Impaired adult hippocampal neurogenesis is a prominent feature of neurodegenerative disorders. The extent of neural stem cell (NSCs) generation in adult brain is highly adaptive and depends on both inflammatory signalling and glial cells. In this study, through immunohistochemical co-labelling of nestin and glial fibrillary acidic protein (GFAP), the authors have demonstrated an enhanced stem astrocyte density in subgranular zone of adult and ageing rats following neonatal lipopolysaccharide (LPS) exposure, which could be attributed as a regenerative attempt evoked to overcome the effects of bacterial infection. However, a second hit of LPS at 12 months of age might have killed the progenitors because of the persistent glial activation leading to a decline in stem astrocyte population. The enhanced density of NSCs is attributed to the activation of the toll-like receptor-4 (TLR-4) by LPS on their surface that in turn influences their proliferative potential. The information generated may be useful for therapeutically modulating the pathway in a way so that the TLR-4 activation following bacterial infection may be checked at a level when it triggers the activation of the innate immune response. Thus, the enhanced number of NSCs can generate a viable number of neurons that will mature and integrate in the hippocampal circuitry to compensate the loss due to bacterial infection.
