Stress resistance genes as the new engineering target for environmental control of airborne bacteria (PI: Dr. LAI Ka Man)
Over the past 70 years, studies have attempted to determine the survival of airborne bacteria and the associated effects of environmental parameters in order to predict the risk of airborne disease transmission (through droplet or droplet nuclei) and design infection control strategy. We know something about airborne bacteria through these studies, but the underlying biological mechanisms affecting the bacterial performance and so these experimental results are still poorly understood. This is problematic because without understanding these, we may misinterpret and misuse the results and could not identify a target to control the bacteria. Many people in Hong Kong spend over 90% of their time in indoor environments, most of which are controlled to different levels of temperature and sometimes RH for ventilation, energy savings and comfort. Little is known about the effects of the indoor climate on bioaerosol survival. This issue is of paramount importance in healthcare settings. Some interesting findings have been reported from bioaerosol studies and animal exposure models; for instance, a temperature of 24oC has been shown to universally decrease bacterial survival, and some studies have reported a U-shaped decay curve with RH. Why do bacteria behave in such a manner? Scant research has addressed the fundamental question of the stress resistance of bacteria during aerosolisation. Our data demonstrated that rpoS mutants had almost completely died in aerosolisation. RpoS regulates various stress resistance genes in some bacteria. Missing this gene means missing a defence mechanism. This result prompts to a new idea that if we can identify the critical stress resistance genes, and the stress they respond to as well as the aerosol and environmental condition interacting with them, we may be able to use these genes as new engineering targets for environmental control of airborne bacteria. For instance, if RpoS-mediated stress resistance is important for bacterial survival, finding ways to suppress it can help to effectively inactivate airborne bacteria. Moreover, since the environmental factors that actually kill or preserve bacteria and the gene response to them will now be better known, we could select and optimise disinfection and control measures to reduce disease transmission e.g. to avoid stimulating or to increase the stress loading on a particular gene through changing the environment. We hypothesise that stress resistance genes are crucial in the defence against aerosolisation stress and this new knowledge could help to predict and reduce transmission risks of airborne bacteria.