Nader Ghasemlou
The Pain Chronobiology & Neuroimmunology Laboratory focuses on understanding how communication between the nervous and immune systems contributes to health and disease, using circadian and diurnal rhythms as a tool to dissect mechanisms of action. Our team uses a translational, patient-oriented approach in all of our studies: preclinical studies inform clinical applications, and vice-versa, with patient-partners providing insight throughout the process.
Key areas of study for the lab include:
- Circadian rhythmicity of neuroimmunity
Intrinsic circadian clocks shape neuroimmune function across health and disease. We are particularly interested in how time-of-day programs in microglia/astrocytes, peripheral immune cells, and neurons regulate inflammation, cellular communication, and pain sensitivity in preclinical models of injury and disease. Using multi-omic approaches, we examine how disruption of these rhythms at the cell- and system-levels alter susceptibility to neuroinflammation. This work aims to define the molecular and cellular mechanisms through which circadian biology governs neuroimmune interactions, and to identify rhythmic pathways that can be targeted to improve disease outcomes through more precise and biologically informed interventions.
- Translational chrononeuroimmunology
Bench-to-bedside translation of circadian neuroimmunology is used to study how time-of-day influences symptoms, immune activity, and treatment responses in people living with multiple sclerosis, chronic pain, and other neuroimmune disorders. By combining patient-reported outcomes, longitudinal sampling, and experimental studies, we aim to identify clinically meaningful rhythmic signatures that can guide diagnosis, stratification, and therapy. This program is grounded in the idea that disease biology is dynamic across the day, and that understanding when pathological processes occur may be as important as understanding how they occur.
- Gut-brain axis in spinal cord injury
Spinal cord injury disrupts communication between the gut, immune system, and central nervous system. We are particularly interested in how gut-resident immune cells and shifts in the microbiome post-injury contribute to neuroinflammation recovery. By studying immune signaling across tissues, we aim to determine how peripheral events following injury shape pathological processes within the gut and spinal cord. This work seeks to uncover new mechanisms linking barrier tissues to neurological outcomes and to identify therapeutic strategies that target the gut-brain axis to reduce complications and improve long-term function after spinal cord injury.
- Tissue-resident immune cell crosstalk with neurons
Tissue-resident immune cells, like dendritic cells in the skin and γδ T cells in the gut, communicate with sensory neurons to regulate sensation, inflammation, and disease progression. These peripheral immune populations define how local immune-neural interactions shape neuroinflammatory states. Our work examines the signaling pathways and context-specific responses that govern this crosstalk in both steady-state and injury conditions. By identifying how immune cells directly modulate neuronal function, we aim to reveal new therapeutic opportunities that interrupt maladaptive signaling while preserving protective and homeostatic functions.