Adrenergic-mediated loss of splenic innate-like B cells contributes to infection susceptibility after stroke

Abstract

Infection is a major complication of acute stroke and causes increased mortality and morbidity, however, there are no current interventions that prevent infection in stroke patients and improve clinical outcome. The mechanisms that underlie susceptibility of stroke patients to infection are poorly understood. Splenic marginal zone (MZ) B cells are innate-like lymphocytes that provide early defence against bacterial infection. Here we show experimental stroke in mice induces a marked loss of MZ B cells, deficiencies in capturing blood-borne antigen and suppression of circulating IgM. These deficits are accompanied by spontaneous bacterial lung infection. IgM levels are similarly suppressed in stroke patients. β-adrenergic receptor antagonism after experimental stroke prevents loss of splenic MZ B cells, preserves IgM levels, and reduces bacterial burden. These findings suggest that adrenergic-mediated loss of MZ B cells contributes to the infection-prone state after stroke and identify systemic B cell disruption as a target for therapeutic manipulation