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Vol. 32. Issue S2.
Psicología y enfermedad inflamatoria intestinal
Pages 55-61 (October 2009)
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Vol. 32. Issue S2.
Psicología y enfermedad inflamatoria intestinal
Pages 55-61 (October 2009)
Psicología y enfermedad inflamatoria intestinal
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Bases celulares y moleculares de la disfunción de la barrera intestinal inducida por estrés experimental
Cellular and molecular bases of intestinal barrier dysfunction induced by experimental stress
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Luis Menchén
Sección de Gastroenterología, Servicio de Aparato Digestivo, Hospital General Universitario Gregorio Marañón, y CIBEREHD, Madrid, España
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Resumen

Existe la impresión generalizada de que las situaciones vitales estresantes influyen en el curso clínico de una amplia variedad de enfermedades gastrointestinales, entre las que se encuentra la enfermedad inflamatoria intestinal. Sin embargo, la demostración causal de esta asociación resulta compleja y los resultados obtenidos en estudios clínicos son discordantes. En los últimos años, la utilización de modelos experimentales de estrés en animales de laboratorio ha proporcionado una sólida evidencia acerca de las consecuencias fisiopatológicas del estrés en el tubo digestivo así como de los mecanismos celulares y moleculares que subyacen a la relación entre el estrés físico y/o psicológico y las enfermedades gastrointestinales. En el caso de la enfermedad inflamatoria intestinal, la marcada disfunción de barrera intestinal relacionada principalmente con el incremento de la permeabilidad epitelial paracelular inducida por estrés podría ser responsable, al menos en parte, de la reactivación y del incremento de la gravedad de la enfermedad inflamatoria intestinal que se ha observado en varios modelos experimentales de estrés.

Palabras clave:
Enfermedad inflamatoria intestinal
Barrera intestinal
Mastocitos
Células epiteliales intestinales
CRF
PPARgamma
Abstract

There is a widespread impression that stressful life situations influence the clinical course of a wide variety of gastrointestinal disorders, including inflammatory bowel disease. However, demonstrating a causal relationship is complex and the results obtained in clinical studies are contradictory. In the last few years, the use of experimental stress models in laboratory animals have provided solid evidence of the physiopathological effects of stress on the digestive tract as well as of the cellular and molecular mechanisms underlying the association between physical and/or psychological stress and gastrointestinal disorders.

In inflammatory bowel disease, the marked intestinal barrier dysfunction, which is mainly related to the stress-induced increase in paracellular epithelial permeability, could be partially responsible for the reactivation and increase in the severity of inflammatory bowel disease observed in various experimental stress models.

Keywords:
Inflammatory bowel disease
Intestinal barrier
Mastocytes
Intestinal epithelials cells
CRF
PPARgamma
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Bibliografía
[1.]
H. Selye.
A syndrome produced by diverse nocuous agents.
Nature, 138 (1936), pp. 32
[2.]
H. Selye.
Stress and the general adaptation syndrome.
Br Med J, 1 (1950), pp. 1383-1392
[3.]
B.S. McEwen.
Protective and damaging effects of stress mediators.
N Engl J Med, 338 (1998), pp. 171-179
[4.]
J.R. Caso, J.C. Leza, L. Menchen.
The effects of physical and psychological stress on the gastro-intestinal tract: lessons from animal models.
Curr Mol Med, 8 (2008), pp. 299-312
[5.]
J. Fioramonti, G.F. Gebhart.
In vivo and transgenic animal models used to study visceral hypersensitivity.
Neurogastroenterol Motil, 19 (2007), pp. 20-28
[6.]
Y. Tache, V. Martínez, M. Million, L. Wang.
Stress and the gastrointestinal tract III. Stress-related alterations of gut motor function: role of brain corticotropin-releasing factor receptors.
Am J Physiol Gastrointest Liver Physiol, 280 (2001), pp. G173-G177
[7.]
J.G. Magalhaes, I. Tattoli, S.E. Girardin.
The intestinal epithelial barrier: how to distinguish between the microbial flora and pathogens.
Semin Immunol, 19 (2007), pp. 106-115
[8.]
J.R. Turner.
Molecular basis of epithelial barrier regulation: from basic mechanisms to clinical application.
Am J Pathol, 169 (2006), pp. 1901-1909
[9.]
L. Ferrier, L. Mazelin, N. Cenac, P. Desreumaux, A. Janin, D. Emilie, et al.
Stress-induced disruption of colonic epithelial barrier: role of interferon-gamma and myosin light chain kinase in mice.
Gastroenterology, 125 (2003), pp. 795-804
[10.]
S. Fagarasan, T. Honjo.
Intestinal IgA synthesis: regulation of front-line body defences.
Nat Rev Immunol, 3 (2003), pp. 63-72
[11.]
