Isaac Chiu

Research Description

Our goal is to understand the role of the nervous system in host defense and inflammation. Nociceptor neurons protect the organism from danger by detecting potentially harmful/noxious stimuli and eliciting the sensation of pain or itch. Celsus defined pain as one of the cardinal signs of inflammation; however, the molecular mechanisms of pain during inflammation are not well understood. We found that nociceptors express specific receptors for pathogen and immune-derived factors, and play a role in modulating immune cell function.

Pathogenic mechanisms of pain

Pain is a component of many infectious diseases, including bacterial and viral infection. We have found that Staphylococcus aureus produces pain by directly activating neurons through N-formylated peptides and the pore-forming toxin alpha-hemolysin. Identifying how pathogens induce nociceptor activation and targeting these mechanisms could be important in the treatment of pain and inflammation.

Somatosensory neuron subsets in inflammation

Nociceptors encode the detection of different sensory modalities including heat and mechanical sensitivity at the molecular level. Similar specification may also mediate different inflammatory conditions. For example, bacterial infection often causes pain, whereas allergic inflammation induces itch. We will use electrophysiology, molecular biology, and animal models to investigate neuronal subsets involved in detection of pathogenic and inflammatory stimuli.

Neuro-immune cross-talk in host defense

Molecular cross-talk between the nervous system and immune system is involved in inflammatory responses. We found that nociceptor-derived neuropeptides alter innate immune cell recruitment and lymph node hypertrophy during infection. We aim to understand the molecular mechanisms by which neurons affect the generation of innate and adaptive immune responses during host defense.