Localized colonic inflammation increases cytokine levels in distant small intestinal segments in the rat

Barada, Kassem; Mourad, Fadi H.; Sawah, Sarah I.; Khoury, Carmen I.; Safieh‐Garabedian, Bared; Nassar, Camille F.; Saadé, Nayef E.

doi:10.1016/j.lfs.2006.06.047

Cited by 20 publications

(10 citation statements)

References 51 publications

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“…In these patients, Peyer's patches in the inflamed ileum appear abnormal with irregular dome and surrounding villous atrophy (51), suggesting these gut-associated lymphoid tissues may be involved in the development of ileal lesions. Indeed, there is a substantial increase in proinflammatory cytokines in the ileum during human colitis and even in rats with experimentally induced colitis (52)(53)(54). In this study, soy peptide supplementation lowered expression of IFNG, TNF, and IL12B, which were all elevated in the POS group.…”

Section: Discussionsupporting

confidence: 44%

Soy-Derived Di- and Tripeptides Alleviate Colon and Ileum Inflammation in Pigs with Dextran Sodium Sulfate-Induced Colitis3

Young

Ibuki

Nakamori

et al. 2012

The Journal of Nutrition

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We evaluated the antiinflammatory activity of soy-derived di- and tripeptides in a dextran sodium sulfate (DSS)-induced pig model of intestinal inflammation. In the DSS-positive control (POS) and DSS-positive with soy peptide treatment (SOY) groups (n = 6/group), DSS was administered to piglets via i.g. catheter for 5 d, followed by a 5-d administration of saline or soy-derived peptides, respectively. A negative control (NEG) group received saline in lieu of the DSS and soy peptides. The severity of inflammation was assessed by clinical signs, morphological and histological measurements, gut permeability, and neutrophil infiltration. Local production of TNF and IL6 were measured by ELISA, colonic and ileal inflammatory gene expression were assessed by real-time RT-PCR, and CD4+CD25+ lymphocyte populations were analyzed by flow cytometry. Crypt elongation and muscle thickness, d-mannitol gut permeation, colonic expression of the inflammatory mediators IFNG, IL1B, TNF, RORC, and IL17A as well as the FOXP3 T-regulatory transcription factor, and myeloperoxidase activity were lower (P < 0.05) in the SOY pigs than in POS pigs. Messenger RNA levels of ileal IFNG, TNF, IL12B, and IL17A were lower (P < 0.05) and FOXP3 expression was greater (P < 0.05) in SOY piglets than in the POS group. In the mesenteric lymph nodes, CD4+CD25+ T cells were higher (P < 0.05) in both the POS and SOY groups than in NEG controls. Soy-derived peptides exert antiinflammatory activity in vivo, suggesting their usefulness for the treatment of inflammatory disorders.

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Section: Discussionsupporting

confidence: 44%

Soy-Derived Di- and Tripeptides Alleviate Colon and Ileum Inflammation in Pigs with Dextran Sodium Sulfate-Induced Colitis3

Young

Ibuki

Nakamori

et al. 2012

The Journal of Nutrition

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“…In addition to neuromuscular plasticity within the region of inflammation, there are often changes in neuromuscular function outside this area. These include reduced small bowel motility or intestinal secretory dysfunction during localized colitis in humans (2,9,35,37,48,58) and in experimental models (3,4,10,23,24,44). Systemic inflammatory cytokines or other endocrine signals may directly stimulate the upper bowel (4), but it is equally likely that there is a neural mechanism for altered upper gut dysfunction.…”

mentioning

confidence: 99%

Enhanced excitability of guinea pig inferior mesenteric ganglion neurons during and following recovery from chemical colitis

