Atypical microglial response to biodiesel exhaust in healthy and hypertensive rats |
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| Affiliation: | 1. Department of Anatomy and Cell Biology, The Stark Neuroscience Research Institute, Indiana University School of Medicine, Indianapolis, IN 46202, USA;2. Department of Biochemistry & Molecular Biology, Virginia Commonwealth University Medical Campus, Richmond, VA 23298, USA;3. Department of Anatomy and Neurobiology, Virginia Commonwealth University Medical Campus, Richmond, VA 23298, USA;4. Environmental Public Health Division, National Health and Environmental Effects Research Laboratory, ORD, U.S. Environmental Protection Agency, Research Triangle Park, NC, 27711, USA;5. Toxicity Assessment Division, National Health and Environmental Effects Research Laboratory, ORD, U.S. Environmental Protection Agency, Research Triangle Park, NC 27711, USA;6. Integrated Systems Toxicology Division, National Health and Environmental Effects Research Laboratory, ORD, U.S. Environmental Protection Agency, Research Triangle Park, NC, 27711, USA;1. Hadassah – Hebrew University Medical Center, Jerusalem, Israel;2. Aspect Imaging, Shoham, Israel;3. Envigo CRS (Israel), Ness Ziona, Israel;4. KadimaStem, Ness Ziona, Israel;5. Sackler School of Medicine, Tel Aviv University, Tel Aviv, and Consultant in Toxicologic Pathology, Timrat, Israel;1. Department of Pediatrics, University of Arkansas for Medical Sciences, College of Medicine, Arkansas Children’s Hospital Research Institute, 13 Children’s Way, Little Rock, AR 72202, USA;2. Department of Pharmacology and Toxicology, University of Arkansas for Medical Sciences, College of Medicine, 4301 West Markham St., Little Rock, AR 72205, USA;3. Department of Research and Development, Central Arkansas Veterans Healthcare System, Little Rock, AR 72205, USA;1. Department of Pharmacobiology, Center for Research and Advanced Studies (CINVESTAV), Mexico City, Mexico;2. Unit for Medical Research in Neurological Diseases, Specialties Hospital, National Medical Center SXXI (CMN-SXXI), Mexico City, Mexico;3. Medicinal Chemistry, Department of Biological Sciences, Faculty of Exact Sciences, National University of La Plata, Buenos Aires, Argentina;4. Department of Neuroscience Research, National Institute of Psychiatry Ramon de la Fuente Muñiz, Mexico City, Mexico;1. Department of Orthopedic Surgery, The 2nd Affiliated Hospital of Harbin Medical University, Harbin, PR China;2. School of Basic Medical Sciences, Hubei University of Chinese Medicine, Wuhan, PR China;3. Department of Neurology, Indiana University School of Medicine, Indianapolis, IN, USA;4. Department of Rehabilitation Medicine, The First Affiliated Hospital of Nanjing Medical University, No. 300 Guangzhou Road, Nanjing, Jiangsu 210029, PR China;1. Department of Medical Laboratory, Xuanwu Hospital, Beijing Children’s Hospital, Capital Medical University, PR China;2. Department of Medical Laboratory, Beijing Children’s Hospital, Capital Medical University, PR China;3. Institute of Applied Cancer Research, MD Anderson Cancer Center, USA;4. Department of Medical Laboratory, Xuanwu Hospital, Capital Medical University, Beijing 100053, PR China |
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| Abstract: | Accumulating evidence suggests a deleterious role for urban air pollution in central nervous system (CNS) diseases and neurodevelopmental disorders. Microglia, the resident innate immune cells and sentinels in the brain, are a common source of neuroinflammation and are implicated in air pollution-induced CNS effects. While renewable energy, such as soy-based biofuel, is of increasing public interest, there is little information on how soy biofuel may affect the brain, especially in people with preexisting disease conditions. To address this, male spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto (WKY) rats were exposed to 100% Soy-based Biodiesel Exhaust (100SBDE; 0, 50, 150 and 500 μg/m3) by inhalation, 4 h/day for 4 weeks (5 days/week). Ionized calcium-binding adapter molecule-1 (IBA-1) staining of microglia in the substantia nigra revealed significant changes in morphology with 100SBDE exposure in rats from both genotypes, where SHR were less sensitive. Aconitase activity was inhibited in the frontal cortex and cerebellum of WKY rats exposed to 100SBDE. No consistent changes occurred in pro-inflammatory cytokine expression, nitrated protein, or arginase1 expression in brain regions from either rat strain exposed to 100SBDE. However, while IBA-1 mRNA expression was not modified, CX3CR1 mRNA expression was lower in the striatum of 100SBDE exposed rats regardless of genotype, suggesting a downregulation of the fractalkine receptor on microglia in this brain region. Together, these data indicate that while microglia are detecting and responding to 100SBDE exposure with changes in morphology, there is reduced expression of CX3CR1 regardless of genetic background and the activation response is atypical without traditional inflammatory markers of M1 or M2 activation in the brain. |
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| Keywords: | Biodiesel Air pollution Brain Microglia Atypical activation Neurotoxicity |
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