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Review
. 2021 Jun 6;18(1):127.
doi: 10.1186/s12974-021-02177-0.

Stroke-induced immunosuppression: implications for the prevention and prediction of post-stroke infections

Júlia Faura  1 , Alejandro Bustamante  2 , Francesc Miró-Mur  3 , Joan Montaner  1   4
Affiliations
Review

Stroke-induced immunosuppression: implications for the prevention and prediction of post-stroke infections

Júlia Faura et al. J Neuroinflammation. .

Abstract

Stroke produces a powerful inflammatory cascade in the brain, but also a suppression of the peripheral immune system, which is also called stroke-induced immunosuppression (SIIS). The main processes that lead to SIIS are a shift from a lymphocyte phenotype T-helper (Th) 1 to a Th2 phenotype, a decrease of the lymphocyte counts and NK cells in the blood and spleen, and an impairment of the defense mechanisms of neutrophils and monocytes. The direct clinical consequence of SIIS in stroke patients is an increased susceptibility to stroke-associated infections, which is enhanced by clinical factors like dysphagia. Among these infections, stroke-associated pneumonia (SAP) is the one that accounts for the highest impact on stroke outcome, so research is focused on its early diagnosis and prevention. Biomarkers indicating modifications in SIIS pathways could have an important role in the early prediction of SAP, but currently, there are no individual biomarkers or panels of biomarkers that are accurate enough to be translated to clinical practice. Similarly, there is still no efficient therapy to prevent the onset of SAP, and clinical trials testing prophylactic antibiotic treatment and β-blockers have failed. However, local immunomodulation could open up a new research opportunity to find a preventive therapy for SAP. Recent studies have focused on the pulmonary immune changes that could be caused by stroke similarly to other acquired brain injuries. Some of the traits observed in animal models of stroke include lung edema and inflammation, as well as inflammation of the bronchoalveolar lavage fluid.

Keywords: Biomarkers; Immunosuppression; Infection; Inflammation; Pneumonia; Stroke.

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Conflict of interest statement

The authors declare that they have no competing interests.

Figures

Fig. 1
Fig. 1
The interplay of local and systemic processes leading to pneumonia in stroke patients. Stroke-associated pneumonia is influenced by systemic and local mechanisms. Locally, there are pulmonary alterations due to stroke itself and the inflammatory processes that develop. BALF inflammation, lung inflammation, and edema seem to be the principal alterations, although there are some discrepancies between studies. On a systemic level, various represented processes lead to 3 main alterations that cause systemic immunosuppression after stroke: an increase of the T-helper (Th) 2/Th1 cytokine ratio; a reduction of the lymphocyte counts in the spleen, thymus, and blood; and a decrease of the antimicrobial defense mechanisms of neutrophils and monocytes. SNS sympathetic nervous system, iNKT invariant natural killer T cells, PNS parasympathetic nervous system, ACh acetylcholine, HPA hypothalamic–pituitary–adrenal, HMGB-1 high motility group box-1, sCD163 soluble cluster of differentiation 163, MZ marginal zone, FasL Fas ligand, BALF bronchoalveolar lavage fluid. Parts of this figure were supported by Servier Medical Art with permission under the Creative Commons Attribution 3.0 Unported License
See this image and copyright information in PMC

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