B. L. Sánchez, José Ángel Gutiérrez Pabello, Gerardo Enrique Medina Basulto, T. R. Evangelista, E. D. Aparicio, S. Oshima
{"title":"禽分枝杆菌亚种。副结核降低铁诱导巨噬细胞中铁portin 1 mrna表达的调控","authors":"B. L. Sánchez, José Ángel Gutiérrez Pabello, Gerardo Enrique Medina Basulto, T. R. Evangelista, E. D. Aparicio, S. Oshima","doi":"10.21753/VMOA.3.1.361","DOIUrl":null,"url":null,"abstract":"Veterinaria Mexico OA ISSN: 2448-6760 Cite this as: Landeros Sanchez B, Gutierrez Pabello JA, Medina Basulto GE, Renteria Evangelista TB, Diaz Aparicio E, Oshima S. Mycobacterium avium subsp. paratuberculosis down-regulates mRNA expression of iron-induced macrophage Ferroportin 1. Veterinaria Mexico OA. 2016;3(1). doi: 10.21753/vmoa.3.1.361 Mycobacterium avium subsp. paratuberculosis (MAP) is the causative agent of Johne’s disease. The mechanisms by which MAP is able to adapt to the innate host response are still unclear. We examined Ferroportin 1 (FPN1) mRNA expression levels via real-time PCR of the mouse macrophage cell line J774 that was incubated in the presence of Mycobacterium avium subsp. paratuberculosis (MAP) or MAP crude protein extract. Infection with live MAP decreased FPN1 mRNA levels in a multiplicity of infection (MOI)-dependent fashion. Macrophages infected with MOIs of 20:1 and 15:1 did not show any change in FPN1 gene expression, whereas MOIs of 10:1 and 5:1 induced a decrease of 50 and 80%, respectively. Macrophages treated with 50, 100, 150 and 200 µg/mL of MAP crude extract (ATCC19698) decreased FPN1 mRNA expression by 25%. Additionally, up-regulation of FPN1 mRNA by an iron overload treatment of 400 µM of ferric nitrilotriacetate (FeNTA) was abrogated by live MAP (MOI 20:1) by approximately 70%. Our data revealed an inhibitory effect of MAP on FPN1 mRNA and suggested a bacterial mechanism that may play a role in host iron regulation. Figure 1. Infection by Mycobacterium avium subsp. paratuberculosis (MAP) down-regulates macrophage fpn1 gene expression. Murine macrophages, J774, were infected with MAP at different multiplicities of infection (MOIs) for 6 hours. Total RNA was extracted and gene expression was measured by real-time PCR. Results were normalized to GAPDH and expressed as units of relative expression (URE). Results are the mean ± standard deviation of 3 independent experiments with 3 replicates each. Statistical significance, P = 0.05.","PeriodicalId":49387,"journal":{"name":"Veterinaria Mexico","volume":null,"pages":null},"PeriodicalIF":0.2000,"publicationDate":"2016-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.21753/VMOA.3.1.361","citationCount":"0","resultStr":"{\"title\":\"El Mycobacterium avium subesp. paratuberculosis disminuye la regulación de la expresión del ARNm de la ferroportina 1 en los macrófagos inducidos con hierro\",\"authors\":\"B. L. Sánchez, José Ángel Gutiérrez Pabello, Gerardo Enrique Medina Basulto, T. R. Evangelista, E. D. Aparicio, S. Oshima\",\"doi\":\"10.21753/VMOA.3.1.361\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Veterinaria Mexico OA ISSN: 2448-6760 Cite this as: Landeros Sanchez B, Gutierrez Pabello JA, Medina Basulto GE, Renteria Evangelista TB, Diaz Aparicio E, Oshima S. Mycobacterium avium subsp. paratuberculosis down-regulates mRNA expression of iron-induced macrophage Ferroportin 1. Veterinaria Mexico OA. 2016;3(1). doi: 10.21753/vmoa.3.1.361 Mycobacterium avium subsp. paratuberculosis (MAP) is the causative agent of Johne’s disease. The mechanisms by which MAP is able to adapt to the innate host response are still unclear. We examined Ferroportin 1 (FPN1) mRNA expression levels via real-time PCR of the mouse macrophage cell line J774 that was incubated in the presence of Mycobacterium avium subsp. paratuberculosis (MAP) or MAP crude protein extract. Infection with live MAP decreased FPN1 mRNA levels in a multiplicity of infection (MOI)-dependent fashion. Macrophages