Relevant bibliographies by topics / Intestine, Small Immunology

Academic literature on the topic 'Intestine, Small Immunology'

Author: Grafiati
Published: 4 June 2021
Last updated: 28 January 2023

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Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters

Journal articles on the topic "Intestine, Small Immunology":

1

Bland, P. W., and M. Bailey. "Immunology of the small intestine." Transplantation Proceedings 30, no. 6 (September 1998): 2560–61. http://dx.doi.org/10.1016/s0041-1345(98)00725-8.

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2

Kunisawa, Jun, Yosuke Kurashima, Morio Higuchi, Masashi Gohda, Izumi Ishikawa, Ikuko Ogahara, Namju Kim, Miki Shimizu, and Hiroshi Kiyono. "Small and large intestinal intraepithelial T lymphocytes show distinct dependency on sphingosine 1-phosphate (42.11)." Journal of Immunology 178, no. 1_Supplement (April 1, 2007): S35. http://dx.doi.org/10.4049/jimmunol.178.supp.42.11.

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Abstract It is known that the composition of intraepithelial T lymphocyte (IEL) differs between small and large intestines, but the mechanism underlying that difference remains obscure. Here, we show that sphingosine 1-phosphate (S1P) plays a key role in regulating intestinal IEL trafficking into the small and large intestines. High levels of type 1 S1P receptor (S1P1) expression was noted on naïve IELs expressing CD4 or CD8αβ, which leads to their preferential migration into the large intestine. In contrast, recent thymic emigrants (RTEs), double-positive thymocytes, and double-negative thymic T cell-committed precursors use S1P-independent trafficking pathway into the intestine. The former two populations exclusively migrate into the small intestine, while the latter double-negative thymic T cell-committed precursors migrate into both the small and large intestines. Hence, down-regulation of S1P1 expression inhibited naïve IEL migration into the intestines but did not affect the migration of thymic IEL precursors. These data are the first to demonstrate that a lipid-mediated system determines whether IELs migrate to the small or large intestine.
3

Brandl, Katharina, George Plitas, Ronald P. DeMatteo, Laura V. Hooper, and Eric G. Pamer. "MyD88-mediated signals induce in vivo production of the bactericidal lectin RegIIIγ and protect against intestinal Listeria monocytogenes infection (44.4)." Journal of Immunology 178, no. 1_Supplement (April 1, 2007): S48. http://dx.doi.org/10.4049/jimmunol.178.supp.44.4.

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Abstract Listeria monocytogenes (L. monocytogenes) is an intracellular bacterium that causes systemic infections after traversing the intestinal mucosa. To test the hypothesis that the Toll-like receptor pathway is involved in defense against intestinal L. monocytogenes infection, we analyzed the role of the common intracellular adaptor molecule myeloid differentiation primary-response protein 88 (MyD88) following oral infection with L. monocytogenes. We found that MyD88 deficient mice have increased susceptibility to intestinal L. monocytogenes infection with higher bacterial burden in spleen, liver, mesenteric lymph nodes, intestinal lumen, and small intestine (lamina propria and intestinal epithelium). Further in vitro and in vivo studies showed that MyD88 mediated protection primarily occurs in the distal small intestine. Recently, it was shown that the intestinal bactericidal lectin RegIIIγ has antibacterial activity against L. monocytogenes. RT-PCR and Western Blot analysis of distal small intestines showed that RegIIIγ is significantly diminished in MyD88 deficient mice. Since optimal expression of RegIIIγ requires MyD88-mediated signals, our findings suggest that increased susceptibility to intestinal L. monocytogenes infection in MyD88-deficient mice results from diminished levels of this bactericidal lectin in the distal small bowel.
4

Chowers, Y., W. Holtmeier, J. Harwood, E. Morzycka-Wroblewska, and M. F. Kagnoff. "The V delta 1 T cell receptor repertoire in human small intestine and colon." Journal of Experimental Medicine 180, no. 1 (July 1, 1994): 183–90. http://dx.doi.org/10.1084/jem.180.1.183.

