Adrenergic-mediated loss of splenic marginal zone B cells contributes to infection susceptibility after stroke

Laura McCulloch, Craig J. Smith and Barry W. McColl ()
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Laura McCulloch: The Roslin Institute and R(D)SVS, University of Edinburgh, Easter Bush
Craig J. Smith: Stroke and Vascular Research Centre, University of Manchester, Manchester Academic Health Science Centre
Barry W. McColl: The Roslin Institute and R(D)SVS, University of Edinburgh, Easter Bush

Nature Communications, 2017, vol. 8, issue 1, 1-16

Abstract: Abstract Infection is a major complication of acute stroke and causes increased mortality and morbidity; however, current interventions do not prevent infection and improve clinical outcome in stroke patients. The mechanisms that underlie susceptibility to infection in these patients are unclear. 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.

Date: 2017
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DOI: 10.1038/ncomms15051

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