Author
Listed:
- 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
Greater Manchester Comprehensive Stroke Centre, Salford Royal NHS Foundation Trust, Salford M6 8HD, UK)
- Barry W. McColl
(The Roslin Institute and R(D)SVS, University of Edinburgh, Easter Bush)
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.
Suggested Citation
Laura McCulloch & Craig J. Smith & Barry W. McColl, 2017.
"Adrenergic-mediated loss of splenic marginal zone B cells contributes to infection susceptibility after stroke,"
Nature Communications, Nature, vol. 8(1), pages 1-16, April.
Handle:
RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_ncomms15051
DOI: 10.1038/ncomms15051
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