Linden

2012

American Journal of Physiology-Gastrointestinal and Liver Physi

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Linden DR. Enhanced excitability of guinea pig inferior mesenteric ganglion neurons during and following recovery from chemical colitis. Am J Physiol Gastrointest Liver Physiol 303: G1067-G1075, 2012. First published September 6, 2012 doi:10.1152/ajpgi.00226.2012.-Postganglionic sympathetic neurons in the prevertebral ganglia (PVG) provide ongoing inhibitory tone to the gastrointestinal tract and receive innervation from mechanosensory intestinofugal afferent neurons primarily located in the colon and rectum. This study tests the hypothesis that colitis alters the excitability of PVG neurons. Intracellular recording techniques were used to evaluate changes in the electrical properties of inferior mesenteric ganglion (IMG) neurons in the trinitrobenzene sulfonic acid (TNBS) and acetic acid models of guinea pig colitis. Visceromotor IMG neurons were hyperexcitable 12 and 24 h, but not 6 h, post-TNBS during "acute" inflammation. Hyperexcitability persisted at 6 days post-TNBS during "chronic" inflammation, as well as at 56 days post-TNBS when colitis had resolved. In contrast, there was only a modest decrease in the current required to elicit an action potential at 24 h after acetic acid administration. Vasomotor neurons from inflamed preparations exhibited normal excitability. The excitatory effects of XE-991, a blocker of the channel that contributes to the M-type potassium current, and heteropodatoxin-2, a blocker of the channel that contributes to the A-type potassium current, were unchanged in TNBS-inflamed preparations, suggesting that these currents did not contribute to hyperexcitability. Riluzole, an inhibitor of persistent sodium currents, caused tonic visceromotor neurons to accommodate to sustained current pulses, regardless of the inflammatory state of the preparation, and restored a normal rheobase in neurons from TNBS-inflamed preparations but did not alter the rheobase of control preparations, suggesting that enhanced activity of voltage-gated sodium channels may contribute to colitis-induced hyperexcitability. Collectively, these data indicate that enhanced sympathetic drive as a result of hyperexcitable visceromotor neurons may contribute to small bowel dysfunction during colitis. intracellular electrophysiology; postganglionic sympathetic; inflammation INFLAMMATION OF THE GASTROINTESTINAL tract is associated with numerous changes in the neuromuscular apparatus. Within the region of inflammation, there is generally smooth muscle hyperplasia with reduced contractility (11,20,43,45,47), enhanced excitability of intrinsic primary afferent neurons (32,33,46), and neuronal cell loss (12,31). In addition to neuromuscular plasticity within the region of inflammation, there are often changes in neuromuscular function outside this area. These include reduced small bowel motility or intestinal secretory dysfunction during localized colitis in humans (2,9,35,37,48,58) and in experimental models (3,4,10,23,24,44). Systemic inflammatory cytokines or other endocrine signals may directly stimulate the upper bow...

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“…Although TNBS is administered in the rectum, it also alters the small intestine without any 249 overt histological lesions in rats suggesting a remote effect of the colitis on the upper 250 intestine. 24,37 In wild-type mice, we did not find any overt duodenitis or ileitis but we 251 observed an increase in pro-inflammatory cytokines (TNF-α and IFN-γ) concentration, 252…”

Section: Ifn-γ and Tnf-α Increase Intestinal Paracellular Permeabilitmentioning

confidence: 72%

“…at a significant distance from the gut 119 injury) without histological lesions. 24 Three days after instillation, mice were sacrificed and 120 the severity of inflammation was assessed ( Figure 2). In the distal colon, TNBS 121 administration induced a robust inflammation as evidenced by decreased body weight, 122 increased disease activity index (DAI), reduced colon length and high macroscopic Wallace 123 damage scores (Figure 2A-D).…”

Section: Gut Injury Leads To Epithelial Nod2 Expression and Cytokine mentioning

confidence: 99%

Nod2 protects remote small intestinal sites in case of colonic inflammation

Hugot

Nabhani

Berrebi

et al. 2019

Preprint

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NOD2 mutations are key risk factors for Crohn's disease (CD). NOD2 contributes to intestinal homeostasis by regulating innate and adaptive immunity together with intestinal epithelial function. However, the roles of NOD2 during gut inflammation is not known. We initially observed that NOD2 expression was increased in epithelial cells remote from inflamed areas in CD patients. To explore this finding, Nod2 mRNA expression, inflammation and gut permeability were examined in the small bowel of wild-type (WT), Nod2 knockout and Nod2 mutant mice after rectal instillation of 2,4,6-trinitrobenzene sulfonic acid (TNBS). In WT mice, Nod2 upregulation remote to rectal injury was associated with pro-inflammatory cytokine expression, recirculating CD4+ T-cells, increased paracellular permeability and myosin like chain kinase activity. Nod2 knockout or mutation led to duodenitis and ileitis demonstrating the remote protective role of Nod2. Bone morrow stem cell (BMSC) transplantations indicated that the small intestinal inflammation was due to NOD2 loss in both hematopoietic and non-hematopoietic compartments. As a whole, WT but not mutant NOD2 prevents disease extension at sites remote from the initial intestinal injury.

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Localized colonic inflammation increases cytokine levels in distant small intestinal segments in the rat

Cited by 20 publications

References 51 publications

Soy-Derived Di- and Tripeptides Alleviate Colon and Ileum Inflammation in Pigs with Dextran Sodium Sulfate-Induced Colitis3

Soy-Derived Di- and Tripeptides Alleviate Colon and Ileum Inflammation in Pigs with Dextran Sodium Sulfate-Induced Colitis3

Enhanced excitability of guinea pig inferior mesenteric ganglion neurons during and following recovery from chemical colitis

Nod2 protects remote small intestinal sites in case of colonic inflammation

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