BACKGROUND: Inflammation affects the brain after stroke with main functions to rapidly eliminate the source of the disturbance, remove damaged tissue and then restore tissue homeostasis. High sensitive C-reactive protein (hsCRP) is a sensitive marker of inflammation and tissue injury in the arterial wall, while fractalkine is a distinct chemokine that promotes inflammatory signaling after neuronal death on ischemic stroke. We aim to investigate the association of fractalkine with hsCRP as a marker of inflammation in ischemic stroke patients.METHODS: This study was designed as a cross-sectional study. Soon after patients with ischemic stroke admitted to hospital, plasma fractalkine and hsCRP concentrations were assesed. Subjects had to be at least 30 years old and maximum 30 days of stroke onset. High inflammation was defined as hsCRP value >3 mg/L.RESULTS: High fractalkine levels were found on 24 ischemic stroke patients (49%) and mean of fractalkine 0.719 ng/mL on patients with stroke onset <7 days was higher than patients with stroke onset 7-30 days. Low fractalkine levels (<0.527 ng/mL) were found on ischemic stroke patients with onset 7-30 days accompanied by high inflammation (hsCRP >3 mg/L), but no significant correlation between fractalkine and hsCRP (p=0.613).CONCLUSION: High inflammation and low plasma fractalkine profile was found after 7 days of onset in ischemic stroke patients. No significant correlation between fractalkine and hsCRP in ischemic stroke patients.KEYWORDS: CRP, fractalkine, inflammation, ischemic stroke

<p>The brain ischemia due to vascular occlusion, especially in the main cerebral artery, could trigger the microglia as a natural immune cell in the brain. These activated microglia will turn up the inflammation cascade in the ischemic area. Interleukin-4 (IL-4) has a vital role in the microglial alteration to become an anti-inflammatory phenotype, which wind up the expression of MHC II and CD11c. Moreover, previous studies has supported that the stimulation of IL-4 in the culture of microglia/macrophage will produce this kind of “alternative” phenotype or neuroprotective phenotype, through the fall of TNF and rise of IGF-1. However, only a few have discussed the role and profile of IL-4 in ischemic stroke. This review article will cover the possibility of IL-4 role as an anti-inflammatory predictor in ischemic stroke.</p><p><strong>Keywords: Interleukin-4, microglia, ischemic stroke, inflammation</strong></p>

BACKGROUND: Central obesity is associated with various chronic metabolic disorders characterized by abnormal cytokine production, increased acute phase reactants, and activation of inflammatory signaling pathways. This study was aimed to investigate the association of waist circumference, chemerin, and retinol binding protein (RBP)-4 with inflammation in men with central obesity.METHODS: The research was conducted with a crosssectional design involving 68 centrally obese male subjects aged 30 to 60 years old, with waist circumference (WC) >90 cm. All subjects fulfilled the inclusion and exclusion criteria. Anthropometric parameters, fasting glucose, creatinine, SGOT, SGPT and hsCRP were measured. Serum concentrations of chemerin and RBP4 were measured by ELISA.RESULTS: The trend lines showed that chemerin, RBP4, and hsCRP increased with WC. Pearson correlation test showed a positively significant correlation between WC and hsCRP (r=0.242, p<0.05); and also between chemerin and hsCRP (r=0.244, p<0.05) and RBP4 (r=0.321, p<0.01). Subjects were stratified into four groups based on their chemerin and RBP4 levels (high chemerin/high RBP4, high chemerin/low RBP4, low chemerin/high RBP4, or low chemerin/low RBP4). Subjects who were in the high chemerin/low RBP4 group were more likely to have high level of inflammation (47.6%), but subjects with high chemerin/high RBP4 showed low level of inflammation (42.9%) as compared with the other three groups.CONCLUSIONS: We concluded that increased WC was correlated with elevated levels of chemerin, RBP4, and hsCRP. High chemerin was correlated with increased level of RBP4 as well as with high level of inflammation.KEYWORDS: waist circumference, chemerin, RBP4, hsCRP, inflammation

Background: About 85% of strokes are ischemic strokes, caused by occlusion of cerebral artery that induced brain inflammation. A deep understanding of ischemic stroke mechanism will lead to better neurorestorative treatment. Objective: This study investigates the dynamics of human mesenchymal stem cells, fractalkine, and M1 microglia/macrophage in ischemic stroke patients. Results:We found the same fractalkine levels and M1 microglia/ macrophage cells on patients with stroke onset 0 to 14 days, then decrease until 30 days of stroke onset. MSCs was increase 7 days after stroke onset, peaked by 14 days, then decreased until 30 days after stroke ischemic onset. Conclusions: This study found an interaction between microglia/ macrophage, fractalkine, and MSCs on ischemic stroke patients, so therapeutic strategy could be developed.