Microglial Activation Modulates Neuroendocrine Secretion During Experimental Sepsis

Author(s)

da Costa, Luis Henrique Angenendt ^[1] ; Santos-Junior, Nilton Nascimento ^[1] ; Catalao, Carlos Henrique Rocha ^[1] ; Rocha, Maria Jose Alves ^{[1, 2, 3]}

Affiliation

^[1] Univ Sao Paulo, Ribeirao Preto Med Sch, Dept Neurosci & Behav Sci, BR-14049900 Ribeirao Preto - Brazil

^[2] Univ Sao Paulo, Sch Dent Ribeirao Preto, Dept Basic & Oral Biol, BR-14040904 Ribeirao Preto - Brazil

^[3] Univ Sao Paulo, Fac Odontol Ribeirao Preto, Dept Biol Basica & Oral, Ave Cafe S-N, BR-14040904 Ribeirao Preto, SP - Brazil

• Document type: Journal article
• Source: Molecular Neurobiology; v. 58, n. 5 JAN 2021.
• Web of Science Citations: 0

Abstract

Sepsis promotes an inflammatory state in the central nervous system (CNS) that may cause autonomic, cognitive, and endocrine changes. Microglia, a resident immune cell of the CNS, is activated in several brain regions during sepsis, suggesting its participation in the central alterations observed in this disease. In this study, we aimed to investigate the role of microglial activation in the neuroendocrine system functions during systemic inflammation. Wistar rats received an intracerebroventricular injection of the microglial activation inhibitor minocycline (100 mu g/animal), shortly before sepsis induction by cecal ligation and puncture. At 6 and 24 h after surgery, hormonal parameters, central and peripheral inflammation, and markers of apoptosis and synaptic function in the hypothalamus were analyzed. The administration of minocycline decreased the production of inflammatory mediators and the expression of cell death markers, especially in the late phase of sepsis (24 h). With respect to the endocrine parameters, microglial inhibition caused a decrease in oxytocin and an increase in corticosterone and vasopressin plasma levels in the early phase of sepsis (6 h), while in the late phase, we observed decreased oxytocin and increased ACTH and corticosterone levels compared to septic animals that did not receive minocycline. Prolactin levels were not affected by minocycline administration. The results indicate that microglial activation differentially modulates the secretion of several hormones and that this process is associated with inflammatory mediators produced both centrally and peripherally. (AU)

• FAPESP's process: 18/02854-0 - Glial activation analysis in the neuroimmunoendocrine alterations in septic rats and the simvastatin neuroprotector effect in survivals
• Grantee: Maria José Alves da Rocha
• Support Opportunities: Regular Research Grants
• FAPESP's process: 16/07803-0 - Effect of inhibition of microglial activation on neuroimmunoendocrine parameters during sepsis
• Grantee: Luís Henrique Angenendt da Costa
• Support Opportunities: Scholarships in Brazil - Doctorate