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V delta 1 bearing T cells comprise the major population of gamma/delta T cells in the human intestinal tract. To gain insight into mechanisms involved in the generation of these cells and the diversity of their repertoire, we have characterized the junctional sequences of V delta 1 T cell receptor transcripts in the human small intestine and colon. Mucosal biopsies obtained from defined regions along the length of the small intestine or colon contained a high frequency of either one or a few identical in frame V delta 1 sequences. Less abundant sequences were also detected repeatedly throughout the length of small intestine or colon. Moreover, the intestinal V delta 1 repertoire in the small intestine and colon appeared compartmentalized and showed no overlap with the V delta 1 repertoire in peripheral blood. Dominant V delta 1 transcripts in each subject differed between the small intestine and colon, and the dominant transcripts within these sites differed among individuals. Analysis of small intestinal transcripts obtained at a 1-yr interval revealed that the V delta 1 repertoire was stable over time. The fact that the majority of V delta 1 transcripts, both dominant and rare, are distributed throughout a several meter length of the adult intestinal tract and are stable over time suggests they are not generated by an ongoing process of in situ VDJ gene rearrangement. Our results favor a model in which the repertoire of V delta 1 T cells in the intestinal tract is shaped by positive selection in response to a limited array of ligands before the migration of V delta 1 cells throughout the small intestine or colon.
5

Beagley, K. W., K. Fujihashi, A. S. Lagoo, S. Lagoo-Deenadaylan, C. A. Black, A. M. Murray, A. T. Sharmanov, M. Yamamoto, J. R. McGhee, and C. O. Elson. "Differences in intraepithelial lymphocyte T cell subsets isolated from murine small versus large intestine." Journal of Immunology 154, no. 11 (June 1, 1995): 5611–19. http://dx.doi.org/10.4049/jimmunol.154.11.5611.

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Abstract Intraepithelial lymphocytes (IELs) have been extensively studied in the murine small intestine. However, to date no studies have assessed IEL in the large intestine, despite the marked differences in function and lumenal environment. In the present study, we isolated IEL from both small and large intestine of three mouse strains (BALB/c, C3H/HeN, C57BL/6) and determined the frequency of CD2, CD4, and CD8 expression on CD3+ IEL, as well as the frequency of alpha beta and gamma delta TCR usage and V beta distribution. Higher numbers of IEL/unit length were always isolated from the small intestine (20-30 x 10(6)/5 mice) compared with large intestine (1.1-2.5 x 10(6)/5 mice). Interestingly, IEL from the large intestine of all strains were predominantly alpha beta TCR+ whereas gamma delta TCR+ IELs predominated in small intestine. Large intestinal IELs were mainly CD4+, in both BALB/c and C3H/HeN mouse strains. IELs from large intestine of C57BL/6 mice were mainly CD8+; however, the CD4+ subset was fourfold higher when compared with small intestine IEL. Potential functional differences between IEL subsets was assessed by determining the relative levels of mRNA for IL-1, 2, 4, 5, 10, IFN-gamma, TGF-beta, and TNF-gamma. Similar patterns of IL-1, IFN-gamma and TNF-alpha were seen while more IL-2, IL-4, IL-5, and IL-10 mRNA was noted in large intestinal IEL. Stimulation of C3H/HeJ IEL with anti-CD3 also resulted in higher levels of IL-3/GM-CSF, IL-4, and IL-6 by IEL from large intestine. These results show that marked differences occur among the T cell subsets present in IELs from mouse small and large intestine.
6

Allenspach, Karin. "Clinical Immunology and Immunopathology of the Canine and Feline Intestine." Veterinary Clinics of North America: Small Animal Practice 41, no. 2 (March 2011): 345–60. http://dx.doi.org/10.1016/j.cvsm.2011.01.004.

