Inflammation-Induced Intestinal Hyperemia in the Rat: Role of Neutrophils

Sekizuka, Eiichi; Grisham, Matthew B.; Ma, Li; Deitch, Edwin A.; Granger, D. Neil

doi:10.1016/s0016-5085(88)80073-8

Cited by 64 publications

(33 citation statements)

References 14 publications

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“…Also, TNBS-increased myeloperoxidase activity, a quantitative index of inflammation in a damaged tissue (Cetinkaya et al, 2005(Cetinkaya et al, , 2006, was inhibited by GFW. This result corresponds to previous studies that antioxidants can suppress intestinal inflammation (Sekizuka et al, 1988;Cetinkaya et al, 2005Cetinkaya et al, , 2006Necefli et al, 2006). Furthermore, our study showed that the TNBS-induced TNF-α expression in rat colon was significantly suppressed by GFW.…”

Section: Discussionsupporting

confidence: 92%

Grifola frondosa water extract alleviates intestinal inflammation by suppressing TNF-α production and its signaling

et al. 2010

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Abbreviations: 5-ASA, 5-aminosalicylic acid; BCECF/AM, 2',7'-bis (2-carboxyethyl)-5(6)-carboxyfluorescein acetoxymethyl ester; DPPH, 2,2-diphenyl-1-picrylhydrazyl; GFW, water extract of Grifola frondosa; IBD, inflammatory bowel disease; MCP-1, monocyte chemoattractant protein-1; ROS, reactive oxygen species; TNBS, trinitrobenzene sulfonic acid; TPA, 12-O-tetradecanoylphorbol-13-acetate Abstract TNF-α is a major cytokine involved in inflammatory bowel disease (IBD). In this study, water extract of Grifola frondosa (GFW) was evaluated for its protective effects against colon inflammation through the modulation of TNF-α action. In coculture of HT-29 human colon cancer cells with U937 human monocytic cells, TNF-α-induced monocyte adhesion to HT-29 cells was significantly suppressed by GFW (10, 50, 100 μg/ml). The reduced adhesion by GFW correlated with the suppressed expression of MCP-1 and IL-8, the major IBD-associated chemokines. In addition, treatment with GFW significantly suppressed TNF-α-induced reactive oxygen species production and NF-κB transcriptional activity in HT-29 cells. In differentiated U937 monocytic cells, LPS-induced TNF-α production, which is known to be mediated through NF-κB activation, was significantly suppressed by GFW. In an in vivo rat model of IBD, oral administration of GFW for 5 days (1 g/kg per day) significantly inhibited the trinitrobenzene sulfonic acid (TNBS)-induced weight loss, colon ulceration, myeloperoxidase activity, and TNF-α expression in the colon tissue. Moreover, the effect of GFW was similar to that of intra-peritoneal injection of 5-aminosalicylic acid (5-ASA), an active metabolite of sulfasalazine, commonly used drug for the treatment of IBD. The results suggest that GFW ameliorates colon inflammation by suppressing production of TNF-α as well as its signaling through NF-κB leading to the expression of inflammatory chemokines, MCP-1 and IL-8. Taken together, the results strongly suggest GFW is a valuable medicinal food for IBD treatment, and thus may be used as an alternative medicine for IBD.

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Section: Discussionsupporting

confidence: 92%

Grifola frondosa water extract alleviates intestinal inflammation by suppressing TNF-α production and its signaling

et al. 2010

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“…Various mediators such as arachidonate metabolites, cytokines and reactive oxygen metabolites were found to be involved in the pathogenesis of inflammation observed in IBD [7, 8, 9]. Although PMNs are commonly observed in the damaged tissue, there is no clear-cut conclusion whether they are the reason or the result of inflammation [3, 4, 5, 6]. Evidence obtained from previous studies focused on reactive oxygen metabolites as being responsible for tissue damage by lipid peroxidation [30].…”

Section: Discussionmentioning

confidence: 99%

“…One potential source for the increased value of reactive oxygen metabolites in IBD is the neutrophil [2]. Although recent studies demonstrated the frequent presence of increased numbers of mucosal neutrophils in many forms of naturally occurring and experimental colitis [3, 4], there is no concluded consensus among investigators about their potential role in the development of mucosal damage [5, 6]. The contributions of different inflammatory mediators, such as arachidonate metabolites, different types of cytokines, including interleukin-1 (IL-1), IL-6, tumor necrosis factor (TNF) and interferon-γ, to the inflammatory response in IBD have been reported [7, 8, 9].…”

