Differential Gene Expression and Immune Modulation Following K. pneumoniae Infection: A Focus on MAPK Signaling

Our current study has revealed significant differential expression of genes following infection by K. pneumoniae. Notably, RSK2 and NFAT2/4 were down-regulated. RSK2 plays a crucial role in the MAPK signaling pathway by regulating gene expression through phosphorylation of various transcription factors. Its down-regulation can disrupt normal gene expression patterns, potentially impacting the expression of genes involved in immune responses and inflammation. NFAT2 (Nuclear Factor of Activated T Cells 2) and NFAT4 (Nuclear Factor of Activated T Cells 4) are transcription factors that play important roles in the MAPK (Mitogen-Activated Protein Kinase) signaling pathway. The decreased expression of NFAT2 and NFAT4 could result in impaired immune cell activation, reduced production of immune mediators, and alterations in gene expression patterns. Consequently, these changes may contribute to an impaired immune response against bacterial infection, potentially influencing the establishment and progression of the infection. Impaired cell proliferation, reduced activation of downstream signaling molecules, and altered gene expression patterns are among the consequences of RSK2 down-regulation in the MAPK signaling pathway. Collectively, the down-regulation of RSK2 in the MAPK signaling pathway following bacterial infection may modulate host cellular responses and influence the infection outcome. Interestingly, TNFR, TRADD, and TAB1 were up-regulated. The up-regulation of TNFR, a cell surface receptor that binds to TNF, suggests activation of the immune response and modulation of cellular processes associated with inflammation.