000109330 001__ 109330
000109330 005__ 20240122154814.0
000109330 0247_ $$2doi$$a10.1111/nmo.13648
000109330 0248_ $$2sideral$$a112951
000109330 037__ $$aART-2019-112951
000109330 041__ $$aeng
000109330 100__ $$0(orcid)0000-0002-5306-9365$$aGrasa, Laura$$uUniversidad de Zaragoza
000109330 245__ $$aTLR2 and TLR4 interact with sulfide system in the modulation of mouse colonic motility
000109330 260__ $$c2019
000109330 5060_ $$aAccess copy available to the general public$$fUnrestricted
000109330 5203_ $$aBackground H2S is a neuromodulator that may inhibit intestinal motility. H2S production in colon is yielded by cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE) enzymes and sulfate-reducing bacteria (SRB). Toll-like receptors (TLRs) recognize intestinal microbiota. The aim of this work was to evaluate the influence of TLR2 and TLR4 on the endogenous and SRB-mediated synthesis of H2S and its consequences on the colonic motility of mouse. Methods Muscle contractility studies were performed in colon from WT, Tlr2(-/-), and Tlr4(-/-) mice. The mRNA levels of TLR2, TLR4, CBS, CSE, and SRB were measured by real-time PCR. Free sulfide levels in colon and feces were determined by colorimetric assays. Results NaHS and GYY4137, donors of H2S, reduced the contractility of colon. Aminooxyacetic acid (AOAA), inhibitor of CBS, and D-L propargylglycine (PAG), inhibitor of CSE, increased the contractility of colon. In vivo treatment with NaHS or GYY4137 inhibited the spontaneous contractions and upregulated TLR2 expression. The in vivo activation of TLR4 with lipopolysaccharide increased the contractile response to PAG, mRNA levels of CSE, and the free sulfide levels of H2S in colon. In Tlr2(-/-) and Tlr4(-/-) mice, the contractions induced by AOAA and PAG and mRNA levels of CBS and CSE were lower with respect to WT mice. Deficiency of TLR2 or TLR4 provokes alterations in free sulfide levels and SRB of colon. Conclusions and Inferences Our study demonstrates interaction between TLR2 and TLR4 and the sulfide system in the regulation of colonic motility and contributes to the pathophysiology knowledge of intestinal motility disorders.
000109330 536__ $$9info:eu-repo/grantAgreement/ES/DGA/B61$$9info:eu-repo/grantAgreement/ES/UZ/JIUZ-2016-BIO-02
000109330 540__ $$9info:eu-repo/semantics/openAccess$$aAll rights reserved$$uhttp://www.europeana.eu/rights/rr-f/
000109330 590__ $$a2.946$$b2019
000109330 591__ $$aCLINICAL NEUROLOGY$$b85 / 204 = 0.417$$c2019$$dQ2$$eT2
000109330 591__ $$aNEUROSCIENCES$$b145 / 270 = 0.537$$c2019$$dQ3$$eT2
000109330 591__ $$aGASTROENTEROLOGY & HEPATOLOGY$$b52 / 88 = 0.591$$c2019$$dQ3$$eT2
000109330 592__ $$a1.33$$b2019
000109330 593__ $$aGastroenterology$$c2019$$dQ1
000109330 593__ $$aPhysiology$$c2019$$dQ1
000109330 593__ $$aEndocrine and Autonomic Systems$$c2019$$dQ2
000109330 655_4 $$ainfo:eu-repo/semantics/article$$vinfo:eu-repo/semantics/acceptedVersion
000109330 700__ $$aAbecia, Leticia
000109330 700__ $$aPeña-Cearra, Ainize
000109330 700__ $$aRobles, Sofía
000109330 700__ $$0(orcid)0000-0001-5573-6144$$aLayunta, Elena$$uUniversidad de Zaragoza
000109330 700__ $$0(orcid)0000-0002-5797-3909$$aLatorre, Eva$$uUniversidad de Zaragoza
000109330 700__ $$0(orcid)0000-0003-4758-3998$$aMesonero, José Emilio$$uUniversidad de Zaragoza
000109330 700__ $$aForcen, Raquel
000109330 7102_ $$11005$$2410$$aUniversidad de Zaragoza$$bDpto. Farmacología y Fisiolog.$$cÁrea Fisiología
000109330 7102_ $$11002$$2050$$aUniversidad de Zaragoza$$bDpto. Bioq.Biolog.Mol. Celular$$cÁrea Biología Celular
000109330 773__ $$g31, 9 (2019), e13648 [12 pp.]$$pNeurogastroenterol. motil.$$tNEUROGASTROENTEROLOGY AND MOTILITY$$x1350-1925
000109330 8564_ $$s1000655$$uhttps://zaguan.unizar.es/record/109330/files/texto_completo.pdf$$yPostprint
000109330 8564_ $$s1028481$$uhttps://zaguan.unizar.es/record/109330/files/texto_completo.jpg?subformat=icon$$xicon$$yPostprint
000109330 909CO $$ooai:zaguan.unizar.es:109330$$particulos$$pdriver
000109330 951__ $$a2024-01-22-15:32:51
000109330 980__ $$aARTICLE