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7

Limon, Natalie M. "The Effects of Childhood, Adolescent and Adult Obesity on Epithelial T Cell Homeostasis in the Intestine." Journal of Immunology 198, no. 1_Supplement (May 1, 2017): 211.10. http://dx.doi.org/10.4049/jimmunol.198.supp.211.10.

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Abstract According to the CDC, 30% of adults in the U.S population are obese, while 17% of children and adolescents are obese. Obesity has resulted in a wide array of complications including disruption of barrier permeability as well as problems with tissue repair. The epithelial layer of the intestines contains intraepithelial intestinal lymphocytes (IEL) that are important in maintaining epithelial homeostasis and repairing tissue. To outline the mechanism by which obesity disrupts intestinal epithelial function among different age groups, childhood, adolescent, and adult mice were placed in a high fat diet (HFD) for 7 weeks to observe IEL number and function. In all age groups, mice administered a HFD exhibit a significant decrease in IEL within the epithelial layer of the small intestine. Notably, in the childhood cohort, IEL seeding is disrupted resulting in limited IEL numbers during adolescence. Interestingly, T cells in the epidermis of the skin are not reduced in number after 7 weeks of HFD suggesting that the intestine is more sensitive to early obesity. This study shows the harmful impact of obesity on the immune system in the small intestine whether obesity occurs in youth or in adulthood.
8

Wang, Jian, Fengqi Li, Haiming Wei, Zhe-Xiong Lian, Rui Sun, and Zhigang Tian. "Respiratory influenza virus infection induces intestinal immune injury via microbiota-mediated Th17 cell–dependent inflammation." Journal of Experimental Medicine 211, no. 12 (November 3, 2014): 2397–410. http://dx.doi.org/10.1084/jem.20140625.

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Influenza in humans is often accompanied by gastroenteritis-like symptoms such as diarrhea, but the underlying mechanism is not yet understood. We explored the occurrence of gastroenteritis-like symptoms using a mouse model of respiratory influenza infection. We found that respiratory influenza infection caused intestinal injury when lung injury occurred, which was not due to direct intestinal viral infection. Influenza infection altered the intestinal microbiota composition, which was mediated by IFN-γ produced by lung-derived CCR9+CD4+ T cells recruited into the small intestine. Th17 cells markedly increased in the small intestine after PR8 infection, and neutralizing IL-17A reduced intestinal injury. Moreover, antibiotic depletion of intestinal microbiota reduced IL-17A production and attenuated influenza-caused intestinal injury. Further study showed that the alteration of intestinal microbiota significantly stimulated IL-15 production from intestinal epithelial cells, which subsequently promoted Th17 cell polarization in the small intestine in situ. Thus, our findings provide new insights into an undescribed mechanism by which respiratory influenza infection causes intestinal disease.
9

Hong, Chun Pyo, Bo Gie Yang, Jung-Hwan Kim, Min Seong Jang, Eun-Jung Lee, Eun Ji Jeun, Chan Kim, Ju-Young Seoh, and Myoung Ho Jang. "High fat diet-induced obesity affects CD4+ T cell differentiation in the small intestine (P3176)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 61.13. http://dx.doi.org/10.4049/jimmunol.190.supp.61.13.

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Abstract Obesity-induced metabolic diseases are caused by the excess infiltration of pro-inflammatory cells to metabolic tissues including adipose and liver. However, systematic understanding of correlation between obesity and alterations of gut immunity is unclear. We hypothesized that immune cells in small intestine may be affected substantially upon high-fat feeding since dietary lipids are absorbed at luminal surface of small intestine. Here we found that small intestinal CD4+ and CD8+ T cells but not B cells were decreased in obese state. In CD4+ T cell subsets, the proportion of TH1 cells was increased in obese state, whereas the proportion of TH17 cells was decreased. The regulation of Intestinal T cells is dependent on antigen presenting cells such as macrophages and dendritic cells. We found intestinal macrophage subsets but not dendritic cells were changed in obese state. We next investigated that which antigen presenting cells from small intestine control CD4+ T cell differentiation during obese state ex vivo. We found that two macrophage subsets control balance of TH1 and TH17 cells inversely. These results show that small intestinal macrophages can have a key role in modulating small intestinal CD4+ T cell differentiation during obesity.
10

Vidal, Jorge E., Bruce A. McClane, Juliann Saputo, Jaquelyn Parker, and Francisco A. Uzal. "Effects of Clostridium perfringens Beta-Toxin on the Rabbit Small Intestine and Colon." Infection and Immunity 76, no. 10 (July 14, 2008): 4396–404. http://dx.doi.org/10.1128/iai.00547-08.