Section: Introductionmentioning

confidence: 99%

Role of Endothelins in Trinitrobenzene Sulfonic Acid-Induced Colitis in Rats

Bm¹,

Kurtel

Güllüoğlu

et al. 1999

Digestion

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To determine the role of endothelins (ET) on experimental colitis, following intracolonic trinitrobenzene sulfonic acid administration, rats were given orally either bosentan (BS), a nonselective ET receptor antagonist (100 mg/kg in 5% arabic gum), or arabic gum by gavage for 2 or 14 days. Macroscopic damage scores obtained in the vehicle (1.4 ± 0.4), acute (4.8 ± 0.6) and chronic (3.8 ± 0.3) colitis groups were significantly higher than in the control group (0). BS treatment reduced the scores in both acute (3 ± 0.5) and chronic (2.3 ± 0.5) colitis groups. Myeloperoxidase (MPO) activities of colonic tissues were elevated in acute and chronic colitis groups (325.1 ± 44.9 and 431.8 ± 54.6 U/g wet weight) as compared with the control group (73.6 ± 11 U/g wet weight). Plasma protein oxidation levels were found to be significantly increased in the chronic colitis group (1,158.1 ± 63.4 nmol/ml) compared with the control, ethanol and acute colitis groups (274.3 ± 23.1, 490 ± 52.2 and 422.2 ± 50.5 nmol/ml). BS treatment significantly reduced both the protein oxidation level (375.5 ± 46.9 nmol/ml) and MPO activity (167.5 ± 35.8 U/g wet weight). The results of the present study suggest the involvement of ETs in the pathogenesis of colonic injury in this animal model of colitis.

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“…These include 1) marked increase in mucosal permeability and possible translocation of inflammatory mediators or infective organisms (9, 38); 2) neutrophil influx, MPO activity, and generation of superoxide radicals (39,40); 3) increased production of arachidonic metabolites, immunoreactive 6-ketoprostaglandin 1␣, leukotriene B 4 , or thromboxane B 2 (18,19,41). Although ACh may be the chief neurotransmitter in the enteric nervous system, it is also likely that other putative neurotransmitters may also be affected during inflammation such as tachykinins, as seen in colitis in canine or in humans (14,42).…”

Section: Colitis Inhibits Colonic Circular Musclementioning

confidence: 99%

Inflammation Inhibits Muscarinic Signaling in In Vivo Canine Colonic Circular Smooth Muscle Cells

Jadcherla

2002

Pediatr Res

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We investigated the effects of experimental colitis on the muscarinic signaling properties and contractile behavior of canine colonic circular smooth muscle. The hypotheses that inflammation 1) inhibits in vivo muscarinic receptor mediated contractions, and 2) alters receptor density or receptor-binding affinities were tested. Muscarine was infused close-intra-arterially in seven conscious dogs during normal and experimental colitis states. Colonic circular muscle contractions were recorded via surgically attached strain gauge transducers. Muscarine stimulated phasic contractions in a dose-dependent manner, whereas colitis was inhibited. The inhibitory concentration 50% dose of M 3 receptor inhibitor was several times lower than that of M 1 , M 2 , and M 4 inhibitors during normal and colitis. However, inflammation induced a significant leftward shift in the circular muscle inhibitory dose-response curve of M 2 inhibitor. Muscarinic receptor density and binding analyses in isolated circular muscle cells was done in normal and colitis states. Inflammation significantly decreased maximum binding from 4082 fmol/mg to 2708 fmol/mg, whereas affinity constant remained unaffected. The conclusions were that 1) spontaneous and muscarine-activated in vivo phasic contractile activity of colonic circular muscle cells is primarily mediated by M 3 receptors; 2) inflammation was associated with a shift in M 2 receptor potency, due chiefly to a decrease in receptor density; and 3) this inhibitory effect was seen in normal and inflamed states, suggesting the importance of M 2 receptor. These findings suggest that changes in muscarinic response during colitis may contribute to the abnormal motility seen with inflammatory bowel disease. ACh, the principal neurotransmitter of the enteric nervous system, is released not only as a result of parasympathetic activation, but also in response to many other gastrointestinal peptides (1). Atropine (nonselective muscarinic antagonist), when administered intravenously or close-intra-arterially (arterial) completely blocks all spontaneous smooth muscle contractions in the gut (1-3). In the gastrointestinal system, muscarinic receptors play a significant role in coordination of peristalsis and propulsion of luminal contents (4).The muscarinic receptors in the gut are localized at presynaptic, postsynaptic, and prejunctional and postjunctional sites (5). These receptors on smooth muscle cells mediate contractions by G-protein coupled mechanisms, whereas those at presynaptic and prejunctional sites modulate the release of ACh by negative feedback. The activation of muscarinic receptors at postsynaptic sites stimulates postsynaptic excitatory and inhibitory neurons to release neurotransmitters. The physiologic mechanisms by which muscarinic receptors stimulate in vivo colonic circular muscle contractions are not completely understood.

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Inflammation-Induced Intestinal Hyperemia in the Rat: Role of Neutrophils

Cited by 64 publications

References 14 publications

Grifola frondosa water extract alleviates intestinal inflammation by suppressing TNF-α production and its signaling

Grifola frondosa water extract alleviates intestinal inflammation by suppressing TNF-α production and its signaling

Role of Endothelins in Trinitrobenzene Sulfonic Acid-Induced Colitis in Rats

Inflammation Inhibits Muscarinic Signaling in In Vivo Canine Colonic Circular Smooth Muscle Cells

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