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Tumor necrosis factor alpha (TNF-α) a cytokine has been shown to be the
key player during the pathogenesis of several autoimmune inflammatory disorders (presumably sterile inflammation) including
rheumatoid arthritis (RA). Several studies have shown that TNF-α is mainly involved in the proinflammatory responses. However recent studies have reported multifunctional role of
TNF-α during the development of RA.
Therefore, in this article we have highlighted the distinct functions of TNF-α during pathogenesis of RA.
Reactive astrogliosis has been implicated in the failure of axonal regeneration in adult mammalian Central Nervous System (CNS).
It is our hypothesis that inflammatory cytokines act upon astrocytes to alter
their biochemical and physical properties, which may in turn be responsible for
the failure of neuronal regeneration. We have therefore examined the effect
of tumor-necrosis factor-alpha (TNF-α) on the ability of astrocytes to support the
survival of the cortical neurons and the growth of the neurites. Mouse astrocytes
and cortical neuronal cultures were prepared. It was observed that when neurons
were cultured in absence of astrocytes only a few of them grew and survived
only for 5-6 days. These neurons had small cell bodies and few, short
neurites. However, when the same numbers of neurons were cultured on the top of
astrocytes, more neurons grew and survived up to 16-18 days. They had
bigger cell bodies and many long branched neurites that formed anestamosing networks. The neurons then coalesced and the neurites formed thick bundles. When
the same numbers of neurons were grown on the top of astrocytes pre-treated
few neurons survived up to 13 days. The neurites of the survived neurons were
shorter than neurites of neurons grown on normal astrocytes and did not form
bundles. In addition, TNF-α stimulated the expression of glial fibrillary acidic protein (GFAP) by
astrocytes. These results support that the pro-inflammatory cytokine, TNF-α modulates the gliosis and that the
astrocytic cell supports neuronal survival and neurite outgrowth.