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ABSTRACT Clostridium perfringens type B and type C isolates, which produce beta-toxin (CPB), cause fatal diseases originating in the intestines of humans or livestock. Our previous studies demonstrated that CPB is necessary for type C isolate CN3685 to cause bloody necrotic enteritis in a rabbit ileal loop model and also showed that purified CPB, in the presence of trypsin inhibitor (TI), can reproduce type C pathology in rabbit ileal loops. We report here a more complete characterization of the effects of purified CPB in the rabbit small and large intestines. One microgram of purified CPB, in the presence of TI, was found to be sufficient to cause significant accumulation of hemorrhagic luminal fluid in duodenal, jejunal, or ileal loops treated for 6 h with purified CPB, while no damage was observed in corresponding loops receiving CPB (no TI) or TI alone. In contrast to the CPB sensitivity of the small intestine, the colon was not affected by 6 h of treatment with even 90 μg of purified CPB whether or not TI was present. Time course studies showed that purified CPB begins to induce small intestinal damage within 1 h, at which time the duodenum is less damaged than the jejunum or ileum. These observations help to explain why type B and C infections primarily involve the small intestine, establish CPB as a very potent and fast-acting toxin in the small intestines, and confirm a key role for intestinal trypsin as an innate intestinal defense mechanism against CPB-producing C. perfringens isolates.
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You might also be interested in the extended bibliographies on the topic 'Intestine, Small Immunology' for particular source types:
Journal articles Dissertations / Theses

Dissertations / Theses on the topic "Intestine, Small Immunology":

1

Masjedi, Mohsen. "Physiological inflammation of the small intestine during weaning in the rat /." Title page, table of contents and summary only, 1998. http://web4.library.adelaide.edu.au/theses/09PH/09phm3973.pdf.

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Thompson, Fiona Marie. "Activation of the mucosal immune system and growth of the small intestine at weaning /." Title page, abstract and contents only, 1994. http://web4.library.adelaide.edu.au/theses/09PH/09pht4677.pdf.

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3

Randrian, Violaine. "Role of myosin IIA in the small intestine immunosurveillance by dendritic cells." Thesis, Sorbonne Paris Cité, 2017. http://www.theses.fr/2017USPCB038/document.

