The central nervous system may infected by a wide range of microorganisms. However, immune response in the central nervous system is too limited and delayed, and penetration of antimicrobials from blood-brain barrier is also limited. The neuroinfections results attributable to the local deficiency in immune system as well as in complement system. The microorganisms can also leads to clinical syndromes such as progressive multifocal leukoencephalopathy (PML), chronic meningitis, herpes simplex encephalitis, West Nile virus neurologic infections, Creutzfeldt–Jakob disease, neurosarcoidosis, AIDS–related viral infections of the nervous system. There is a prompt medical attention required for the therapy of neuroinfectious disease. Most of the neural infections are life threatening. The molecular and cellular studies reveal the interactions between host response to pathogens, microglia crosstalk, and pathobiology of neuroinflammation.
Mast cells are multifunctional cells which play a central & vital role in classic IgE-associated allergic disorders and have a protective role in host defense against microorganisms such as parasites, bacteria, fungi and viruses in the context of both innate and adaptive immune responses. They are the major form of link between neurons and inflammation via neuropeptides which may induce human mast cell degranulation and chemokine production. The host response to pathogens differs among individuals which depends on the individual’s current immune status and efficiency of immune responses. Some non-neuronal cells release pro-inflammatory signals which induce glial cells.
Activation of P2 receptors by ATP stimulates the release of IL-33. As a result I1-6, IL-13 & monocyte chemoattractant protein 1 releases which in turns affect the microglial activity. Another study reveals that PAR-2 has been a novel therapeutic target for the treatment of brain disorders. It has been observed fatty acid amide named N-palmitoylethanolamine (PEA) has neuroprotective effects. It was also useful against amyloid β-peptide-induced learning and memory impairment in mice. In short enzymatic regulation of PEA represents a novel therapeutic approach to treat neuroinflammation.