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10.3892/mmr.2016.4869

http://scihub22266oqcxt.onion/10.3892/mmr.2016.4869
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C4768980!4768980!26846714
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suck abstract from ncbi


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pmid26846714      Mol+Med+Rep 2016 ; 13 (3): 2439-46
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  • Wnt3a suppresses Pseudomonas aeruginosa-induced inflammation and promotes bacterial killing in macrophages #MMPMID26846714
  • CHEN K; FU Q; LI D; WU Y; SUN S; ZHANG X
  • Mol Med Rep 2016[Mar]; 13 (3): 2439-46 PMID26846714show ga
  • 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 ?-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 ?-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.
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