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Plusieurs méthodes de capture antigénique ont été décrites dans l’intestin grêle, surtout en cas d’infection: échantillonnage direct par les cellules dendritiques (DC), capture par les macrophages qui délivrent ensuite l’antigène aux DC du stroma, passage des antigènes à travers les cellules caliciformes. Des travaux antérieurs in vitro dans le laboratoire ont montré l’importance de la myosine IIA dans la coordination de la migration des DC avec la capture et de l’apprêtement antigénique. L’objectif de ma thèse était de combiner plusieurs méthodes d’imagerie telle que la microscopie intravitale, la microscopie confocale ex vivo et l’immunofluorescence sur tissus à la cytométrie en flux pour déterminer l’impact de la myosine IIA sur la capture antigénique in vivo. Cette étude montre que les DC patrouillent en permanence dans l’épithélium de l’intestin grêle, y compris hors conditions infectieuses. Elles sont recrutées dans la lamina propria (LP) et pénètrent dans l’épithélium par transmigration à travers la membrane basale qui sépare ces deux compartiments. La myosine IIA est indispensable à la transmigration de CD103+CD11b+DC. Ces événements de transmigration surviennent plus fréquemment dans les parties proximales de l’intestin grêle, duodénum and jéjunum, que dans l’iléon. Chez les souris adultes, ces DC ne sont pas recrutées sous l’influence du microbiote mais sont sensibles au rétinal, un métabolite de la vitamine A qu’elles transforment en une molécule active l’acide trans-rétinoïque (AtRA). D’après notre analyse transcriptomique, les DC intra-épithéliales constituent une population homogène dont le profil est distinct de celui de leurs homologues de la LP. Elles sont enrichies en ARN des voies liées à l’apprêtement antigénique, l’autophagie et les lysosomes. Ces résultats suggèrent qu’elles ont une fonction différente des CD103+CD11b+DC de la LP: elles n’agissent pas sur la prolifération ni la différenciation des lymphocytes T mais contrôlent spécifiquement l’effectif des lymphocytes intra-épithéliaux CD8+αβ. Ces découvertes reflètent l’importance de l’épithélium comme première ligne de défense contre les pathogènes. Elles soulèvent également de nouvelles questions concernant la régulation de la réponse immune dans l’épithélium et les interactions mutuelles entre la lumière intestinale, l’épithélium et le stroma des villosités
Several routes for antigen capture have been described in the small intestine, mainly upon pathogenic infection: direct sampling by Dendritic Cells (DCs), sampling by macrophages that deliver antigens to DCs in the stroma, antigenic passage through goblet cells. Previous in vitro work in the lab showed that myosin IIA is essential to coordinate antigen uptake and processing with DC migration. The objective of my thesis was to combine several imaging methods including intravital microscopy, ex vivo confocal microscopy and immunofluorescence on gut tissue to flow cytometry in order to unravel the impact of myosin IIA on DC physiology in vivo. My work shows that CD103+CD11b+ DCs, which are unique to the gut, constantly patrol the epithelium of the small intestine at steady state: they are recruited from the lamina propria (LP) and penetrate into the epithelium by transmigrating through the basal membrane that separates these two compartments. DC transmigration requires myosin IIA in vivo. Remarkably, we found that DC transmigration into the epithelium occurs mainly in the upper parts of the small intestine, the duodenum and the jejunum, but is not observed in the ileum. DC transmigration does not require the gut microbiota but relies on retinal, a vitamin A metabolite of that they convert into its active form all-trans retinoic acid (AtRA). Strikingly, single cell RNA-seq showed that intra-epithelial CD103+CD11b+ DCs constitute a homogenous cell population with a distinct transcriptomic signature from their LP counterpart. They are enriched with RNA related to antigen presentation, autophagy and lysosome pathways. Our results further suggest that these cells have a different function from LP CD103+CD11b+ DCs, as they do not significantly impact proliferation or differentiation of T helper lymphocytes but control the CD8+αβ intraepithelial lymphocytes (IELs) pool. These findings highlight the importance of the epithelial tissue as a first line of defense against pathogens in the upper parts of the small intestine. They also raise new questions about the regulation of the immune response in the epithelium and the mutual influences between lumen, epithelium and intestinal lamina propria
4

Moghaddami, Mahin. "Characterization of isolated lymphoid aggregations in the mucosa of the small intestine /." Title page, abstract and contents only, 1999. http://web4.library.adelaide.edu.au/theses/09PH/09phm6959.pdf.

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Thesis (Ph.D.)--University of Adelaide, Dept. of Microbiology and Immunology, 1999.
Errata & addenda tipped in behind back end paper. Copies of author's previously published articles in pocket on back end-paper. Bibliography: leaves 147-194.
5

Guo, Weihong, and 郭衛紅. "The immune mechanisms and novel immunosuppressive approaches in experimental small bowel transplantation." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2001. http://hub.hku.hk/bib/B3124175X.

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6

Li, Xiaosong. "The mechanism study of novel approaches to control chronic allograft rejection in rat orthotopic small bowel transplantation." Click to view the E-thesis via HKUTO, 2006. http://sunzi.lib.hku.hk/hkuto/record/B36395778.

