-2-infection and epithelial mechanisms of the kinin-kallikrein-system at the kinin B2 receptor level in SARS-CoV-2-infection that is of direct translational relevance. From acute SARS-CoV-2-positive study participants and -negative controls, transcriptomes of nasal curettages were analyzed. Primary airway epithelial cells (NHBEs) were infected with SARS-CoV-2 and treated with the approved B2R-antagonist icatibant. SARS-CoV-2 RNA RT-qPCR, cytotoxicity assays, plaque assays, and transcriptome analyses were performed. The treatment effect was further studied in a murine airway inflammation model in vivo. Here, we report a broad and strong upregulation of kallikreins and the kinin B2 receptor (B2R) in the nasal mucosa of acutely symptomatic SARS-CoV-2-positive study participants. A B2R-antagonist impeded SARS-CoV-2 replication and spread in NHBEs, as determined in plaque assays on Vero-E6 cells. B2R-antagonism reduced the expression of SARS-CoV-2 entry receptor ACE2, G protein-coupled receptor signaling, and ion transport in vitro and in a murine airway inflammation in vivo model. In summary, this study provides evidence that treatment with B2R-antagonists protects airway epithelial cells from SARS-CoV-2 by inhibiting its replication and spread, through the reduction of ACE2 levels and the interference with several cellular signaling processes. Future clinical studies need to shed light on the airway protection potential of approved B2R-antagonists, like icatibant, in the treatment of early-stage COVID-19. KEY MESSAGES: Induction of kinin B2 receptor in the nose of SARS-CoV-2-positive patients. Treatment with B2R-antagonist protects airway epithelial cells from SARS-CoV-2. B2R-antagonist reduces ACE2 levels in vivo and ex vivo. Protection by B2R-antagonist is mediated by inhibiting viral replication and spread.
