Michelle Erickson, Ph.D.
Research Biologist, VA Puget Sound Healthcare System, Seattle, WA, USA
Research Assistant Professor, Department of Medicine- Division of Gerontology and Geriatric Medicine, University of Washington, Seattle, WA, USA
Background. The blood-brain barrier facilitates bidirectional communication between the CNS and periphery, and thus is an interface for neuroimmune interactions. The lungs are constantly exposed to the external environment through breathed air, which includes pathogenic microbes and environmental toxicants that can cause pulmonary inflammation. Emerging work in Taiwan, Mexico, The United States, and Europe suggests that exposure to air pollution, such as ozone, may increase risk for cognitive decline and Alzheimer’s disease. This presentation will cover aspects of lung-brain communication in which the blood-brain barrier may contribute to ozone-induced CNS dysfunction.
Method. Female Balb/c mice were exposed to ozone concentrations ranging from 1-3 parts per million for 4 hours, which promotes an inflammatory response in the lung that is comparable to humans exposed to ozone at environmentally relevant concentrations. Concentrations of cytokines, chemokines, and serum amyloid A were measured in blood, brain, lungs, and liver using bead-based multiplex assays, ELISAs, or immunoblots. Pulmonary inflammation in bronchoalveolar lavage was assessed by Hemacolor staining. Transport of 125-I-labeled serum amyloid A across the blood-brain barrier was measured using multiple-time regression analysis.
Result. Ozone exposure significantly increased serum amyloid A levels in lungs, blood, liver, and brain. However, ozone did not induce proinflammatory cytokine response in blood or brain. Serum amyloid A levels in blood significantly correlated with pulmonary inflammation. We found that ozone did not induce upregulation of serum amyloid A mRNA in brain, but that both hepatic acute phase isoforms of serum amyloid A could cross the intact blood-brain barrier.
Conclusion. Emerging data suggest that serum amyloid A could contribute to neurological conditions such as Alzheimer’s disease and depression. Our work suggests that serum amyloid A could be an important mediator of CNS dysfunction in response to ozone-induced pulmonary inflammation.
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