A. Ponferrada, J.R. Caso, L. Alou, A. Colon, D. Sevillano, M.A. Moro, et al.
The role of PPARgamma on restoration of colonic homeostasis after experimental stress-induced inflammation and dysfunction.
Gastroenterology, 132 (2007), pp. 1791-1803
[12.]
M.A. McGuckin, R. Eri, L.A. Simms, T.H. Florin, G. Radford-Smith.
Intestinal barrier dysfunction in inflammatory bowel diseases.
Inflamm Bowel Dis, 15 (2009), pp. 100-113
[13.]
F. Casellas, S. Aguade, B. Soriano, A. Accarino, J. Molero, L. Guarner.
Intestinal permeability to 99mTc-diethylenetriaminopentaacetic acid in inflammatory bowel disease.
Am J Gastroenterol, 81 (1986), pp. 767-770
[14.]
D. Hollander, C.M. Vadheim, E. Brettholz, G.M. Petersen, T. Delahunty, J.I. Rotter.
Increased intestinal permeability in patients with Crohn's disease and their relatives. A possible etiologic factor.
Ann Intern Med, 105 (1986), pp. 883-885
[15.]
K.D. Katz, D. Hollander, C.M. Vadheim, C. McElree, T. Delahunty, V.D. Dadufalza, et al.
Intestinal permeability in patients with Crohn's disease and their healthy relatives.
Gastroenterology, 97 (1989), pp. 927-931
[16.]
S. Buhner, C. Buning, J. Genschel, K. Kling, D. Herrmann, A. Dignass, et al.
Genetic basis for increased intestinal permeability in families with Crohn's disease: role of CARD15 3020insC mutation?.
[17.]
J.D. Soderholm, G. Olaison, K.H. Peterson, L.E. Franzen, T. Lindmark, M. Wiren, et al.
Augmented increase in tight junction permeability by luminal stimuli in the non-inflamed ileum of Crohn's disease.
Gut, 50 (2002), pp. 307-313
[18.]
P. Marteau, J.F. Colombel, J. Nemeth, J.P. Vaerman, J.C. Dive, J.C. Rambaud.
Immunological study of histologically non-involved jejunum during Crohn's disease: evidence for reduced in vivo secretion of secretory IgA.
Clin Exp Immunol, 80 (1990), pp. 196-201
[19.]
S. Balzan, C. De Almeida Quadros, R. De Cleva, B. Zilberstein, I. Cecconello.
Bacterial translocation: overview of mechanisms and clinical impact.
J Gastroenterol Hepatol, 22 (2007), pp. 464-471
[20.]
W. Strober, I. Fuss, P. Mannon.
The fundamental basis of inflammatory bowel disease.
J Clin Invest, 117 (2007), pp. 514-521
[21.]
Q. Aziz, D.G. Thompson.
Brain-gut axis in health and disease.
Gastroenterology, 114 (1998), pp. 559-578
[22.]
H.R. Berthoud, L.A. Blackshaw, S.J. Brookes, D. Grundy.
Neuroanatomy of extrinsic afferents supplying the gastrointestinal tract.
Neurogastroenterol Motil, 16 (2004), pp. 28-33
[23.]
P.A. Anton, F. Shanahan.
Neuroimmunomodulation in inflammatory bowel disease. How far from “bench” to “bedside”?.
Ann N Y Acad Sci, 840 (1998), pp. 723-734
[24.]
M. Gue, C. Bonbonne, J. Fioramonti, J. More, C. Del Río-Lacheze, C. Comera, et al.
Stress-induced enhancement of colitis in rats: CRF and arginine vasopressin are not involved.
Am J Physiol, 272 (1997), pp. G84-91
[25.]
A.L. Colon, J.L. Madrigal, L.A. Menchen, M.A. Moro, I. Lizasoain, P. Lorenzo, et al.
Stress increases susceptibility to oxidative/nitrosative mucosal damage in an experimental model of colitis in rats.
Dig Dis Sci, 49 (2004), pp. 1713-1721
[26.]
R. Glaser, J.K. Kiecolt-Glaser.
Stress-induced immune dysfunction: implications for health.
Nat Rev Immunol, 5 (2005), pp. 243-251
[27.]
P.R. Saunders, P. Miceli, B.A. Vallance, L. Wang, S. Pinto, G. Tougas, et al.
Noradrenergic and cholinergic neural pathways mediate stress-induced reactivation of colitis in the rat.
Auton Neurosci, 124 (2006), pp. 56-68
[28.]
P.R. Saunders, N.P. Hanssen, M.H. Perdue.
Cholinergic nerves mediate stress-induced intestinal transport abnormalities in Wistar-Kyoto rats.
