Acquired Immunoglobulin G deficiency in stroke patients and experimental brain ischemia

Liesz, Arthur; Roth, Stefan; Zorn, Markus; Sun, Li; Hofmann, Kerstin; Veltkamp, Roland

doi:10.1016/j.expneurol.2015.04.021

Cited by 20 publications

(20 citation statements)

References 15 publications

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“…As described in previous studies, infection was also associated with greater initial stroke severity41252. Our data are consistent with a recent study showing lower IgG levels in stroke patients which was associated with bacterial infection, however, these deficits were not associated with a B-cell-dependent mechanism53. In conjunction with our mouse MCAO data, it is reasonable to speculate that deficits in innate-like B-cell function, including IgM production, could mediate the effects of greater stroke severity on infection risk in patients.…”

Section: Discussionsupporting

confidence: 92%

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

2017

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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.

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Section: Discussionsupporting

confidence: 92%

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

2017

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“…We have shown, for the first time that circulating IgG1, IgG4 and IgA concentrations were reduced in the first 7 d after stroke in comparison to non-stroke controls. This is in agreement with previous data showing that pan-IgG concentrations were reduced in patients after stroke although subclasses of IgG were not assessed in that study and no reduction in IgA was found at the 7 d time point assessed 16 . IgA is the most predominant immunoglobulin isotype at mucosal surfaces including the respiratory tract and is crucial for antibacterial protection at these sites 17 .…”

Section: Discussionsupporting

confidence: 93%

Interleukin-1 receptor antagonist treatment in acute ischaemic stroke does not alter systemic markers of anti-microbial defence

McCulloch

Allan

Smith

et al. 2019

Preprint

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AimBlockade of the cytokine interleukin-1 (IL-1) with IL-1 receptor antagonist (IL-1Ra) is a candidate treatment for stroke entering phase II/III trials, which acts by inhibiting harmful inflammatory responses. Infection is a common complication after stroke that significantly worsens outcome and is related to stroke-induced deficits in systemic immune function thought to be mediated by the sympathetic nervous system. Therefore, immunomodulatory treatments for stroke, such as IL-1Ra, carry a risk of aggravating stroke-associated infection. Our primary objective was to determine if factors associated with antibody-mediated antibacterial defences were further compromised in patients treated with IL-1Ra after stroke.MethodsWe assessed plasma concentrations of immunoglobulin isotypes and complement components in stroke patients treated with IL-1Ra or placebo and untreated non-stroke controls using multiplex protein assays. Activation of the SNS was determined by measuring noradrenaline, a major SNS mediator.ResultsThere were significantly lower plasma concentrations of IgM, IgA, IgG1 and IgG4 in stroke-patients compared to non-stroke controls, however there were no differences between stroke patients treated with placebo or IL-1Ra. Concentrations of complement components associated with the classical pathway were increased and those associated with the alternative pathways decreased in stroke patients, neither being affected by treatment with IL-1Ra. Noradrenaline concentrations were increased after stroke in both placebo and IL-1Ra-treated stroke patients compared to non-stroke controls.ConclusionThese data show treatment with IL-1Ra after stroke does not alter circulating immunoglobulin and complement concentrations, and is therefore unlikely to further aggravate stroke-associated infection susceptibility through reduced availability of these key anti-microbial mediators.

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“…Recently, an acquired hypogammaglobulinemia has been detected in stroke as well as in the MCAO model of experimental stroke following ischemia [15].…”

Section: Introductionmentioning

confidence: 99%

Stroke induces specific alteration of T memory compartment controlling auto-reactive CNS antigen-specific T cell responses

Klehmet

Höffmann

Walter

et al. 2016

Journal of the Neurological Sciences

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Acquired Immunoglobulin G deficiency in stroke patients and experimental brain ischemia

Cited by 20 publications

References 15 publications

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

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

Interleukin-1 receptor antagonist treatment in acute ischaemic stroke does not alter systemic markers of anti-microbial defence

Stroke induces specific alteration of T memory compartment controlling auto-reactive CNS antigen-specific T cell responses

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