Further Observations on a Delayed Hypersensitivity Reaction in the Guinea Pig Colon

Bicks, Richard O.; Brown, Geron; Hickey, Haryuo; Rosenberg, Elizabeth

doi:10.1016/s0016-5085(65)80002-6

Cited by 19 publications

(5 citation statements)

References 9 publications

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“…The formation of the LTC4 from this model of immediate hypersensitivity is most probably from mast cells resident in the colon. The DNCB model ofcolitis in the guinea-pig is produced via a cell-mediated, delayed hypersensitivity response (Bicks et al, 1965;1967) and therefore it is unlikely that a release of LTC4 from mast cells would occur. The low levels of LTB4 formed in the present study by inflamed colonic tissue in which there is considerable polymorphonuclear leucocyte infiltration may be due to the tissue preparation and incubation conditions used.…”

Section: Discussionmentioning

confidence: 99%

“…Inflammation of the guinea-pig colon was produced by a method similar to that of Bicks et al (1965). Guinea-pigs (male, 300-350 g) were sensitized by applying to a shaved area on the back a 2.5% ethanolic solution of DNCB (50 pl) once daily for 3 consecutive days; control animals received ethanol (50 gil) alone.…”

Section: Model Of Colitismentioning

confidence: 99%

“…To elucidate further the involvement of arachidonate metabolites in ulcerative colitis, we have investigated the metabolism of arachidonic acid in inflamed colonic tissue taken from an animal model of inflammatory bowel disease (IBD). An immune model of colitis was used (Bicks et al, 1965;1967) in which a delayed hypersensitivity reaction was induced in guinea-pigs by skin sensitization and subsequent intracolonic challenge with the chemical hapten dinitrochlorobenzene (DNCB). In a previous study, the level of PGE2 was elevated in inflamed colonic mucosa taken from guinea-pigs with DNCB-induced colitis (Norris et al, 1982a).…”

Section: Introductionmentioning

confidence: 99%

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Increased metabolism of arachidonic acid in an immune model of colitis in guinea‐pigs

Boughton‐Smith

Whittle

1985

British J Pharmacology

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Inflammation of the guinea‐pig colon was produced by skin sensitization and subsequent intracolonic challenge with the chemical hapten, dinitrochlorobenzene. Metabolism of [14C]‐arachidonic acid by homogenates of control colon was very low, although metabolites co‐migrating on thin layer chromatography (t.l.c.) with prostaglandin E2 (PGE2), PGF2α, PGD2, 6‐keto‐PGF1α, thromboxane B2 (TXB2), HHT and 11‐, 12‐, 15‐HETE were formed. There was an overall 3 fold increase in metabolism of [14C]‐arachidonic acid by homogenates of inflamed mucosa. The greatest increase in metabolite formation was of PGE2, with smaller increases in HHT, 11‐, 12‐, 15‐HETE, PGD2, TXB2, PGF2α and 6‐keto‐PGF1α. The formation of these metabolites was inhibited both by indomethacin and the dual pathway inhibitor, BW755C. The formation of immunoreactive PGE2, TXB2 and 6‐keto‐PGF1α was also increased in homogenates of inflamed guinea‐pig colon. The small level of immunoreactive LTB4 detected in control colon was not changed in inflamed colonic tissue. The dinitrochlorobenzene model of colitis offers a means of studying arachidonic acid metabolism in an immune‐mediated inflammatory response in intestinal tissue.

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Section: Discussionmentioning

confidence: 99%

Section: Model Of Colitismentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Increased metabolism of arachidonic acid in an immune model of colitis in guinea‐pigs

Boughton‐Smith

Whittle

1985

British J Pharmacology

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“…Received for publication 26 May 1976 postulated as important in causing disease in the colon, and, in an animal model in swine, contact hypersensitivity to DNCB in the colon has produced changes similar to those of ulcerative colitis (Bicks et al, 1965;Bicks et al, 1967). Preliminary studies in mice had shown that fetal colon could be transplanted in a similar way to small intestine, and the growth of colonic isografts has been studied in more detail here.…”

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confidence: 99%

Histopathology of cell mediated immune reaction in mouse colon--allograft rejection.

Holden¹,

Ferguson²

1976

Gut

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SUMmARY Grafts of mouse fetal colon, implanted beneath the renal capsule of adult hosts, have been used to study the growth and development of colonic isografts and the rejection of colonic allografts. Isografts grew normally and maintained a structure similar to normal colon. Grafts between strains with H2 histocompatibility differences were rejected by 13 days after transplantation. Early progressive infiltration of the grafts by lymphoid cells was followed by increasing damage to, and subsequent loss of, the epithelial cell layer and destruction of the underlying muscle, changes which parallel those seen in rejection of skin and small bowel. The increase in survival time which is seen in allografts between strains with H2 identity was longer in the colon than has been seen in the skin or small bowel; none of the allografts of colon were completely rejected before 30 days, and some remained viable at 50 days. Comparison of the appearances of rejection in the colon withthose of ulcerative colitis and colonic Crohn's disease does not show the striking similarity which is seen between small bowel rejection and coeliac disease. Many of the individual features of these diseases are, however, present in the course of colonic rejection.

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“…In this model of colitis, animals were presensitized to develop colitis, where the sensitivity is passively transferred by lymphocytes[ 36 ] and immune-suppression will mitigate the bowel injury. [ 37 38 ] This model also shares some of the histological features associated with idiopathic human colitis. [ 39 ]…”

Section: Discussionmentioning

confidence: 99%

Curcumin half analog modulates interleukin-6 and tumor necrosis factor-alpha in inflammatory bowel disease

et al. 2015

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Background:The present study was aimed at examining the effect of dehydrozingerone (DHZ), half analogue of curcumin which is the active constituent of turmeric (Curcuma longa) in the di-nitrochlorobenzene (DNCB) induced model for inflammatory bowel disease (IBD).Materials and Methods:Male Wistar rats (200–220 g) were divided into four groups (n = 6). Chemical induction of IBD was done by sensitizing with 300 µL of 20 g/L of DNCB (in acetone) onto the nape of rats for 14 days followed by intra-colonic instillation of 250 µL of DNCB (0.1% DNCB in 50% alcohol) solution on day 15. Rats in Group 1 (normal control) and Group 2 (DNCB control) were treated with vehicle. Rats in Group 3 were treated with DHZ (100 mg/kg, p.o.; 8 days) and Group 4 animals were treated with sulfasalazine (SS) (100 mg/kg, p.o.; 8 days). On 24th day, the rats were killed, colon removed and the macroscopic, biochemical, and histopathological evaluations were performed.Results:The levels of myeloperoxidase, thiobarbituric acid reactive substrate, and nitrite increased significantly (P < 0.05) in the DNCB group whereas reduced significantly in the DHZ and SS treated groups. Serum nitrite levels were found to be insignificant between the different groups. Interleukin-6, tumor necrosis factor-alpha level was significantly high in the DNCB group.Conclusion:These findings show that DHZ can be a promising molecule for the treatment of IBD.

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Further Observations on a Delayed Hypersensitivity Reaction in the Guinea Pig Colon

Cited by 19 publications

References 9 publications

Increased metabolism of arachidonic acid in an immune model of colitis in guinea‐pigs

Increased metabolism of arachidonic acid in an immune model of colitis in guinea‐pigs

Histopathology of cell mediated immune reaction in mouse colon--allograft rejection.

Curcumin half analog modulates interleukin-6 and tumor necrosis factor-alpha in inflammatory bowel disease

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