Regulation of γδT17 cells by Mycobacterium vaccae through interference with Notch/Jagged1 signaling pathway.

The objective of this study was to investigate the effect of Mycobacterium vaccae on Jagged 1 and gamma delta T17 (γδT17) cells in asthmatic mice. An asthma mouse model was established through immunization with ovalbumin (OVA). Gamma-secretase inhibitor (DAPT) was used to block the Notch signaling pathway. M. vaccae was used to treat asthma, and related indicators were measured. Blocking Notch signaling inhibited the production of γδT17 cells and secretion of cytokine interleukin (IL)-17, which was accompanied by a decrease in Jagged1 mRNA and protein expression in the treated asthma group compared with the untreated asthma group. Similarly, treatment with M. vaccae inhibited Jagged1 expression and γδT17 cell production, which was associated with decreased airway inflammation and reactivity. The Notch signaling pathway may play a role in the pathogenesis of asthma through the induction of Jagged1 receptor. On the other hand, the inhibitory effect of M. vaccae on Jagged1 receptor in γδT17 cells could be used for the prevention and treatment of asthma.

Regulation of γδT17 cells by Mycobacterium vaccae through interference with Notch/Jagged1 signaling pathway

The objective of this study was to investigate the effect of Mycobacterium vaccae on Jagged 1 and gamma delta T17 (γδT17) cells in asthmatic mice. An asthma mouse model was established through immunization with ovalbumin (OVA). Gamma-secretase inhibitor (DAPT) was used to block the Notch signaling pathway. M. vaccae was used to treat asthma, and related indicators were measured. Blocking Notch signaling inhibited the production of γδT17 cells and secretion of cytokine interleukin (IL)-17, which was accompanied by a decrease in Jagged1 mRNA and protein expression in the treated asthma group compared with the untreated asthma group. Similarly, treatment with M. vaccae inhibited Jagged1 expression and γδT17 cell production, which was associated with decreased airway inflammation and reactivity. The Notch signaling pathway may play a role in the pathogenesis of asthma through the induction of Jagged1 receptor. On the other hand, the inhibitory effect of M. vaccae on Jagged1 receptor in γδT17 cells could be used for the prevention and treatment of asthma.

Imbalance of γδT17/γδTreg cells in the pathogenesis of allergic asthma induced by ovalbumin.

We aimed to explore the imbalance between the T helper 17 γδT cells (γδT17) and the regulatory γδT cells (γδTreg) in asthmatic mice. Male Balb/c mice were randomly divided into the normal control group and the asthmatic model group. The asthmatic model group mice were intraperitoneally injected with the mixture of ovalbumin (OVA)/Al(OH)3 and then activated by exposure of the animals to OVA atomization. Airway hyperresponsiveness (AHR) was determined by a non-invasive lung function machine. Hematoxylin and eosin and Alcian blue-periodic acid Schiff staining were done for histopathological analysis. Interleukin (IL)-17 and IL-35 levels in bronchoalveolar lavage fluid were detected by ELISA. The percentage of IL-17+ γδT cells and Foxp3+ γδT cells in spleen cells suspension were detected and the transcription levels of RORγt and Foxp3 in the lung tissue were determined. Compared with the normal control, the severity of airway inflammation and AHR were higher in the asthmatic mice. Furthermore, mice in the asthmatic group displayed significant increases of IL-17+ γδT cells, expression of IL-17A, and RORγt, whereas control mice displayed marked decreases of Foxp3+ γδT cells, expression of IL-35, and transcription factor Foxp3. In addition, the mRNA expression of RORγt was positively correlated with the percentage of IL-17+γδT cells, and the mRNA level of Foxp3 was positively correlated with the percentage of Foxp3+ γδT cells. The imbalance of γδT17/γδTreg in the asthmatic mice may contribute to the pathogenesis of OVA-induced asthma.

Imbalance of γδT17/γδTreg cells in the pathogenesis of allergic asthma induced by ovalbumin

We aimed to explore the imbalance between the T helper 17 γδT cells (γδT17) and the regulatory γδT cells (γδTreg) in asthmatic mice. Male Balb/c mice were randomly divided into the normal control group and the asthmatic model group. The asthmatic model group mice were intraperitoneally injected with the mixture of ovalbumin (OVA)/Al(OH)3 and then activated by exposure of the animals to OVA atomization. Airway hyperresponsiveness (AHR) was determined by a non-invasive lung function machine. Hematoxylin and eosin and Alcian blue-periodic acid Schiff staining were done for histopathological analysis. Interleukin (IL)-17 and IL-35 levels in bronchoalveolar lavage fluid were detected by ELISA. The percentage of IL-17+ γδT cells and Foxp3+ γδT cells in spleen cells suspension were detected and the transcription levels of RORγt and Foxp3 in the lung tissue were determined. Compared with the normal control, the severity of airway inflammation and AHR were higher in the asthmatic mice. Furthermore, mice in the asthmatic group displayed significant increases of IL-17+ γδT cells, expression of IL-17A, and RORγt, whereas control mice displayed marked decreases of Foxp3+ γδT cells, expression of IL-35, and transcription factor Foxp3. In addition, the mRNA expression of RORγt was positively correlated with the percentage of IL-17+γδT cells, and the mRNA level of Foxp3 was positively correlated with the percentage of Foxp3+ γδT cells. The imbalance of γδT17/γδTreg in the asthmatic mice may contribute to the pathogenesis of OVA-induced asthma.

Primeras experiencias clínicas en Cuba sobre el uso de la electroterapia en cuatro pacientes con tumores sólidos malignos superficiales / First clinical experiences in Cuba with the use of the electrotherapy in four patients with superficial malignant solid tumors

Los primeros estudios clínicos en Cuba fueron realizados para evaluar la seguridad y efectividad de la electroterapia en 4 pacientes con tumor sólido superficial maligno. Se empleó básicamente el equipo chino multifuncional ZAY-6B, en el que además de insertar electrodos en la base perpendicular al eje mayor, se utilizó un arreglo de cátodos y ánodos alternos. Los pacientes fueron cuidadosamente observados durante y después de la sesión con electroterapia para poder evaluar sus efectos terapéuticos. Se obtuvo un retardo significativo del crecimiento tumoral después del tratamiento, particularmente del carcinoma ductal invasor de mama, aunque se logró la remisión parcial de todos los neoplasmas malignos tratados con electricidad. Un hecho interesante fue que las 2 pacientes con carcinoma ductal invasor de mama inoperable, pudieron ser intervenidas quirúrgicamente luego de haber recibido electroterapia.. La necrosis de los 4 tumores malignos se produjo inmediatamente después de la terapia. Transcurridos 8 meses, los hallazgos histopatológicos y peritumorales en el carcinoma ductal invasor de mama de la segunda paciente, revelaron gran necrosis tumoral, congestión vascular, infiltraciones de monocitos y linfocitos y una respuesta inflamatoria crónica. Los resultados preliminares derivados de este adiestramiento indican que la terapia con corriente eléctrica directa de baja intensidad puede ser introducida en el Sistema Nacional de Salud Pública por constituir un método seguro, simple, económico, eficaz, apenas traumático y muy factible para tratar a los pacientes con tumores inoperables en estadios avanzados (III y IV), que no toleran la radioterapia y quimioterapia o en quienes la aplicación de estos métodos oncoespecíficos no proporcionó la respuesta objetiva esperada