Persistent alterations in colonic afferent innervation in a rat model of postinfectious gut dysfunction: Role for changes in peripheral neurotrophic factors

2016 ◽  
Vol 28 (5) ◽  
pp. 693-704
Author(s):  
F. Jardí ◽  
J. A. Fernández-Blanco ◽  
V. Martínez ◽  
P. Vergara
Keyword(s):  
Rat Model ◽  
Neurotrophic Factors ◽  
Gut Dysfunction ◽  
Afferent Innervation

Mo2036 Remodeling of Colonic Sensory Afferents in a Rat Model of Post-Infectious Gut Dysfunction: Implication of Neurotrophic Factors

2014 ◽  
Vol 146 (5) ◽  
pp. S-724
Author(s):  
Ferran Jardi ◽  
Joan Antoni Fernandez-Blanco ◽  
Vicente Martinez ◽  
Patri Vergara
Keyword(s):  
Rat Model ◽  
Neurotrophic Factors ◽  
Sensory Afferents ◽  
Gut Dysfunction ◽  
Post Infectious

scholarly journals Oxycodone regulates incision-induced activation of neurotrophic factors and receptors in an acute post-surgery pain rat model

2018 ◽  
Vol Volume 11 ◽  
pp. 2663-2674 ◽  
Author(s):  
Baowen Liu ◽  
Yi Liu ◽  
Ningbo Li ◽  
Jin Zhang ◽  
Xianwei Zhang
Keyword(s):  
Rat Model ◽  
Neurotrophic Factors ◽  
Post Surgery

16 Differential Effects of PAR-2 Activation on Barrier Function and Motility During Acute and Chronic Inflammation in a Rat Model of Postinfectious Gut Dysfunction

2012 ◽  
Vol 142 (5) ◽  
pp. S-4-S-5
Author(s):  
Joan Antoni Fernandez-Blanco ◽  
Ferran Jardi ◽  
Morley D. Hollenberg ◽  
Vicente Martinez ◽  
Patri Vergara
Keyword(s):  
Chronic Inflammation ◽  
Rat Model ◽  
Barrier Function ◽  
Differential Effects ◽  
Gut Dysfunction ◽  
Acute And Chronic Inflammation

T2059 Persistent Epithelial Barrier Alterations in a Rat Model of Post-Inflammatory Gut Dysfunction

2010 ◽  
Vol 138 (5) ◽  
pp. S-623
Author(s):  
Joan Antoni Fernandez-Blanco ◽  
Vicente Martinez ◽  
Maite Martin ◽  
Patri Vergara
Keyword(s):  
Rat Model ◽  
Epithelial Barrier ◽  
Gut Dysfunction

Stimulation of neurotrophic factors and inhibition of proinflammatory cytokines by exogenous application of triiodothyronine in the rat model of ischemic stroke

2017 ◽  
Vol 35 (1) ◽  
pp. 50-55 ◽  
Author(s):  
Fatemeh Sabbaghziarani ◽  
Keywan Mortezaee ◽  
Mohammad Akbari ◽  
Iraj Ragerdi Kashani ◽  
Mansooreh Soleimani ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Proinflammatory Cytokines ◽  
Rat Model ◽  
Neurotrophic Factors ◽  
Exogenous Application ◽  
Stimulation Of

Insulin-dependent Diabetes and Gut Dysfunction: The BB Rat Model

2004 ◽  
Vol 36 (9) ◽  
pp. 585-594 ◽  
Author(s):  
W. J. Malaisse ◽  
P. Courtois ◽  
F. W. Scott
Keyword(s):  
Rat Model ◽  
Insulin Dependent Diabetes ◽  
Bb Rat ◽  
Gut Dysfunction ◽  
Insulin Dependent

PAR-2-mediated control of barrier function and motility differs between early and late phases of postinfectious gut dysfunction in the rat

2013 ◽  
Vol 304 (4) ◽  
pp. G390-G400 ◽  
Author(s):  
Juan A. Fernández-Blanco ◽  
Morley D. Hollenberg ◽  
Vicente Martínez ◽  
Patri Vergara
Keyword(s):  
Ion Transport ◽  
Rat Model ◽  
Barrier Function ◽  
Early Phase ◽  
Trichinella Spiralis ◽  
Late Phase ◽  
Organ Bath ◽  
Motor Responses ◽  
Gut Dysfunction

Proteinase-activated receptor-2 (PAR-2) and mast cell (MC) mediators contribute to inflammatory and functional gastrointestinal disorders. We aimed to characterize jejunal PAR-2-mediated responses and the potential MC involvement in the early and late phases of a rat model of postinfectious gut dysfunction. Jejunal tissues of control and Trichinella spiralis-infected (14 and 30 days postinfection) rats, treated or not with the MC stabilizer, ketotifen, were used. Histopathology and immunostaining were used to characterize inflammation, PAR-2 expression, and mucosal and connective tissue MCs. Epithelial barrier function (hydroelectrolytic transport and permeability) and motility were assessed in vitro in basal conditions and after PAR-2 activation. Intestinal inflammation on day 14 postinfection (early phase) was significantly resolved by day 30 (late phase) although MC counts and epithelial permeability remained increased. PAR-2-mediated ion transport (Ussing chambers, in vitro) and epithelial surface PAR-2 expression were reduced in the early phase, with a trend toward normalization during the late phase. In control conditions, PAR-2 activation (organ bath) induced biphasic motor responses (relaxation followed by excitation). At 14 days postinfection, spontaneous contractility and PAR-2-mediated relaxations were enhanced; motor responses were normalized on day 30. Postinfectious changes in PAR-2 functions were not affected by ketotifen treatment. We concluded that, in the rat model of Trichinella spiralis infection, alterations of intestinal PAR-2 function and expression depend on the inflammatory phase considered. A lack of a ketotifen effect suggests no interplay between MCs and PAR-2-mediated motility and ion transport alterations. These observations question the role of MC mediators in PAR-2-modulating postinfectious gut dysfunction.

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