The β-adrenergic receptor blocker and anti-inflammatory drug propranolol mitigates brain cytokine expression in a long-term model of Gulf War Illness

Growing evidence suggests that Gulf War Illness (GWI) is the result of underlying neuroimmune dysfunction. For example, previously we found that several Gulf War-relevant organophosphate, acetylcholinesterase inhibitors produce heightened neuroinflammatory responses following a sub chronic stressor exposure. The goal of the study was to evaluate the potential for the β-adrenergic receptor inhibitor and anti-inflammatory drug, propranolol, to treat neuroinflammation in a novel long-term mouse model of GWI. We established that our long-term GWI model produces enhanced and prolonged neuroinflammation that is dependent upon Gulf War-relevant organophosphate exposure. Propranolol treatment abrogated the neuroinflammation instigated in our model specifically, having no treatment effects in non-DFP exposed groups. Our results indicate that propranolol may be a promising therapy for GWI by treating the underlying neuroinflammation associated with Gulf War-relevant physiological stress and organophosphate exposures.