The immune system safeguards the health of complex organisms by rapidly eliminating invading pathogens, curbing infection-induced tissue disruptions, and maintaining tissue homeostasis. Many bacterial pathogens evade host antimicrobial mechanisms and persist in infected tissues at low levels for long periods of time even in the presence of innate and adaptive immune resistance. During persistent infection, the immune system simultaneously orchestrates antimicrobial responses to contain the pathogen, repairs damaged tissue, regulates nutrient resources, and maintains other tissue physiologic functions to ensure host survival. Failure of any of these tasks leads to uncontrolled infection, devastating disease, and even death. The goals of our research are to understand:

1)What are the innate and adaptive immune cellular mechanisms that contain pathogens during persistent infection?

2)How are tissue physiological functions, such as tissue repair and nutrient regulation, maintained during persistent infection?

3)How do pathogens survive innate and adaptive antimicrobial mechanisms in infected tissues?

4)How does persistent infection impact host immunity to secondary infections of a similar or different pathogen?

Through investigating these fundamental questions, we may be able to decode the underlying cellular and molecular mechanisms that can be harnessed to eradicate infections, promote tissue resilience, and restore health after an infectious insult. We employ animal infection models and bring together immunology, tissue biology, microbiology, and genetics to uncover the mechanisms of tissue immunity and immunophysiology during persistent infection from the molecular to organismal level.

Current areas of research:
•Development, maintenance, and plasticity of macrophage functional diversity in infected tissue
•Tissue repair and nutrient regulation during persistent infection
•Cellular dynamics and bacterial persistence in lymphoid organs