Pseudomonas aeruginosa infection stimulates mitogen‐activated protein kinases signaling pathway in human megakaryocytes

Abstract

Pseudomonas aeruginosa is a major cause of nosocomial infections and contributes to higher mortality in hospitalized individuals. Infection by P. aeruginosa triggers host immune response through activation of pathogen recognition receptors, which are present in innate cells. Several studies have reported the mechanism of P. aeruginosa induced innate immunity in multiple cell types. But so far there is no reports on response of megakaryocytes to P. aeruginosa infection. Hence, our aim was to investigate the precise role and signaling mechanism of megakaryocytes during P. aeruginosa infection. In this study, we used Mo7e cells as representatives of human megakaryocyte and found that P. aeruginosa infection induces cytotoxicity in these cells. We further demonstrated that P. aeruginosa infection modulates p38 and extracellular signal regulated kinase pathways in Mo7e cells. Protein expression profiling in P. aeruginosa lipopolysaccharide‐treated Mo7e cells revealed upregulation of importin subunit β and downregulation of metabolic enzymes. Our results suggest that P. aeruginosa infection regulates mitogen‐activated protein kinases signaling pathway and importin in Mo7e cells and that this is a potential mechanism for nuclear translocation of nuclear factor binding near the κ light‐chain gene in B cells and c‐Jun N‐terminal kinases to induce cell cytotoxicity.

Understanding the complications of pseudomonas aeruginosa biofilm exudates on wound healing

“…Herein, JNK pathway was downregulated by PAO1 BCM, with a concomitant decrease in c-Jun levels. Similar to this dissertation, P. aeruginosa has been reported to exploit kinase pathways as well by inducing apoptosis in human conjunctiva epithelial cells and human megakaryocytes through JNK pathway activation (Gopala Krishnan et al, 2019;Jendrossek et al, 2001). Additionally, Losa et al (2014) have reported that apoptosis induced in airway epithelial cells by P. aeruginosa is caused by increased gap junction expression and this increase in gap junction is regulated by JNK signalling inhibition.…”

Kit activates interleukin‐4 receptor and effector signal transducer and activator of transcription 6 independent of its cognate ligand in mouse mast cells

“…A total of 3–6 µg of antibody was used per immunoprecipitation, and antibody–protein complexes were collected with 50–75 µl protein A‐Sepharose. Western blotting was performed, as previously described …”