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Li, Xiaosong, and 李小松. "The mechanism study of novel approaches to control chronic allograft rejection in rat orthotopic small bowel transplantation." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B36395778.

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8

Lemmey, Andrew Bruce. "Effects of insulin-like growth factors (IGFS) on recovery from gut resection in rats : a thesis submitted to the University of Adelaide, South Australia for the degree of Doctor of Philosophy." 1992, 1993. http://web4.library.adelaide.edu.au/theses/09PH/09phl554.pdf.

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Includes bibliographical references (leaves 159-213) Shows that IGF-I peptides are effective in diminishing post-surgical catabolism and enhancing adaptive gut hyperplasia in rats recovering from massive small bowel resection.
9

Ou, Gangwei. "Human intestinal epithelial cells in innate immunity : interactions with normal microbiota and pathogenic bacteria." Doctoral thesis, Umeå : Umeå University, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-18388.

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10

Galvao, Flávio Henrique Ferreira. "Modelo experimental de doença do enxerto versus hospedeiro após transplante de intestino delgado." Universidade de São Paulo, 1998. http://www.teses.usp.br/teses/disponiveis/5/5132/tde-13072011-171433/.

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A doença do enxerto versus hospedeiro (DEVH) é uma grave complicação do transplante de órgãos sólidos, com alta mortalidade. Seu estudo tem sido limitado pela carência de modelos experimentais apropriados. Descreve-se um modelo de DEVH baseado no aumento do quimerismo, sua evolução clínica, histopatológica, do número das células quiméricas, do perfil das citocinas e da tolerância imunológica. Ratos Lewis (LEW) foram submetidos a transplante simultâneo de intestino delgado e medula óssea provenientes de ratos ACI (grupo de estudo - E) ou LEW (grupo controle - C), tratados com FK-506 (1 mg/Kg/dia) entre o 0 e 13o PO, e uma dose semanal daí por diante. Os ratos foram divididos nos seguintes grupos: E1- 6 ratos sacrificados no 120o PO. E2- 8 ratos após apresentarem sinais clínicos graves de DEVH entre o 189o e o 271o PO. Como controle, ratos LEW foram receptores dos mesmos tipos de enxertos provenientes de ratos LEW, submetidos à mesma imunossupressão e foram assim divididos: C1- 6 ratos sacrificados no 120o PO, C2- 5 ratos sacrificados entre o 223o e o 270o PO. A citometria de fluxo foi realizada para quantificar a porcentagem das células linfóides de ACI doadores no sangue periférico nos E1, E2 em 6 períodos: 30o PO, 65o PO, 95o PO, 120o PO, 160o PO, 200o PO. Os animais foram examinados 2 vezes por semana à procura de sinais de DEVH (rash cutâneo, perda de peso, de pelo e hiperqueratose). No sacrifício dos animais do grupo E1 e C1, foram colhidas amostras de língua (LI), de linfonodos cervicais (LC), intestino delgado do receptor e do enxerto para análise das citocinas IL-2, IL-4, IL-6, IL-10, IFN-gama e TNF-alfa por meio da reação em cadeia da polimerase. Em todos os grupos foram também colhidas amostras destes órgãos para histopatologia e nos animais do grupo E2 linfonodos cervicais foram processados para análise da reatividade celular por meio da reação mista dos linfócitos (MLR). A evolução clínica e histopatológica foi graduada de 0 a 3 de acordo com a severidade dos sintomas e do infiltrado mononuclear das amostras. Os ratos dos grupos E1 e E2 iniciaram sinais da DEVH entre o 84o e 115o PO. Os ratos dos grupos C1 e C2 não apresentaram evidência de DEVH. Amostras de LI e LC dos ratos do grupo E1 apresentaram alterações histopatológicas grau 2 e do grupo E2 apresentaram alterações histopatológicas grau 3, respectivamente. Nenhuma alteração histopatológica foi encontrada nos ratos do grupo controle e em amostras do ID. Nenhuma alteração histopatológica foi encontrada no intestino delgado do receptor e do enxerto. O aumento da