It has long been thought that astrocytes, like other glial cells, simply provide a support mechanism for neuronal function in the healthy and inflamed central nervous system (CNS). However, recent evidence suggests that astrocytes play an active and dual role in CNS inflammatory diseases such as multiple sclerosis (MS). Astrocytes not only have the ability to enhance immune responses and inhibit myelin repair, but they can also be protective and limit CNS inflammation while supporting oligodendrocyte and axonal regeneration. The particular impact of these cells on the pathogenesis and repair of an inflammatory demyelinating process is dependent upon a number of factors, including the stage of the disease, the type and microenvironment of the lesion, and the interactions with other cell types and factors that influence their activation. In this review, we summarize recent data supporting the idea that astrocytes play a complex role in the regulation of CNS autoimmunity. Keywordsanimal models; astrocyte; chemokines; cytokines; demyelination; multiple sclerosis; neuroinflammation; remyelination Initiated by the breakdown of the blood-brain barrier (BBB), multiple sclerosis (MS) has classically been considered a T cell-mediated autoimmune disorder of the central nervous system (CNS), characterized by inflammatory cell infiltration and myelin destruction [1]. Focal demyelinated lesions in the white matter are the traditional hallmarks of MS. However recent evidence suggests more widespread damage to the brain and spinal cord, particularly during the progressive phase of disease. Such global injury includes axonal damage, diffuse damage to areas of white matter distant from inflammatory lesions, and demyelination of deep and cortical gray matter [2]. Clinical deficits in MS range from relapsing-remitting to chronic-progressive patterns of expression. Spontaneous remyelination occurs early in relapsing-remitting disease, which restores neurophysiological function in animal models of MS, and likely represents a remission period in human MS [3]. However, recurrent inflammatory attacks and the failure of myelin repair during later progressive phases of disease ultimately lead to permanent debilitation [3]. It is well understood that oligodendrocyte progenitor cells (OPCs) are responsible for remyelinating lesions in the CNS [4], and thus the failure of myelin repair has been attributed to deficiencies in the generation of mature oligodendrocytes or their ability to myelinate, and/or to neurodegeneration and axons that are unreceptive to myelination [5].

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Smoke-free legislation was associated with significant early improvements in symptoms, spirometry measurements, and systemic inflammation of bar workers. Asthmatic bar workers also had reduced airway inflammation and improved quality of life.

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