Development of Anxiolytic and Depression-like Behavior in Mice Infected with Mycobacterium lepraemurium

Ponce-Regalado, None; Salazar-Juárez, Alberto; Oscar, Rojas-Espinosa; de, Arturo Contis-Montes; Hurtado‐Alvarado, Gabriela; Arce‐Paredes, Patricia; Pérez‐Sánchez, Gilberto; Pavón, Lenin; Girón-Pérez, Manuel Iván; Hernández-Pando, Rogelio; Álvarez-Sánchez, María Elizbeth; Becerril-Villanueva, Enrique

doi:10.1016/j.neuroscience.2022.03.021

Cited by 1 publication

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“…Systemic inflammation produces neuroinflammation and neuronal damage caused by oxidative stress and activating microglia that impair cognitive function, including learning and memory, and can contribute to neurobehavioral changes, including the development of neuropsychiatric disorders [39][40][41]. In the absence of brain bacteria, we have shown that Mtb lung infection caused neuroinflammation and behavioral impairments [25], and similar results have been described in Mycobacterium lepraemurium [42,43]. The results of this work showed that low doses of DEX IT and IN in combination with AB reduced sickness behavior, reduced anxiety-like behavior, decreased depression-like behavior, improved neurological outcomes, and enhanced short-and long-term memory in TB mice.…”

Section: Discussionsupporting

confidence: 80%

Effect of Low Doses of Dexamethasone on Experimental Pulmonary Tuberculosis

et al. 2023

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Tuberculosis (TB) is the deadliest disease caused by a bacterial agent. Glucocorticoids (GCs) have a typical anti-inflammatory effect, but recently it has been shown that they can present proinflammatory activity, mainly by increasing molecules from innate immunity. In the current study, we evaluated the effect of low doses of dexamethasone on Mycobacterium tuberculosis in vivo and in vitro. We used an established mice model of progressing tuberculosis (TB) in the in vivo studies. Intratracheal or intranasal dexamethasone therapy administered with conventional antibiotics in the late stage of the disease decreased the lung bacilli load and lung pneumonia, and increased the survival of the animals. Finally, the treatment decreased the inflammatory response in the SNC and, therefore, sickness behavior and neurological abnormalities in the infected animals. In the in vitro experiments, we used a cell line of murine alveolar macrophages infected with Mtb. Low-dose dexamethasone treatment increased the clearance capacity of Mtb by MHS macrophages, MIP-1α, and TLR2 expression, decreased proinflammatory and anti-inflammatory cytokines, and induced apoptosis, a molecular process that contributes to the control of the mycobacteria. In conclusion, the administration of low doses of dexamethasone represents a promising adjuvant treatment for pulmonary TB.

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