My lab is interested in understanding the various interactions occurring between the virulence factors produced by bacterial pathogens, primarily, and the different arms of the host immune system with special focus on skin immunity. During the initial stages of infection by a pathogen, the host niche facing the threat produces different signalling and protective molecules to initiate the immune protective mechanisms, mainly the innate immune repertoire. The pathogen, on the other hand, produces various effector molecules, called virulence factors, to counter the host immune measures. My research interest is to understand these interactions, with special focus on the host signalling and molecular mechanisms, with the ultimate aim of designing better and more efficient host-directed preventives and therapeutics. With this underlying objectives, my lab is aiming to bioengineer host signalling molecules and repurpose available drugs, as well as look for potential natural products that might contribute to ameliorate disease conditions through improved host immunomodulation.

Another focus of my lab is to understand the etiopathologies of various skin conditions, like psoriasis and delayed wound healing post infection. Skin is the largest organ of the human body and acts as the first protective barrier against different invading pathogens. Thus, it is extremely important to maintain skin barrier and immunity functions in top notch condition, for the overall prevention of pathogen invasion into the deeper sites of the body. My previous work has demonstrated that LL-37, the only human antimicrobial peptide from the cathelicidin family, protects the skin against Group A streptococcal soft tissue invasive infection through immunomodulation of the host responses. It was a novel finding which implicated the immune-signalling function of LL-37 using specific host receptors during bacterial infection, rather than the canonical direct antimicrobial activity of LL-37. On the other hand, the same immune-signalling property of LL-37 appeared to contribute to the pathogenesis of the immune-mediated skin condition called psoriasis. Hence, understanding the role of such immune molecules with dual functionality might provide better clues to the mechanism of immune protection and perturbations that are effected inside the host body depending on the disease conditions. The future aim is to harness the potency of such natural antimicrobials produced by living organisms, including human and using them to either enhance or ease immunomodulatory functions to ameliorate the host pathogenic condition.