Microbial sensing and inflammation are critical for host defense against pathogens. Professional phagocytes, including macrophages and neutrophils, sense microbial signatures, alarmins as well as metabolic cues during infection. Within infected tissue, processing and integration of these signals require a tight control for efficient pathogen disposal with minimal collateral damage. Phagocyte versatility, their crosstalk with parenchyma cells and in situ dynamics of immune cells control patterns of the inflammatory responses, thereby balancing host protective versus destructive inflammation. Our laboratory investigates regulation of pathogen-induced inflammation at the tissue level, deciphering intercellular networking, and at the molecular level, elucidating cell-intrinsic events in the context of infections with intracellular pathogens relevant for livestock and human health.
Our research contributes to new concepts for a comprehensive understanding of the host-pathogen interaction in diseases caused by zoonotic agents and organisms developing antimicrobial resistance. This knowledge will aid in the design of novel intervention strategies to fight infection.
Immunity to mycobacteria
- Deciphering host-adaptation of M. tuberculosis complex (MTC) members.
- Investigations on early events controlling pulmonary inflammation and susceptibility to tuberculosis.
- Targeting myeloid cell biology within host-directed therapy for tuberculosis.
Regulators of inflammation
- Compartmentalization of and crosstalk between microbial sensing platforms.
- Myeloid-derived suppressor cells in bacterial and viral diseases.
- Disease tolerance in mammalian and avian species during respiratory infections.