porcentagem de células do doador no sangue periférico do receptor foi progressivo chegando a 5,4±2.3% no 10o período, 21±4,6% no 3o período e 39,3±4% no 6o período. IL-2, IL-6, IL-10, IFN-gma e TNF-alfa estiveram aumentados em língua e IL-4, IL-6, IL-10, IFN-gama e TNF-alfa em linfonodos cervicais. Os linfócitos de ratos do grupo E2 mostraram hiporreatividade aos de ratos ACI e hiperreatividade aos de ratos PVG (terceira parte) denotando tolerância imunológica. Neste modelo experimental há uma inexorável evolução imunológica para DEVH; existe correlação direta entre o aumento do quimerismo em sangue periférico e da expressão de citocinas em língua e linfonodos cervicais e a severidade da DEVH, além da indução de tolerância imunológica do rato do grupo E2 quimérico ao rato ACI normal.
Graft-versus-host disease (GVHD) has been a major concern after small bowel transplantation (SBTX) and the lack of suitable experimental models has limited the study of GVHD after solid organ transplantation. Here we describe a re1evant experimental model of GVHD after fully allogeneic SBTX based on chimerism augmentation, its clinical and histophatological evolution, cytokine involvement, responsible donor cell and immunologic tolerance analysis. LEW rat recipients received orthotopic SBTX and simultaneous donor bone marrow cell infusion (250x106), from ACI rats (experimental group - E) or LEW (control group C). FK-506 was administered dayly at a dose of 1 mg/kg on day 0 to 13, then continued as a weekly injection of same dose until the experimental end point. The recipients were divided in the following groups: E1 - 6 rats sacrificed at 120° POD. E2 - 8 rats sacrificed with critical GVHD between DPO 189 to 271. LEW recipient of LEW grafts, under the same immunossupression were used as control and divided as: C1 - 6 rats sacrificed at POD 120; C2- 5 rats sacrificed between 223 and 270 POD the number of donor cell in the recipient circulation was determined by flowcytometry in 6 pos-operative time: 30, 65, 95, 120, 160, 200. The rats were analyzed twice a week for body weigh and searching for signs of GVHD (cutaneous rush, hiperkeratosis and loss of hair and body weigh). At the sacrificed, samples from tongue (TG), cervical lymph node (CLN), donor (SBD) and recipient (SBR) small bowel were taken from all animals for histophatology and from E1 and C1l animals for IL-2, IL-4, IL-6, IL-10, IFN-gama e TNF-alfa cytokines analysis using reverse transcription polymerase chain reaction. Samples from cervical lynph nodes of 5 animals from group E2 were used for mixed lymphocyte reaction for tolerance analysis. The clinical and histophatological evolution of the disease were evaluated from degree 0 to 3 according to the severity. GVHD in E1 and E2 animals started between 84 and 115 POD. Histophatological analysis of TG and CLN showed that E1 animals present GVHD grade 2 and E2 animals grade 3. The increase of donors cells in the recipient circulation was progressive and account for 5.4± 2.3% at POD 30, 21.4±4.6% at POD 95 and 39.3±4% at POD 200. IL-4, IL-6, IL-10, IFN-gama e TNF-alfa were upregulated in CLN and IL-2, IL-6, IL-10, IFN-gama e TNF-alfa were upregulated in TG when compared with the respective controls. The lymphocytes from E2 group showed hyporeactivety to lymphocytes of normal ACI and hypereactivety to those of PVG, meaning tolerance. No cytokines alteration was noted in SBD neither SBR. Animals from group C1 and C2 did not present any sign of disease. This result show that GVHD is a inexoravel evolution under the experimental conditions of this study and the evolution of the disease is near correlated with the augmentation of the donor cells in the recipient circulation and upregulation of cytokines gene expression in target organs. Tolerance to the same donor strain lynphocytes was also noted.
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Books on the topic "Intestine, Small Immunology":

1

N, Marsh Michael, ed. Immunopathology of the small intestine. Chichester [West Sussex]: Wiley, 1987.

