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LULLING IMMUNITY, PAIN, AND STRESS TO SLEEP WITH CORTISTATIN
Autor
Afiliación
Spanish National Research Council (CSIC). Institute of Parasitology and Biomedicine Lopez-Neyra. Granada, Spain.
Spanish National Research Council (CSIC). Institute of Parasitology and Biomedicine Lopez-Neyra. Granada, Spain.
Spanish National Research Council (CSIC). Institute of Parasitology and Biomedicine Lopez-Neyra. Granada, Spain.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Rio de Janeiro, RJ, Brasil
Spanish National Research Council (CSIC). Institute of Parasitology and Biomedicine Lopez-Neyra. Granada, Spain.
Spanish National Research Council (CSIC). Institute of Parasitology and Biomedicine Lopez-Neyra. Granada, Spain.
Spanish National Research Council (CSIC). Institute of Parasitology and Biomedicine Lopez-Neyra. Granada, Spain.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Rio de Janeiro, RJ, Brasil
Spanish National Research Council (CSIC). Institute of Parasitology and Biomedicine Lopez-Neyra. Granada, Spain.
Resumen en ingles
Cortistatin is a neuropeptide isolated from cortical brain regions, showing high structural homology and sharing
many functions with somatostatin. However, cortistatin exerts unique functions in the central nervous and immune
systems, including decreasing locomotor activity, inducing sleep-promoting effects, and deactivating inflammatory
and T helper (TH)1/TH17–driven responses in preclinical models of sepsis, arthritis, multiple sclerosis, and colitis.
Besides its release by cortical and hippocampal interneurons, cortistatin is produced by macrophages, lymphocytes,
and peripheral nociceptive neurons in response to inflammatory stimuli, supporting a physiological role of cortistatin
in the immune and nociceptive systems. Cortistatin-deficient mice have been shown to have exacerbated nociceptive
responses to neuropathic and inflammatory pain sensitization. However, a paradoxical effect has been observed in
studies of immune disorders, in which, despite showing competent inflammatory/autoreactive responses, cortistatindeficient
mice were partially resistant to systemic autoimmunity and inflammation. This unexpected phenotype was
associated with elevated circulating glucocorticoids and anxiety-like behavior. These findings support cortistatin as a
novel multimodal therapeutic approach to treat autoimmunity and clinical pain and identify it as a key endogenous
component of the neuroimmune system related to stress responses.
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