ABSTRACT
La enfermedad periodontal requiere de un hospedero susceptible para su desarrollo y progresión. Dentro de las características del hospedero se encuentra la respuesta T reguladora, que otorga tolerancia frente a antígenos propios, participa durante las enfermedades infecciosas limitando el daño tisular, sin disminuir la respuesta antibacteriana. El presente estudio tiene por objetivo determinar la presencia, reclutamiento y función de Tregs en pacientes con periodontitis crónica. En 10 biopsias de tejido periodontal sano y con periodontits crónica se realizó inmunohistoquímica para marcadores (CD4, CD25, Foxp3), quimioquinas (CCL17, CCL22) y citoquinas (TGF-B, IL-10) de Tregs. Además de Western-Blot para detectar las citoquinas. Los resultados obtenidos sugieren una posible asociación entre células Tregs y la infección periodontal, ya que se confirma su reclutamiento y presencia. Sin embargo, son necesarios más estudios del posible desbalance con su contraparte pro-inflamatoria Th17, que expliquen en parte la compleja etiopatogenia de la enfermedad periodontal.
Periodontal disease requires a susceptible host to initiation, development and progression. T regulatory response is one of these inmunoregulatory characteristics of the susceptible host, which provide tolerance, tissular protection during infection without impairing the control of periodontopathogens. The aim of this study is to determinate the presence, homing and function of T regulatory cells (Tregs) in patients with chronic periodontitis. Ten biopsies were taken from pockets, the presence of Tregs markers (CD4, CD25, Foxp3), chemokines (CCL17, CCL22) and cytokines (TGF-p, IL-10) were determinate by immunohistochemistry. Cytokines also were detected with Western-Blot. Our results suggest a possible association between Tregs and periodontal infection, confirming homing and presence of Tregs. However, further studies are required to determine the possible imbalance with pro-inflammatory part Th17, that might explain the complex etiopathogenesis of periodontal disease.
Subject(s)
Humans , Male , Female , Adult , T-Lymphocytes, Regulatory/immunology , Chronic Periodontitis/immunology , Blotting, Western , Chemokines , Cytokines , Forkhead Transcription Factors , ImmunohistochemistryABSTRACT
The bovine model is extremely interesting to study several basic aspects of mucosal local immunity. Many reports have shown that, in young calves, the infectivity of enterotoxigenic Escherichia coli may be inhibited by passively administered antibodies anti K99 pilus. We have measured, by immunoradiometric assays, the IgG response anti K99 pilus in the serum of calves, deprived of colostrum and orally inoculated with enteropathogenic K99+ E. coli. Although variable levels of IgG anti K99 pilus were detected, their protective value could not be ascertained in vivo due to the acute development of the infection. In an effort to correlate the presence of serum antibodies anti K99 pilus with their protective capacity, an ex-vivo assay to monitor the interaction of radiolabeled K99 pilus with the bovine mucosa was standardized. Paradoxically, although K99 pilus, purified by standard procedures, was recognized by polyclonal rabbit and calf antisera, its interaction with the bovine intestinal mucosa, quantitated in the ex-vivo system, was not inhibited by these reagents, indicating that the antibodies did not effectively block those K99 pilus domains involved in the interaction with mucosal receptors