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2

R, Grant David, and Wood Richard F. M, eds. Small bowel transplantation. London: E. Arnold, 1994.

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3

Small Bowel Transplantation (Hodder Arnold Publication). A Hodder Arnold Publication, 1996.

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4

E, Deltz, Thiede Arnulf, and Hamelmann H, eds. Small-bowel transplantation: Experimental and clinical fundamentals. Berlin: Springer-Verlag, 1986.

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Deltz, Eberhard, and Arnluf Thiede. Small-Bowel Transplantation: Experimental and Clinical Fundamentals. Springer-Verlag, 1987.

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6

Deltz, Eberhard. Small-Bowel Transplantation: Experimental and Clinical Fundamentals. Springer, 2011.

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7

Deltz, Eberhard, Arnulf Thiede, and Horst Hamelmann. Small-Bowel Transplantation: Experimental and Clinical Fundamentals. Springer London, Limited, 2012.

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8

Effects of immune cells and inflammation on smooth muscle and enteric nerves. Boca Raton, Fla: CRC Press, 1991.

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Book chapters on the topic "Intestine, Small Immunology":

1

Judge, Thomas. "The Small Bowel in Immunology." In Clinical Imaging of the Small Intestine, 29–37. New York, NY: Springer New York, 1999. http://dx.doi.org/10.1007/978-0-387-21565-5_3.

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2

Esses, Steven J., and Lloyd Mayer. "Mucosal Immunology of the Intestine." In Practical Gastroenterology and Hepatology: Small and Large Intestine and Pancreas, 23–27. Oxford, UK: Wiley-Blackwell, 2010. http://dx.doi.org/10.1002/9781444328417.ch4.

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3

Greney, Ph, E. Candolfi, and T. T. Kien. "Specific IgA response in small intestine during experimental toxoplasmosis." In Advances in Mucosal Immunology, 829–30. Dordrecht: Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-009-1848-1_261.

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Cummins, A. G., F. M. Thompson, L. Spargo, and G. Mayrhofer. "Maturation of the small intestine at weaning in the nude hypothymic rat." In Advances in Mucosal Immunology, 481–82. Dordrecht: Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-009-1848-1_142.

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Mowat, A. Mcl, A. J. Edwards, and I. N. Crispe. "T cell receptor expression by CD8+ intraepithelial lymphocytes from mouse small intestine." In Advances in Mucosal Immunology, 83–85. Dordrecht: Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-009-1848-1_21.

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Simister, N. E., and K. E. Mostov. "Functional expression of an Fc receptor cloned from neonatal rat small intestine." In Advances in Mucosal Immunology, 293–97. Dordrecht: Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-009-1848-1_83.

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Ferguson, Anne, and T. T. MacDonald. "Effects of Local Delayed Hypersensitivity on the Small Intestine." In Ciba Foundation Symposium 46 - Immunology of the Gut, 305–27. Chichester, UK: John Wiley & Sons, Ltd., 2008. http://dx.doi.org/10.1002/9780470720288.ch15.

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Trejdosiewicz, L. K., G. Malizia, S. Badr-el-Din, C. J. Smart, D. J. Oakes, J. Southgate, P. D. Howdle, G. Janossy, L. W. Poulter, and M. S. Losowsky. "T Cell and Mononuclear Phagocyte Populations of the Human Small and Large Intestine." In Recent Advances in Mucosal Immunology, 465–73. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-5344-7_54.

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9

Felstein, M. V., and A. McI Mowat. "Induction of Proliferative and Destructive Graft-Versus-Host Reactions in the Small Intestine." In Recent Advances in Mucosal Immunology, 653–60. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-5344-7_77.

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Nemirovsky, M. S., and N. Després. "Immunological and Immunopathological Characterization of a Mucosal Antigen from Guinea Pig Small Intestine." In Recent Advances in Mucosal Immunology, 783–89. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-5344-7_91.

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