ABSTRACT
The ability of nematodes to manipulate the immune system of their host towards a Th2 and T regulatory responses has been proposed to suppress the inflammatory response. Clinical trials have proposed a useful effect of helminth infections on improvement of inflammatory disorders. In this study, we investigated the immunomodulatory effect of Syphacia obvelata infection to induce intestinal tolerance in C57BL/6 mice. Mice were infected through the cagemates with self-infected BALB/c mice. Four weeks post-infection, expression levels of IFN-γ, TNF-α, IL-17, and IL-10 were assessed in the supernatant of mesenteric lymph node (MLN) culture. Foxp3⁺Treg were measured in MLN cells by flow cytometry. In the S. obvelata-infected group, the percentage of Tregs (5.2±0.4) was significantly higher than the control (3.6±0.5) (P<0.05). The levels of IL-10 (55.3±2.2 vs 35.2±3.2), IL-17 (52.9±3.8 vs 41±1.8), IFN-γ (44.8±4.8 vs 22.3±2.3) and TNF-α (71.1±5.8 vs 60.1±3.3) were significantly increased in infected mice compared to the control group (P<0.05). The above results showed the potential effects of S. obvelata to induce intestinal tolerance. Therefore, it seems that S. obvelata may increase the immunological suppressive function in the intestinal tract.
Subject(s)
Animals , Mice , Flow Cytometry , Helminths , Hope , Immune System , Interleukin-10 , Interleukin-17 , Lymph Nodes , OxyuroideaABSTRACT
La Diabetes Mellitus Tipo 1 (DM1) es una de las patologías más estudiadas en la actualidad, no solo por el aumento de su incidencia, sino también por su aparición a edades cada vez más tempranas. La DM1 es una enfermedad autoinmune de una alta complejidad genética y donde la susceptibilidad a factores ambientales parece jugar un papel preponderante. Elementos como parto por cesárea, deficiencia de vitamina D, exposición temprana a proteínas de la leche de vaca, exposición limitada a microorganismos durante la infancia y el incremento en la incidencia de obesidad infantil han sido relacionados con el desarrollo de esta entidad, convergiendo todos estos factores en un punto clave: la pérdida de la tolerancia inmunológica intestinal y la participación de células T auto-reactivas en pacientes susceptibles. Por su parte, la leche materna ofrece una serie de factores de crecimiento, inmunológicos, e incluso insulina, que son capaces de inducir una respuesta tolerogénica en el microambiente intestinal con la subsecuente disminución de la autoinmunidad. En esta revisión se expondrá la evidencia y los mecanismos fisiopatológicos propuestos por medio de los cuales los elementos mencionados desencadenarían una alteración de la inmunomodulación intestinal y un incremento en la predisposición al desarrollo de DM1.
Type 1 Diabetes Mellitus (T1DM) is one of the most studied pathologies to date, not only due to the elevating incidence but also because it is being diagnosed at even earlier ages. T1DM is an autoimmune disease with a very complex genetic background where environmental factors seem to play a very important triggering role. Elements like cesarean section, vitamin D deficiency, early exposure to cow milk proteins, limited exposure to microorganisms during infancy, and the increase of childhood obesity have been related to the development of this disease, converging all the factors into one key feature: loss of intestinal immunological tolerance and the participation of auto-reactive T cells from a susceptible patient. On the other hand, breast milk offers a series of growth and immunological factors, even insulin, which are able to induce a tolerogenic response in the intestinal microenvironment, lowering the probability of any autoimmune phenomena. The following review will expose evidence of the pathophysiological mechanisms involved in each environmental element associated with intestinal immunomodulation and the increase risk of T1DM.