infected with MOIs of 20:1 and 15:1 did not show any change in FPN1 gene expression, whereas MOIs of 10:1 and 5:1 induced a decrease of 50 and 80%, respectively. Macrophages treated with 50, 100, 150 and 200 µg/mL of MAP crude extract (ATCC19698) decreased FPN1 mRNA expression by 25%. Additionally, up-regulation of FPN1 mRNA by an iron overload treatment of 400 µM of ferric nitrilotriacetate (FeNTA) was abrogated by live MAP (MOI 20:1) by approximately 70%. Our data revealed an inhibitory effect of MAP on FPN1 mRNA and suggested a bacterial mechanism that may play a role in host iron regulation. Figure 1. Infection by Mycobacterium avium subsp. paratuberculosis (MAP) down-regulates macrophage fpn1 gene expression. Murine macrophages, J774, were infected with MAP at different multiplicities of infection (MOIs) for 6 hours. Total RNA was extracted and gene expression was measured by real-time PCR. Results were normalized to GAPDH and expressed as units of relative expression (URE). Results are the mean ± standard deviation of 3 independent experiments with 3 replicates each. 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El Mycobacterium avium subesp. paratuberculosis disminuye la regulación de la expresión del ARNm de la ferroportina 1 en los macrófagos inducidos con hierro
Veterinaria Mexico OA ISSN: 2448-6760 Cite this as: Landeros Sanchez B, Gutierrez Pabello JA, Medina Basulto GE, Renteria Evangelista TB, Diaz Aparicio E, Oshima S. Mycobacterium avium subsp. paratuberculosis down-regulates mRNA expression of iron-induced macrophage Ferroportin 1. Veterinaria Mexico OA. 2016;3(1). doi: 10.21753/vmoa.3.1.361 Mycobacterium avium subsp. paratuberculosis (MAP) is the causative agent of Johne’s disease. The mechanisms by which MAP is able to adapt to the innate host response are still unclear. We examined Ferroportin 1 (FPN1) mRNA expression levels via real-time PCR of the mouse macrophage cell line J774 that was incubated in the presence of Mycobacterium avium subsp. paratuberculosis (MAP) or MAP crude protein extract. Infection with live MAP decreased FPN1 mRNA levels in a multiplicity of infection (MOI)-dependent fashion. Macrophages infected with MOIs of 20:1 and 15:1 did not show any change in FPN1 gene expression, whereas MOIs of 10:1 and 5:1 induced a decrease of 50 and 80%, respectively. Macrophages treated with 50, 100, 150 and 200 µg/mL of MAP crude extract (ATCC19698) decreased FPN1 mRNA expression by 25%. Additionally, up-regulation of FPN1 mRNA by an iron overload treatment of 400 µM of ferric nitrilotriacetate (FeNTA) was abrogated by live MAP (MOI 20:1) by approximately 70%. Our data revealed an inhibitory effect of MAP on FPN1 mRNA and suggested a bacterial mechanism that may play a role in host iron regulation. Figure 1. Infection by Mycobacterium avium subsp. paratuberculosis (MAP) down-regulates macrophage fpn1 gene expression. Murine macrophages, J774, were infected with MAP at different multiplicities of infection (MOIs) for 6 hours. Total RNA was extracted and gene expression was measured by real-time PCR. Results were normalized to GAPDH and expressed as units of relative expression (URE). Results are the mean ± standard deviation of 3 independent experiments with 3 replicates each. Statistical significance, P = 0.05.
期刊介绍:
Veterinaria México OA (ISSN 2448-6760) is an online scientific journal edited by Universidad Nacional Autónoma de México (UNAM). The journal is Open Access and follows UNAM''s initiative, to transmit knowledge free of charge to the readership and authors, with no Article Processing Charges.
This journal publishes advances in Veterinary Sciences and Animal Production, and to reach more lectures across the world the journal was updated since 2014 from its predecessor printed in paper Veterinaria México (ISSN 0301-5092) and its digital version (ISSN 2007-5472).