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 heterogeneity and 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 phagocyte heterogeneity and cellular networking, and at the molecular level, elucidating cell-intrinsic events in the context of infections with intracellular pathogens (i.e. Mycobacterium spp.) relevant for livestock (i.e. cattle) and human health.
Immunity to mycobacteria
- Host-adaptation of M. tuberculosis complex (MTC) members.
- Early events controlling pulmonary inflammation and susceptibility to tuberculosis.
- Myeloid cells and host-directed therapy for tuberculosis.
- Granuloma immunobiology.
Regulators of inflammation
- Myeloid-derived suppressor cells in bacterial and viral diseases.