Silica sulfuric acid (SSA) was firstly used as an efficient catalyst to promote the synthesis of rctt configurational calix[4]resorcinarenes via one-pot condensation between resorcinol and aromatic aldehydes. The structure of 4- cyanophenyl-calix[4]resorcinarene (3b) has been determined by single crystal X-ray diffraction.

Background. Respiratory syncytial virus (RSV) is the main pathogen causing acute bronchiolitis, which is common in infants and young children. A previous study revealed the possible involvement of POU class 2 associating factor 1 (POU2AF1) in RSV‐triggered acute bronchiolitis. We attempted to clarify the specific action mechanism of POU2AF1 underlying RSV‐triggered inflammation. Methods. RT‐qPCR measured POU2AF1 levels in RSV‐infected children, mice, and airway epithelial cell lines (HBECs). HE staining showed histopathological features in the lung tissue of RSV‐infected mice. ELISA examined the contents of proinflammatory cytokines in RSV‐infected mice. Western blotting evaluated the protein abundance of proinflammatory cytokines in RSV‐infected HBECs and assessed NF‐κB pathway‐associated protein expression in RSV‐infected mice and RSV‐treated HBECs. Results. POU2AF1 presented depletion in RSV‐infected children, mice, and HBECs. RSV‐infected triggered lung injury and inflammatory cell infiltration in the mouse lung tissue, while POU2AF1 overexpression rescued these changes. RSV‐infected induced inflammatory impairment in HBECs, whereas POU2AF1 reversed this effect. POU2AF1 suppressed the upregulated NF‐κB pathway‐associated protein expression in mice and HBECs under RSV infection. Conclusion. POU2AF1 exerts a protective impact on RSV‐induced acute bronchiolitis in vitro and in vivo through the NF‐κB pathway. Our research may provide a novel direction for better therapy of RSV‐triggered acute bronchiolitis.