Rat anti Mouse IL4 monoclonal antibody, clone 41451S

Understanding the mechanisms of glial scar formation by reactive astrocytes is crucial for elaborating a therapeutic strategy to brain and spinal cord injury. However, the extrinsic mechanisms that drive the polarization of reactive astrocytes, the first step in glial scar formation, remain poorly understood. Here, using an in vitro chemotaxis assay as an experimental model for polarization, we observed that Il4-M2 macrophages are stronger inducers of reactive astrocytes' polarization, compared to naive or M1 macrophages. Then, we showed that both beta 1-integrin and Wnt/beta-catenin pathways in astrocytes are required for this polarization in vitro and in vivo after spinal cord crush injury in mice. These findings provide molecular targets for manipulating the polarization of reactive astrocytes in order to potentially enhance the healing of SCI lesions.

Background: The aim of this article was to evaluate the cognitive status of remitted patients with bipolar disorder (BD) using Mini-Mental State Examination (MMSE), Frontal Assessment Battery, and Brief Assessment of Cognition in Affective Disorders (BAC-A). The BAC-A is a comprehensive test battery addressing the cognitive domains compromised in BD. We also aimed to analyze potential clinical and immune predictors of cognitive performance in BD. Methods: Remitted patients with BD (M +/- S.E: 43.80 +/- 10.87 years) and age-matched controls (M +/- S.E: 43.52 +/- 11.72) were administered clinical questionnaires and cognitive tests. Inflammatory plasma levels (IL-2, IL-4, IL-6, IL-10, IFN-gamma, TNF alpha, IL-17A, sTNFR1, and sTNFR2) were measured using an enzyme-linked immunosorbent assay. We generated a global cognitive performance index based on BAC-A scores. Multivariate analyses compared cognitive and immune measures across groups. A regression analysis was performed to examine the relationship between global cognitive performance, clinical and immune parameters in BD. Results: Remitted patients with BD performed poorly on tasks of affective processing, verbal memory, working verbal memory, and executive functioning. Patients with BD presented higher plasma levels sTNFR1, TNF alpha, IFN, IL2, IL4, IL6, IL10, and IL17compared with controls. Education and MMSE were found to be positively correlated with global cognitive performance. IL6 plasma levels were negatively correlated with global cognitive performance. Conclusion: The major determinants of poor cognitive performance in BD were education and IL6 plasma levels.