Person:
González Bris, Álvaro

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First Name
Álvaro
Last Name
González Bris
URI
https://hdl.handle.net/20.500.14352/86236
Affiliation
Universidad Complutense de Madrid
Faculty / Institute
Medicina
Department
Farmacología y Toxicología
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2015 - 201912020 - 20211
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Author: Leza Cerro, Juan Carlos ×

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    Periodontal diseases and depression: A pre‐clinical in vivo study
    (Journal of Clinical Periodontology, 2021) Martínez, María; Martín‐Hernández, David; Virto Ruiz, Leire; Mac-Dowell Mata, Karina Soledad; Leza Cerro, Juan Carlos; García Bueno, Borja; Figuero Ruiz, Elena; Ambrosio Elejalde, Nagore; Herrera González, David; Montero Solís, Eduardo; González Bris, Álvaro; Marín Cuenda, María José; Sanz Martín, Mariano
    Aim: To analyse, through a pre-clinical in vivo model, the possible mechanisms linking depression and periodontitis at behavioural, microbiological and molecular levels. Materials and methods: Periodontitis (P) was induced in Wistar:Han rats (oral gavages with Porphyromonas gingivalis and Fusobacterium nucleatum) during 12 weeks, followed by a 3-week period of Chronic Mild Stress (CMS) induction. Four groups (n = 12 rats/group) were obtained: periodontitis and CMS (P+CMS+); periodontitis without CMS; CMS without periodontitis; and control. Periodontal clinical variables, alveolar bone levels (ABL), depressive-like behaviour, microbial counts and expression of inflammatory mediators in plasma and brain frontal cortex (FC), were measured. ANOVA tests were applied. Results: The highest values for ABL occurred in the P+CMS+ group, which also presented the highest expression of pro-inflammatory mediators (TNF-α, IL-1β and NF-kB) in frontal cortex, related to the lipoprotein APOA1-mediated transport of bacterial lipopolysaccharide to the brain and the detection of F. nucleatum in the brain parenchyma. A dysregulation of the hypothalamic-pituitary-adrenal stress axis, reflected by the increase in plasma corticosterone and glucocorticoid receptor levels in FC, was also found in this group. Conclusions: Neuroinflammation induced by F. nucleatum (through a leaky mouth) might act as the linking mechanism between periodontal diseases and depression.
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    Bacterial translocation affects intracellular neuroinflammatory pathways in a depression-like model in rats
    (Neuropharmacology, 2015) Martín Hernández, David; Caso Fernández, Javier Rubén; González Bris, Álvaro; Maus, Sandra R.; Muñoz Madrigal, José Luis; García Bueno, Borja; Mac-Dowell Mata, Karina Soledad; Alou Cervera, Luis; Gómez-Lus Centelles, María Luisa; Leza Cerro, Juan Carlos
    Recent studies have suggested that depression is accompanied by an increased intestinal permeability which would be related to the inflammatory pathophysiology of the disease. This study aimed to evaluate whether experimental depression presents with bacterial translocation that in turn can lead to the TLR-4 in the brain affecting the mitogen-activated protein kinases (MAPK) and antioxidant pathways. Male Wistar rats were exposed to chronic mild stress (CMS) and the intestinal integrity, presence of bacteria in tissues and plasma lipopolysaccharide levels were analyzed. We also studied the expression in the prefrontal cortex of activated forms of MAPK and some of their activation controllers and the effects of CMS on the antioxidant Nrf2 pathway. Our results indicate that after exposure to a CMS protocol there is increased intestinal permeability and bacterial translocation. CMS also increases the expression of the activated form of the MAPK p38 while decreasing the expression of the antioxidant transcription factor Nrf2. The actions of antibiotic administration to prevent bacterial translocation on elements of the MAPK and Nrf2 pathways indicate that the translocated bacteria are playing a role in these effects. In effect, our results propose a role of the translocated bacteria in the pathophysiology of depression through the p38 MAPK pathway which could aggravate the neuroinflammation and the oxidative/nitrosative damage present in this pathology. Moreover, our results reveal that the antioxidant factor Nrf2 and its activators may be involved in the consequences of the CMS on the brain