Guillermina J Baay-Guzmán, Aaron Pavel Rodríguez-Hernández, D Anaya-Estrada, M Rodriguez-Jimenez, J E Cocoletzi-Bautista, D Hernández-Cueto, R Luria-Perez
{"title":"[通过药物调节HIF-1在小鼠肺过敏性炎症模型中调节IL-33和IL-17的表达]。","authors":"Guillermina J Baay-Guzmán, Aaron Pavel Rodríguez-Hernández, D Anaya-Estrada, M Rodriguez-Jimenez, J E Cocoletzi-Bautista, D Hernández-Cueto, R Luria-Perez","doi":"10.29262/ram.v70i3.1273","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>To evaluate the effect of pharmacological modulation of HIF-1 on the expression of IL-33 and IL-17 in a murine model of allergic pulmonary inflam- mation (API) with different degrees of severity.</p><p><strong>Methods: </strong>5 mice/group received ovalbumin (OVA) 1(mild), 2(moderate) or 3(severe) challenges via i.t. prior to allergen sensitization, in addition to the HIF-1 induction or inhibition groups, received EDHB (OVA+EDHB) i.p. or 2ME (OVA+2ME) i.t. respectively. Control groups received saline solution (SS) in the same way. HE (inflammatory infiltrate), PAS (mucus production) and immunohistochemical staining for HIF-1a, IL-33, IL-17 were performed, quantitatively analyzing by digital pathology.</p><p><strong>Results: </strong>We obtained different degrees of severity with a greater number of challenges, increasing the expression of HIF-1, correlating with the expression of IL-33/IL-17. Increasing or decreasing, respectively by pharmacological modulation.</p><p><strong>Conclusions: </strong>The above suggests that the high expression of HIF-1 favors the production of IL-33 and IL-17 contributing to the damage in lung tissue and the severity of the disease and these can be regulated through the modulation of HIF- 1.</p>","PeriodicalId":101421,"journal":{"name":"Revista alergia Mexico (Tecamachalco, Puebla, Mexico : 1993)","volume":"70 4","pages":"190"},"PeriodicalIF":0.0000,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"[Regulación de la expresión de IL-33 e IL-17 por la modulación farmacológica de HIF-1 en un modelo murino de inflamación alérgica pulmonar].\",\"authors\":\"Guillermina J Baay-Guzmán, Aaron Pavel Rodríguez-Hernández, D Anaya-Estrada, M Rodriguez-Jimenez, J E Cocoletzi-Bautista, D Hernández-Cueto, R Luria-Perez\",\"doi\":\"10.29262/ram.v70i3.1273\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Objective: </strong>To evaluate the effect of pharmacological modulation of HIF-1 on the expression of IL-33 and IL-17 in a murine model of allergic pulmonary inflam- mation (API) with different degrees of severity.</p><p><strong>Methods: </strong>5 mice/group received ovalbumin (OVA) 1(mild), 2(moderate) or 3(severe) challenges via i.t. prior to allergen sensitization, in addition to the HIF-1 induction or inhibition groups, received EDHB (OVA+EDHB) i.p. or 2ME (OVA+2ME) i.t. respectively. Control groups received saline solution (SS) in the same way. HE (inflammatory infiltrate), PAS (mucus production) and immunohistochemical staining for HIF-1a, IL-33, IL-17 were performed, quantitatively analyzing by digital pathology.</p><p><strong>Results: </strong>We obtained different degrees of severity with a greater number of challenges, increasing the expression of HIF-1, correlating with the expression of IL-33/IL-17. Increasing or decreasing, respectively by pharmacological modulation.</p><p><strong>Conclusions: </strong>The above suggests that the high expression of HIF-1 favors the production of IL-33 and IL-17 contributing to the damage in lung tissue and the severity of the disease and these can be regulated through the modulation of HIF- 1.</p>\",\"PeriodicalId\":101421,\"journal\":{\"name\":\"Revista alergia Mexico (Tecamachalco, Puebla, Mexico : 1993)\",\"volume\":\"70 4\",\"pages\":\"190\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2023-09-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Revista alergia Mexico (Tecamachalco, Puebla, Mexico : 1993)\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.29262/ram.v70i3.1273\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Revista alergia Mexico (Tecamachalco, Puebla, Mexico : 1993)","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.29262/ram.v70i3.1273","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
[Regulación de la expresión de IL-33 e IL-17 por la modulación farmacológica de HIF-1 en un modelo murino de inflamación alérgica pulmonar].
Objective: To evaluate the effect of pharmacological modulation of HIF-1 on the expression of IL-33 and IL-17 in a murine model of allergic pulmonary inflam- mation (API) with different degrees of severity.
Methods: 5 mice/group received ovalbumin (OVA) 1(mild), 2(moderate) or 3(severe) challenges via i.t. prior to allergen sensitization, in addition to the HIF-1 induction or inhibition groups, received EDHB (OVA+EDHB) i.p. or 2ME (OVA+2ME) i.t. respectively. Control groups received saline solution (SS) in the same way. HE (inflammatory infiltrate), PAS (mucus production) and immunohistochemical staining for HIF-1a, IL-33, IL-17 were performed, quantitatively analyzing by digital pathology.
Results: We obtained different degrees of severity with a greater number of challenges, increasing the expression of HIF-1, correlating with the expression of IL-33/IL-17. Increasing or decreasing, respectively by pharmacological modulation.
Conclusions: The above suggests that the high expression of HIF-1 favors the production of IL-33 and IL-17 contributing to the damage in lung tissue and the severity of the disease and these can be regulated through the modulation of HIF- 1.