Abstract
Stroke is a devastating disease with a strong inflammatory component. It has been shown that part of this response is mediated by IL17+ γδT cells. γδT cells constitute a lymphocyte population with innate features that mainly populates epithelial surfaces including skin, intestine, and airways. We have shown that in the context of stroke, T cells migrate from the small intestine to the meninges but whether they can migrate from other epithelial surfaces is still unknown. Because of its proximity, one possible source of stroke-associated IL17+ γδT cells could be the Nasal-Associated Lymphoid Tissue (NALT) from which T cells could migrate along olfactory nerve sheaths through the cribriform plate into the brain and/or meninges. In order to study the role of NALT as a source for immune cells and/or inflammatory mediators in the context of stroke, we analyzed the effect of NALT ablation on immune cell infiltration and infarct volume after stroke. Infarct volume analysis did not show any significant difference between sham and NALT-ablated animals. In addition, no significant differences were found in immune cell infiltration in the brain or meninges of stroke animals subjected to NALT or Sham-ablation surgery. In conclusion, NALT ablation does not affect ischemic brain damage or immune cell infiltration in the meninges or brain after stroke.
Highlights
One important component of stroke pathophysiology involves the inflammatory response that induces secondary damage
Our results show that Nasal-Associated Lymphoid Tissue (NALT) ablation did not affect the accumulation of IL-17-expressing T cells in the brain and meninges after brain ischemia and had no effect on the extent of ischemic brain injury
Because we have observed that γδT cells might traffic from the intestine to the meninges after stroke [2], it is possible that other epithelial-associated lymphatic tissues hosting γδT cells may contribute IL-17+ γδT cells during the immune response observed after ischemic brain injury
Summary
One important component of stroke pathophysiology involves the inflammatory response that induces secondary damage. This response involves the participation of peripheral immune cells that enter the ischemic territory and surrounding structures such as the meninges [1]. It is generally accepted that innate immune cells are predominant during the acute stages of stroke, while cells pertaining to the adaptive branch of the immune system are found later in disease development [1]. One of the innate immune cell types found in the meninges early after ischemic brain injury are γδT cells [2]. We and others have previously shown that γδT cells are crucial inducers of post-ischemic brain inflammation by producing IL-17 [2,3,4]
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