Acquired Immunoglobulin G deficiency in stroke patients and experimental brain ischemia
| Autor: | Kerstin Hofmann, Roland Veltkamp, Stefan Roth, Markus Zorn, Arthur Liesz, Li Sun |
|---|---|
| Rok vydání: | 2015 |
| Předmět: |
Male
Pathology medicine.medical_specialty Time Factors medicine.medical_treatment Sensitivity and Specificity Severity of Illness Index Statistics Nonparametric Transient Hypogammaglobulinemia Brain ischemia Hypogammaglobulinemia Excretion Mice Developmental Neuroscience medicine Animals Humans Biotinylation IgG Deficiency Stroke Aged Analysis of Variance biology business.industry Immunosuppression Middle Aged medicine.disease Disease Models Animal Neurology Ischemic Attack Transient Brain Injuries Immunoglobulin G Luminescent Measurements Immunology biology.protein Female IgG deficiency Antibody business |
| Zdroj: | Experimental Neurology. 271:46-52 |
| ISSN: | 0014-4886 |
| Popis: | Background and purpose Acute brain injuries induce a systemic immune depression syndrome (SIDS) that predisposes patients to bacterial infections. While cellular compartments of this syndrome have been well characterized, the contribution of humoral immune mechanisms and particularly immunoglobulins to SIDS has not been investigated so far. Methods We determined serum immunoglobulin levels and infectious complications at several time points in 159 ischemic and hemorrhagic stroke patients. Additionally, findings were verified in a transient middle cerebral artery occlusion model. A novel immunoassay was established to analyze the IgG excretion ratio in mice. Results We identified a transient IgG reduction in patients suffering from substantial ischemic or hemorrhagic brain injuries. The IgG-reduction was associated with subsequent bacterial infections. Similarly, transient hypogammaglobulinemia was detected in a murine stroke model. We then used this animal model to further distinguish the mechanism of the IgG reduction by an IgG transfer paradigm. Excretional loss rather than deficient production of IgG was demonstrated to underlay hypogammaglobulinemia. Conclusions This is the first report of transient hypogammaglobulinemia after ischemic and hemorrhagic stroke suggesting involvement in infectious complications. These findings pave the road for further studies investigating post-stroke hypogammaglobulinemia as a druggable target for stroke-induced complications. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full Text from ScienceDirect