Am J Physiol, 273 (1997), pp. G486-G490
[29.]
A.J. Kiliaan, P.R. Saunders, P.B. Bijlsma, M.C. Berin, J.A. Taminiau, J.A. Groot, et al.
Stress stimulates transepithelial macromolecular uptake in rat jejunum.
Am J Physiol, 275 (1998), pp. G1037-G1044
[30.]
L.C. Yu, M.H. Perdue.
Role of mast cells in intestinal mucosal function: studies in models of hypersensitivity and stress.
Immunol Rev, 179 (2001), pp. 61-73
[31.]
G. Barbara, V. Stanghellini, R. De Giorgio, R. Corinaldesi.
Functional gastrointestinal disorders and mast cells: implications for therapy.
Neurogastroenterol Motil, 18 (2006), pp. 6-17
[32.]
T.-J. Lin, A.D. Befus.
Mast cells in mucosal defenses and pathogenesis.
3rd ed., pp. 703-715
[33.]
J. Santos, M. Benjamin, P.C. Yang, T. Prior, M.H. Perdue.
Chronic stress impairs rat growth and jejunal epithelial barrier function: role of mast cells.
Am J Physiol Gastrointest Liver Physiol, 278 (2000), pp. G847-G854
[34.]
I. Castagliuolo, J.T. Lamont, B. Qiu, S.M. Fleming, K.R. Bhaskar, S.T. Nikulasson, et al.
Acute stress causes mucin release from rat colon: role of corticotropin releasing factor and mast cells.
Am J Physiol, 271 (1996), pp. G884-G892
[35.]
T.C. Theoharides, R. Letourneau, P. Patra, L. Hesse, X. Pang, W. Boucher, et al.
Stress-induced rat intestinal mast cell intragranular activation and inhibitory effect of sulfated proteoglycans.
Dig Dis Sci, 44 (1999), pp. 87S-93S
[36.]
B.S. Qiu, B.A. Vallance, P.A. Blennerhassett, S.M. Collins.
The role of CD4+ lymphocytes in the susceptibility of mice to stress-induced reactivation of experimental colitis.
Nat Med, 5 (1999), pp. 1178-1182
[37.]
M.E. Truckenmiller, M.F. Princiotta, C.C. Norbury, R.H. Bonneau.
Corticosterone impairs MHC class I antigen presentation by dendritic cells via reduction of peptide generation.
J Neuroimmunol, 160 (2005), pp. 48-60
[38.]
M.D. Elftman, C.C. Norbury, R.H. Bonneau, M.E. Truckenmiller.
Corticosterone impairs dendritic cell maturation and function.
Immunology, 122 (2007), pp. 279-290
[39.]
N. Fazal, M. Shamim, S.S. Khan, R.L. Gamelli, M.M. Sayeed.
Neutrophil depletion in rats reduces burn-injury induced intestinal bacterial translocation.
Crit Care Med, 28 (2000), pp. 1550-1555
[40.]
M.F. Kagnoff, L. Eckmann.
Epithelial cells as sensors for microbial infection.
J Clin Invest, 100 (1997), pp. 6-10
[41.]
H.C. Jung, L. Eckmann, S.K. Yang, A. Panja, J. Fierer, E. Morzycka-Wroblewska, et al.
A distinct array of proinflammatory cytokines is expressed in human colon epithelial cells in response to bacterial invasion.
J Clin Invest, 95 (1995), pp. 55-65
[42.]
Y. Yu, S. Sitaraman, A.T. Gewirtz.
Intestinal epithelial cell regulation of mucosal inflammation.
Immunol Res, 29 (2004), pp. 55-68
[43.]
T.L. Bale, W.W. Vale.
CRF and CRF receptors: role in stress responsivity and other behaviors.
Annu Rev Pharmacol Toxicol, 44 (2004), pp. 525-557
[44.]
Y. Tache, M.H. Perdue.
Role of peripheral CRF signalling pathways in stress-related alterations of gut motility and mucosal function.
Neurogastroenterol Motil, 16 (2004), pp. 137-142
[45.]
Y. Tache, B. Bonaz.
Corticotropin-releasing factor receptors and stress-related alterations of gut motor function.
J Clin Invest, 117 (2007), pp. 33-40
[46.]
M.G. Gareau, J. Jury, P.C. Yang, G. MacQueen, M.H. Perdue.
Neonatal maternal separation causes colonic dysfunction in rat pups including impaired host resistance.
[47.]
J. Santos, P.R. Saunders, N.P. Hanssen, P.C. Yang, D. Yates, J.A. Groot, et al.
Corticotropin-releasing hormone mimics stress-induced colonic epithelial pathophysiology in the rat.
Am J Physiol, 277 (1999), pp. G391-G399
[48.]
H.J. Lenz.
