Expression of microbiota recognition receptors and intestinal serotoninergic system in two mouse models of colitis

Layunta, E. (Universidad de Zaragoza) ; Latorre, E. ; Grasa, L. (Universidad de Zaragoza) ; Castro, M. (Universidad de Zaragoza) ; Plaza, M.A. (Universidad de Zaragoza) ; Pardo, J. ; Santiago, L. ; Medina de Sánchez , F. ; Martínez-Augustin, O. ; Ocón, B. ; Aranda, C. ; Mesonero, J.E. (Universidad de Zaragoza) ; Alcalde, A.I.

Resumen: Background: The intestinal microbiota patterns recognition receptors TLRs and NODs (PRRs), and the intestinal serotoninergic system, may contribute to intestinal responses to microbiota and alter intestinal homeostasis/inflammation e.g. in inflammatory bowel disease.
Aim: We examined two mouse colitis models (Dextran Sulfate Sodium (DSS) or Lymphocyte Transfer (LT) mouse colitis) and compared the expression of PRRs, implicated in innate immunity, and some elements of the intestinal serotoninergic system.
Methods: In ileum and colon from DSS or LT mouse colitis animals, TLRs, NODs, serotonin transporter (SERT) and serotonin receptors (5-HTRs) mRNA expression was measured by RT-qPCR. SERT protein expression was analyzed by western blotting.
Results: In DSS ileum, TLR9, 5HTR1A, 5-HTR4 and 5-HTR7 mRNA levels were over-expressed, and SERT expression reduced; in DSS colon, NOD2, TLR2, TLR9, and 5-HTR7 mRNAs were increased; however, 5HTR1A, 5-HTR2B, 5-HTR3, and 5HTR4 mRNA levels were diminished, as well as SERT expression. On the other hand, in LT ileum, TLR9, 5-HTR1A, 5- HT2A, and 5-HT2B mRNAs were reduced and, although SERT mRNA was not altered, SERT protein level was reduced; in colon of LT mouse model, TLR2, TLR9, 5-HTR1A, and 5-HTR7 mRNA levels and SERT expression were increased; however, TLR4, NOD1, 5- HTR2B, 5-HT3, 5-HT4 mRNA levels were reduced.

Idioma: Inglés

Año: 2015

Publicado en: Acta Physiologica 214, Suppl. 701 (2015), 6 [I3]
ISSN: 1748-1708

Factor impacto JCR: 4.066 (2015)

Categ. JCR: PHYSIOLOGY rank: 13 / 83 = 0.157 (2015) - Q1 - T1

Factor impacto SCIMAGO: 1.654 - Physiology (Q1)

Financiación: info:eu-repo/grantAgreement/ES/DGA/ARAINF-012-2008
Financiación: info:eu-repo/grantAgreement/ES/DGA/B022-13
Financiación: info:eu-repo/grantAgreement/ES/DGA/B105-11
Financiación: info:eu-repo/grantAgreement/ES/DGA/B61
Financiación: info:eu-repo/grantAgreement/ES/MICINN-FEDER/BFU2009-08149
Financiación: info:eu-repo/grantAgreement/ES/MICINN-FEDER/BFU2010-18971
Financiación: info:eu-repo/grantAgreement/ES/MICINN-FEDER/SAF2011-22922
Financiación: info:eu-repo/grantAgreement/ES/MICINN-FEDER/SAF22812

Tipo y forma: Comunicación congreso (Versión definitiva)

Área (Departamento): Área Fisiología (Dpto. Farmacología y Fisiolog.)