Wnt3a suppresses Pseudomonas aeruginosa-induced inflammation and promotes bacterial killing in macrophages.

Pseudomonas aeruginosa (PA) is a common Gram‑negative bacterium and can cause serious infections, including hospital‑acquired pneumonia, suppurative bacterial keratitis and acute burn wound infection. The pathogenesis of PA infections is closely associated with excessive inflammatory responses and bacterial virulence factors. Wingless‑type MMTV integration site family, member 3A (Wnt3a), an upstream mediator in the canonical Wnt signaling pathway, has been implicated as a regulator of inflammation. However, its role in PA‑induced inflammation and bacterial clearance remains unknown. In the present study, the efficacy of Wnt3a conditioned media (Wnt3a‑CM) was assessed using western blotting and immunofluorescence, which showed that β‑catenin, a downstream molecule of Wnt3a, was upregulated and translocated to the nucleus following exposure to 50% Wnt3a‑CM for 6 h. To explore the role of Wnt3a in PA‑induced inflammation, the mRNA levels of pro‑inflammatory cytokines and apoptosis in macrophages were measured using reverse transcription‑quantitative polymerase chain reaction and flow cytometry, respectively. This indicated that Wnt3a suppressed inflammation by reducing the production of pro‑inflammatory cytokines and by promoting apoptosis in macrophages. Furthermore, the mechanism of macrophage‑mediated bacterial killing was investigated, and the results indicated that Wnt3a enhanced macrophage‑mediated intracellular bacterial killing via the induction of the production of cathelicidin‑related antimicrobial peptide and β‑defensins 1. Taken together, the current study explored the role of Wnt3a in inflammation and bacterial invasion, which may provide an improved understanding of host resistance to PA infection.