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Blood viscosity may affect the mechanisms of stroke and early neurological deterioration (END). We aimed to investigate the relationship between blood viscosity, stroke mechanisms, and END in patients with middle cerebral artery (MCA) infarction. Patients with symptomatic MCA atherosclerosis (≥ 50% stenosis) were recruited. Blood viscosity was compared across patients with different mechanisms of symptomatic MCA disease: in situ thrombo-occlusion (sMCA-IST), artery-to-artery embolism (sMCA-AAE), and local branch occlusion (sMCA-LBO). END was defined as four points increase in the National Institutes of Health Stroke Scale score from baseline during the first week. The association between blood viscosity and END was also evaluated. A total of 360 patients (76 with sMCA-IST, 216 with sMCA-AAE, and 68 with sMCA-LBO) were investigated. Blood viscosity was highest in patients with sMCA-IST, followed by sMCA-AAE and sMCA-LBO (P < 0.001). Blood viscosity was associated with END in patients with MCA disease. Low shear viscosity was associated with END in patients with sMCA- LBO (adjusted odds ratio, aOR 1.524; 95% confidence interval, CI 1.035–2.246), sMCA- IST (aOR 1.365; 95% CI 1.013–1.839), and sMCA- AAE (aOR 1.285; 95% CI 1.010–1.634). Blood viscosity was related to END in patients with stroke caused by MCA disease. [ABSTRACT FROM AUTHOR]

Basophils are rare, circulating granulocytes proposed to be involved in T helper (TH) type 2 immunity, mainly through secretion of interleukin (IL)-4. In addition to IL-4, basophils produce IL-6 and tumor necrosis factor (TNF)-α in response to immunoglobulin E (IgE) crosslinking. Differentiation of TH17 cells requires IL-6 and transforming growth factor (TGF)-β, but whether basophils play a significant role in TH17 induction is unknown. Here we show a role for basophils in TH17 cell development by using in vitro T cell differentiation and in vivo TH17-mediated inflammation models. Bone marrow derived-basophils (BMBs) and splenic basophils produce significant amounts of IL-6 as well as IL-4 following stimulation with IgE crosslink or cholera toxin (CT). In addition, through IL-6 secretion, BMBs cooperate with dendritic cells to promote TH17 cell differentiation. In the TH17 lung inflammation model, basophils are recruited to the inflamed lungs following CT challenge, and TH17 responses are significantly reduced in the absence of basophils or IL-6. Furthermore, reconstitution with wild-type, but not IL-6-deficient, basophils restored CT-mediated lung inflammation. Lastly, basophil-deficient mice showed reduced phenotypes of TH17-dependent experimental autoimmune encephalomyelitis. Therefore, our results indicate that basophils are an important inducer of TH17 cell differentiation, which is dependent on IL-6 secretion. [ABSTRACT FROM AUTHOR]

Basophils are rare, circulating granulocytes proposed to be involved in T helper (T H ) type 2 immunity, mainly through secretion of interleukin (IL)-4. In addition to IL-4, basophils produce IL-6 and tumor necrosis factor (TNF)-α in response to immunoglobulin E (IgE) crosslinking. Differentiation of T H 17 cells requires IL-6 and transforming growth factor (TGF)-β, but whether basophils play a significant role in T H 17 induction is unknown. Here we show a role for basophils in T H 17 cell development by using in vitro T cell differentiation and in vivo T H 17-mediated inflammation models. Bone marrow derived-basophils (BMBs) and splenic basophils produce significant amounts of IL-6 as well as IL-4 following stimulation with IgE crosslink or cholera toxin (CT). In addition, through IL-6 secretion, BMBs cooperate with dendritic cells to promote T H 17 cell differentiation. In the T H 17 lung inflammation model, basophils are recruited to the inflamed lungs following CT challenge, and T H 17 responses are significantly reduced in the absence of basophils or IL-6. Furthermore, reconstitution with wild-type, but not IL-6-deficient, basophils restored CT-mediated lung inflammation. Lastly, basophil-deficient mice showed reduced phenotypes of T H 17-dependent experimental autoimmune encephalomyelitis. Therefore, our results indicate that basophils are an important inducer of T H 17 cell differentiation, which is dependent on IL-6 secretion., Competing Interests: The authors declare no competing financial interests.