Manipulation of host Kruppel-like factor (KLF) function by exotoxins from diverse bacterial pathogens.
Diverse pathogenic bacteria have developed similar mechanisms to subvert host cell responses. In this Progress article, we focus on bacterial virulence factors with different enzymatic activities that can increase the expression of the Kruppel-like factor (KLF) family of mammalian transcriptional regulators through their ability to modify the activity of a common host-cell target - the Rho protein family. By using a common virulence strategy, both Gram-negative and Gram-positive pathogens exploit the KLF regulatory cascade to modulate nuclear factor kappaB activation, pro-inflammatory cytokine expression, actin cytoskeletal dynamics and phagocytosis.
O'Grady
Eoin
E
BIOMERIT Research Centre, Department of Microbiology, University College Cork, Cork, Ireland.
Mulcahy
Heidi
H
Adams
Claire
C
Morrissey
John P
JP
O'Gara
Fergal
F
D000818:Animals; D002460:Cell Line; D005098:Exotoxins / Q000494:pharmacology*; D005786:Gene Expression Regulation; D006090:Gram-Negative Bacteria / Q000472:pathogenicity*; D006094:Gram-Positive Bacteria / Q000472:pathogenicity*; D006801:Humans; D000075723:Kruppel-Like Factor 6; D051741:Kruppel-Like Transcription Factors / Q000378:metabolism*; D011518:Proto-Oncogene Proteins / Q000378:metabolism; D015398:Signal Transduction; D037521:Virulence Factors / Q000494:pharmacology*
D005098:Exotoxins; C096161:KLF2 protein, human; C105465:KLF6 protein, human; D000075723:Kruppel-Like Factor 6; D051741:Kruppel-Like Transcription Factors; D011518:Proto-Oncogene Proteins; D037521:Virulence Factors