Abstract
Haemophilus parasuis is known as a commensal organism discovered in the upper respiratory tract of swine where the pathogenic bacteria survive in various adverse environmental stress. QseC, a histidine protein kinase of the two-component regulatory systems CheY/QseC, is involved in the environmental adaptation in bacteria. To investigate the role of QseC in coping with the adverse environment stresses and survive in the host, we constructed a qseC mutant of H. parasuis serovar 13 strain (ΔqseC), MY1902. In this study, we found that QseC was involved in stress tolerance of H. parasuis, by the ΔqseC exhibited a decreased resistance to osmotic pressure, oxidative stress, and heat shock. Moreover, the ΔqseC weakened the ability to take up iron and biofilm formation. We also found that the QseC participate in sensing the epinephrine in environment to regulate the density of H. parasuis.
Highlights
Haemophilus parasuis is a causative agent of Glässer’s disease what characterized by fibrinous polyserositis, polyarthritis, and meningitis (Cai et al, 2005)
In order to determine the similarity between QseC, we aligned the protein sequences of QseC from H. parasuis (SH0165) with Actinobacillus pleuropneumoniae (L20), H. influenzae (Rd KW20), S. enterica subsp
Bacteria have multiple mechanisms for sensing the environment and regulate gene expressions in response to different niches of their host organisms, which is frequently mediated by Two-component signal transduction system (TCSTS) (Labandeira-Rey et al, 2010; Xu et al, 2014)
Summary
Haemophilus parasuis is a causative agent of Glässer’s disease what characterized by fibrinous polyserositis, polyarthritis, and meningitis (Cai et al, 2005). After invading the respiratory tract and lung tissue, H. parasuis exposes to stress conditions, such as osmotic pressure, oxidative stress, and temperature These stresses may affect bacterial survival, and result in protein denaturation and misfolding (Frees et al, 2004). QseC, as a transmembrane protein with histidine protein kinase, QseC Mediates Osmotic Stress Resistance is activated in response to host and bacterial signals, and phosphorylates the QseB response regulator, a transcription factor that regulates relevant virulence gene expression (Walters and Sperandio, 2006; Hughes et al, 2009). In addition to affect biofilm formation as reported in E. coli and Salmonella, we found that QseC function in bacterial response to a variety of stimuli such as osmotic pressure, oxidative stress, and heat shock.
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