The Response of Neuroimmune System During Inflammation
Journal of Pharmacology and Therapeutic Research is an open access, peer reviewed journal that focuses on the interdisciplinary research offering therapeutic solutions to various neurological, genetics, psychological, and respiratory issues affecting the human beings.
Glial cells Microglia are recognized as the innate immune cells of the central nervous system. Microglia actively survey their environment through, and change their cell morphology significantly in response to neural injury. Acute inflammation in the brain is typically characterized by rapid activation of microglia. During this period, there is no peripheral immune response. Over time, however, chronic inflammation causes the degradation of tissue and of the blood–brain barrier. During this time, microglia generate reactive oxygen species and release signals to recruit peripheral immune cells for an inflammatory response.
Astrocytes are glial cells that are the most abundant cells in the brain. They are involved in maintenance and support of neurons and compose a significant component of the blood–brain barrier. After insult to the brain, such as traumatic brain injury, astrocytes may become activated in response to signals released by injured neurons or activated microglia. Once activated, astrocytes may release various growth factors and undergo morphological changes. For example, after injury astrocytes form the glial scar composed of a proteoglycan matrix that hinders axonal regeneration.
Cytokines are a class of proteins that regulates inflammation, cell signaling, and various cell processes such as growth and survival. Chemokines are a subset of cytokines that regulate cell migration, such as attracting immune cells to a site of infection or injury various cell types in the brain may produce cytokines and chemokines such as microglia, astrocytes, endothelial cells, and other glial cells. Physiologically, chemokines and cytokines function as neuromodulators that regulate inflammation and development. In the healthy brain, cells secrete cytokines to produce a local inflammatory environment to recruit microglia and clear the infection or injury. However, in neuroinflammation, cells may have sustained release of cytokines and chemokines which may compromise the blood–brain barrier. Peripheral immune cells are called to the site of injury via these cytokines and may now migrate across the compromised blood brain barrier into the brain. Common cytokines produced in response to brain injury include: interleukin-6 (IL-6), which is produced during astrogliosis, and interleukin-1 beta (IL-1β) and tumor necrosis factor alpha (TNF-α), which can induce neuronal cytotoxicity. Although the pro-inflammatory cytokines may cause cell death and secondary tissue damage, they are necessary to repair the damaged tissue. For example, TNF-α causes neurotoxicity at early stages of neuroinflammation, but contributes to tissue growth at later stages of inflammation.
Journal of Pharmacology and Therapeutic Research