Regulation of duodenal bicarbonate secretion during stress by corticotropin-releasing factor and beta-endorphin.
Proc Natl Acad Sci USA, 86 (1989), pp. 1417-1420
[49.]
J.B. Meddings, M.G. Swain.
Environmental stress-induced gastrointestinal permeability is mediated by endogenous glucocorticoids in the rat.
Gastroenterology, 119 (2000), pp. 1019-1028
[50.]
D. Moriarty, N. Selve, A.W. Baird, J. Goldhill.
Potent NK1 antagonism by SR-140333 reduces rat colonic secretory response to immunocyte activation.
Am J Physiol Cell Physiol, 280 (2001), pp. C852-C858
[51.]
K. Ikeda, K. Miyata, A. Orita, H. Kubota, T. Yamada, K. Tomioka.
RP67580, a neurokinin1 receptor antagonist, decreased restraint stress-induced defecation in rat.
Neurosci Lett, 198 (1995), pp. 103-106
[52.]
I. Castagliuolo, S.E. Leeman, E. Bartolak-Suki, S. Nikulasson, B. Qiu, R.E. Carraway, et al.
A neurotensin antagonist, SR 48692, inhibits colonic responses to immobilization stress in rats.
Proc Natl Acad Sci USA, 93 (1996), pp. 12611-12615
[53.]
F. Barreau, C. Cartier, L. Ferrier, J. Fioramonti, L. Bueno.
Nerve growth factor mediates alterations of colonic sensitivity and mucosal barrier induced by neonatal stress in rats.
Gastroenterology, 127 (2004), pp. 524-534
[54.]
S.J. Middleton, M. Shorthouse, J.O. Hunter.
Increased nitric oxide synthesis in ulcerative colitis.
Lancet, 341 (1993), pp. 465-466
[55.]
D. Rachmilewitz, J.S. Stamler, D. Bachwich, F. Karmeli, Z. Ackerman, D.K. Podolsky.
Enhanced colonic nitric oxide generation and nitric oxide synthase activity in ulcerative colitis and Crohn's disease.
Gut, 36 (1995), pp. 718-723
[56.]
B. Zingarelli, S. Cuzzocrea, C. Szabo, A.L. Salzman.
Mercaptoethylguanidine, a combined inhibitor of nitric oxide synthase and peroxynitrite scavenger, reduces trinitrobenzene sulfonic acidinduced colonic damage in rats.
J Pharmacol Exp Ther, 287 (1998), pp. 1048-1055
[57.]
L.A. Menchen, A.L. Colon, M.A. Moro, J.C. Leza, I. Lizasoain, P. Menchen, et al.
N-(3-(aminomethyl)benzyl)acetamidine, an inducible nitric oxide synthase inhibitor, decreases colonic inflammation induced by trinitrobenzene sulphonic acid in rats.
Life Sci, 69 (2001), pp. 479-491
[58.]
L. Menchen, A.L. Colon, J.L. Madrigal, L. Beltrán, S. Botella, I. Lizasoain, et al.
Activity of inducible and neuronal nitric oxide synthases in colonic mucosa predicts progression of ulcerative colitis.
Am J Gastroenterol, 99 (2004), pp. 1756-1764
[59.]
S. Heikkinen, J. Auwerx, C.A. Argmann.
PPARgamma in human and mouse physiology.
Biochim Biophys Acta, 1771 (2007), pp. 999-1013
[60.]
C. Blanquart, O. Barbier, J.C. Fruchart, B. Staels, C. Glineur.
Peroxisome proliferator-activated receptors: regulation of transcriptional activities and roles in inflammation.
J Steroid Biochem Mol Biol, 85 (2003), pp. 267-273
[61.]
P. Delerive, J.C. Fruchart, B. Staels.
Peroxisome proliferator-activated receptors in inflammation control.
J Endocrinol, 169 (2001), pp. 453-459
[62.]
L. Fajas, D. Auboeuf, E. Raspe, K. Schoonjans, A.M. Lefebvre, R. Saladin, et al.
The organization, promoter analysis, and expression of the human PPARgamma gene.
J Biol Chem, 272 (1997), pp. 18779-18789
[63.]
C.G. Su, X. Wen, S.T. Bailey, W. Jiang, S.M. Rangwala, S.A. Keilbaugh, et al.
A novel therapy for colitis utilizing PPAR-gamma ligands to inhibit the epithelial inflammatory response.
J Clin Invest, 104 (1999), pp. 383-389
[64.]
J.D. Lewis, G.R. Lichtenstein, J.J. Deren, B.E. Sands, S.B. Hanauer, J.A. Katz, et al.
Rosiglitazone for active ulcerative colitis: a randomized placebo-controlled trial.
Gastroenterology, 134 (2008), pp. 688-695
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