Abstract

Bacterial infection of the central nervous system (CNS) is a severe and life-threatening condition with high mortality, and it may lead to permanent neurological deficits in survivors. Increasing evidence indicates that astrocytes, as the most abundant CNS glial cell population, regulate innate and adaptive immune responses in the CNS under pathological conditions in addition to their role in the maintenance of CNS homeostasis and neuronal function. Following antigen recognition, astrocytes participate in the initiation of innate immune responses, and prompt an adaptive immune response to recruit peripheral immune cells. Investigations have been conducted to understand the immunological role of astrocytes in CNS disease and injury, however, their part in bacterial infections of the CNS has not been fully evaluated. A better understanding will permit the identification of successful therapeutic targets for an improved prognosis and disease outcome.

Highlights

  • Invasion of the central nervous system (CNS) by infectious agents is a major global healthcare concern, and is associated with high morbidity and mortality (John et al, 2015; Robertson et al, 2018)

  • The use of gp130 to block IL6 can reduce astrocytosis in glial fibrillary acidic protein (GFAP)-IL6/sgp130 mice (Campbell et al, 2014). These findings suggest that chronic expression of IL-6 by astrocytes has a critical role in neuropathological effects during CNS immune responses

  • Astrocytes play a progressive role in maintaining CNS homeostasis, in both physiological and pathological conditions, such as bacterial infection

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Summary

Introduction

Invasion of the CNS by infectious agents is a major global healthcare concern, and is associated with high morbidity and mortality (John et al, 2015; Robertson et al, 2018). GRAPHICAL ABSTRACT | Astrocyte plays an important role in the CNS innate and adaptive immune responses to bacterial pathogens. Ancillary to facilitating innate immune responses, reactive astrocytes express MHC class II and costimulatory molecules, such as CD80 (B7-1) and CD86 (B72), that may contribute to T cell activation and integrate communication between resident CNS cells and hematopoietic cells, driving an adaptive immune response (Carpentier et al, 2005).

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