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Objectives: Patients with chronic obstructive pulmonary disease (COPD) constitute a potentially susceptible group towards environmental exposures such as livestock farm emissions, given their compromised respiratory health status. The primary aim of this study was to examine the association between livestock exposure and comorbidities and coexisting symptoms and infections in COPD patients., Methods: Data were collected from 1828 COPD patients (without co-occurring asthma) registered in 23 general practices and living in a rural area with a high livestock density. Prevalence of comorbid diseases/disorders and coexisting symptoms/infections were based on electronic health records from the year 2012. Various indicators of individual exposure to livestock were estimated based on residential addresses, using a geographic information system., Results: At least one comorbid disorder was present in 69% of the COPD patients (especially cardiac disorders and depression, while 49% had at least one coexisting symptom and/or infection (especially upper respiratory tract infections, respiratory symptoms and pneumonia). Half of the COPD-patients resided less than 500m of the nearest farm. Some positive as well as inverse associations were found between the examined outcomes and exposure estimates, although not consistent., Conclusions: Despite the high prevalence of coexisting chronic and acute conditions presented in primary care by in COPD patients, this investigation found no convincing evidence for an association with livestock exposure estimates. There is a need for a replication of the present findings in studies with a longitudinal design, on different groups of potentially susceptible patients. Future research should also elucidate the biological plausibility of possible protective effects of exposure., (Copyright © 2017 Elsevier GmbH. All rights reserved.)

Although the primary cause of multiple sclerosis (MS) is unknown, the widely accepted view is that aberrant (auto)immune responses possibly arising following infection(s) are responsible for the destructive inflammatory demyelination and neurodegeneration in the central nervous system (CNS). This notion, and the limited access of human brain tissue early in the course of MS, has led to the development of autoimmune, viral and toxin-induced demyelination animal models as well as the development of human CNS cell and organotypic brain slice cultures in an attempt to understand events in MS. The autoimmune models, collectively known as experimental autoimmune encephalomyelitis (EAE), and viral models have shaped ideas of how environmental factors may trigger inflammation, demyelination and neurodegeneration in the CNS. Understandably, these models have also heavily influenced the development of therapies targeting the inflammatory aspect of MS. Demyelination and remyelination in the absence of overt inflammation are better studied in toxin-induced demyelination models using cuprizone and lysolecithin. The paradigm shift of MS as an autoimmune disease of myelin to a neurodegenerative disease has required more appropriate models reflecting the axonal and neuronal damage. Thus, secondary progressive EAE and spastic models have been crucial to develop neuroprotective approaches. In this review the current in vivo and in vitro experimental models to examine pathological mechanisms involved in inflammation, demyelination and neuronal degeneration, as well as remyelination and repair in MS are discussed. Since this knowledge is the basis for the development of new therapeutic approaches for MS, we particularly address whether the currently available models truly reflect the human disease, and discuss perspectives to further optimise and develop more suitable experimental models to study MS., (Copyright © 2011 Elsevier B.V. All rights reserved.)