Stem Cells Attenuate the Inflammation Crosstalk Between Ischemic Stroke and Multiple Sclerosis: A Review

Abstract

The immense neuroinflammation induced by multiple sclerosis (MS) promotes a favorable environment for ischemic stroke (IS) development, making IS a deadly complication of MS. The overlapping inflammation in MS and IS is a prelude to the vascular pathology, and an inherent cell death mechanism that exacerbates neurovascular unit (NVU) impairment in the disease progression. Despite this consequence, no therapies focus on reducing IS incidence in patients with MS. To this end, the preclinical and clinical evidence we review here argues for cell-based regenerative medicine that will augment the NVU dysfunction and inflammation to ameliorate IS risk.

Keywords: ischemic stroke; multiple sclerosis; neuroinflammation; stem cells.

Figure 1.

This figure exemplifies the role of MS-induced neuroinflammation in prompting atherosclerosis and IS via pro-inflammatory immune cell and cytokine infiltration. On the left, MS induces inflammatory cytokines, Th17, Th1, and inflammatory microglia proliferation in the circulation. These mediators induce atherosclerosis and eventual ischemic stroke as shown on the right. The middle panel demonstrates how stem cells can reduce this inflammation by increasing Treg and anti-inflammatory microglial proliferation, ultimately reducing stroke and MS damage. Once MS neuroinflammation is downregulated, the relationship between atherosclerosis, stroke, and MS would be theoretically negligible, as described in the middle panel. MS: multiple sclerosis; IS: ischemic stroke.