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Microglial priming through the lung-brain axis: the role of air pollution-induced circulating factors.

ABSTRACT: Air pollution is implicated in neurodegenerative disease risk and progression and in microglial activation, but the mechanisms are unknown. In this study, microglia remained activated 24 h after ozone (O3) exposure in rats, suggesting a persistent signal from lung to brain. Ex vivo analysis of serum from O3-treated rats revealed an augmented microglial proinflammatory response and ?-amyloid 42 (A?42) neurotoxicity independent of traditional circulating cytokines, where macrophage-1 antigen-mediated microglia proinflammatory priming. Aged mice exhibited reduced pulmonary immune profiles and the most pronounced neuroinflammation and microglial activation in response to mixed vehicle emissions. Consistent with this premise, cluster of differentiation 36 (CD36)(-/-) mice exhibited impaired pulmonary immune responses concurrent with augmented neuroinflammation and microglial activation in response to O3 Further, aging glia were more sensitive to the proinflammatory effects of O3 serum. Together, these findings outline the lung-brain axis, where air pollutant exposures result in circulating, cytokine-independent signals present in serum that elevate the brain proinflammatory milieu, which is linked to the pulmonary response and is further augmented with age.-Mumaw, C. L., Levesque, S., McGraw, C., Robertson, S., Lucas, S., Stafflinger, J. E., Campen, M. J., Hall, P., Norenberg, J. P., Anderson, T., Lund, A. K., McDonald, J. D., Ottens, A. K., Block, M. L. Microglial priming through the lung-brain axis: the role of air pollution-induced circulating factors.

SUBMITTER: Mumaw CL

PROVIDER: S-EPMC4836369 | biostudies-literature | 2016 May

REPOSITORIES: biostudies-literature

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Microglial priming through the lung-brain axis: the role of air pollution-induced circulating factors.

Mumaw Christen L CL Levesque Shannon S McGraw Constance C Robertson Sarah S Lucas Selita S Stafflinger Jillian E JE Campen Matthew J MJ Hall Pamela P Norenberg Jeffrey P JP Anderson Tamara T Lund Amie K AK McDonald Jacob D JD Ottens Andrew K AK Block Michelle L ML

FASEB journal : official publication of the Federation of American Societies for Experimental Biology 20160210 5

Air pollution is implicated in neurodegenerative disease risk and progression and in microglial activation, but the mechanisms are unknown. In this study, microglia remained activated 24 h after ozone (O3) exposure in rats, suggesting a persistent signal from lung to brain. Ex vivo analysis of serum from O3-treated rats revealed an augmented microglial proinflammatory response and β-amyloid 42 (Aβ42) neurotoxicity independent of traditional circulating cytokines, where macrophage-1 antigen-media ...[more]

PMID: 26864854

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Project description:ObjectiveLung cancer is a leading cause of cancer death in the United States. Exposure to outdoor air pollution (OAP) is associated with increased lung cancer incidence, however little is known about the association of OAP and survival after diagnosis.MethodsWe investigated the effects of OAP and lung cancer survival in Pennsylvania using data from Pennsylvania Cancer Registry. The study population consisted of 252,123 patients diagnosed between 1990 and 2017. The Environmental Protection Agency's ambient air monitoring network provided information on OAP exposure of NO2, O3, PM2.5, and PM10. Mean OAP exposures were calculated by interpolating exposure concentrations from the five nearest monitors within a 50-kilometer radius of each patient's residential address from date of diagnosis to date of death or last contact. Cox proportional-hazards models were used to estimate the hazard ratios (HR) for OAP exposures for overall and lung cancer-specific survival. Statistical analyses were stratified by SEER cancer stage groupings (localized, regional, and distant) and adjusted for individual-level and area-level covariates.ResultsMedian survival time was 0.76 [CIs: 0.75, 0.77] years for the study population and for localized, regional, and distant site diagnosis were 2.2 [CIs: 2.17, 2.23], 1.13 [CIs: 1.12, 1.15], and 0.42 [CIs: 0.41, 0.43] years, respectively. NO2 indicated the greatest HR which increased with increasing magnitude of exposure across all cancer staging groups for deaths before 2-years post-diagnosis. HRs varied by stage and magnitude of OAP exposure with greatest overall effects shown in NO2 followed by PM2.5, O3, and PM10. A subgroup analysis of patients with treatment status information (2010-2017) showed similar associations of increasing HRs with increasing exposure.ConclusionThese findings supported the hypotheses that OAP can influence the carcinogenic process, impairing chemotherapy treatment, and provide important public health implications since environmental factors are not often considered in prognosis of survival after diagnosis.

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Microglial priming through the lung-brain axis: the role of air pollution-induced circulating factors.

Publications

Microglial priming through the lung-brain axis: the role of air pollution-induced circulating factors.

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