Carrageenan: Effects in Animals

Maillet, M.; Bonfils, S; Lister, R. E.

doi:10.1016/s0140-6736(70)90023-1

Cited by 33 publications

(15 citation statements)

References 3 publications

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“…In contrast to the studies of Maillet et al [2] and Sharratt et al [3] and in a manner more significant than that noted by Marcus and Watt [1], this experiment demonstrated that universal colitis can be acutely induced in CFi mice fed a 10% solution of degraded carrageenan. The mucosal reaction was more severe in the proximal colon where there is presumably greater exposure to carrageen, but tissue damage was also extensive in the distal colon.…”

Section: Discussioncontrasting

confidence: 92%

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Degraded Carrageenan-Induced Colitis in CF<sub>1</sub> Mice

et al. 1984

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Delivery of 10% carrageen (degraded carrageenan, Glaxo, France) for 10 days in the drinking water to CF₁ mice induced bloody diarrhea, pericryptal inflammation, and marked dilatation of the cecum and ascending colon. Histologically, the mucosa was characterized by distorted crypt architecture, inflammatory infiltration of the lamina propria, and ulceration, conditions which were more pronounced in the proximal colon but were also present in the distal colon. Treatment with hydrocortisone and levamisole reduced the severity of all phases of the reaction. Alterations in colonic epithelial cell proliferation corresponded with the clinical and histopathological findings. Labeling indices (LI) significantly increased over control values in both proximal (12.9 ± 4.9 vs. 7.6 ± 2.9) and distal colon (13.9 ± 5.2 vs. 7.2 ± 2.4), effectively doubling the number of proliferating cells per crypt column in both areas. However, DNA-synthesizing cells extended further upward along the cryptal wall of the proximal colon reflecting greater mucosal damage. Only in the proximal colon did the proliferative compartment (PC) extend to the upper third of the glands, normally not a proliferative zone. Hydrocortisone and levamisole administered concurrently with 10% carrageen were less effective in protecting the proximal colon since LI and numbers of labeled cells per crypt column were consistently lower in the distal colon. Moreover, hydrocortisone alone significantly depressed DNA synthesis only in the distal colon. All distal colonic crypts were not equally protected by administration of hydrocortisone since some continued to express large numbers of proliferating cells and an extended PC, well characterized preneoplastic defects in regulatory control of colonic epithelial cell proliferation. The clinical presentation, histopathology, proliferative alterations, potential premalignancy, and response to pharmaceutic intervention of carrageen-induced colitis in mice support its continued investigation as an animal model for human ulcerative colitis.

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Section: Discussioncontrasting

confidence: 92%

“…In mice, however, focal cellular infil tration of the colonic mucosa was the sole manifestation of carrageenan's toxicity. Sub sequent investigators confirmed the ulcero genic potential of degraded carrageenan in rabbits and guinea pigs, but not in rats or mice [2][3][4],…”

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confidence: 97%

Degraded Carrageenan-Induced Colitis in CF<sub>1</sub> Mice

et al. 1984

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“…Despite its wide application, the safety of carrageenan is controversial. Earlier work demonstrated that intake of carrageenan may cause anabasis or cancer of the gut in animal models [1, 6–11]. Moreover, carrageenan has been used to study mediators of inflammation [6, 9, 12].…”

Section: Introductionmentioning

confidence: 99%

κ-Carrageenan Enhances Lipopolysaccharide-Induced Interleukin-8 Secretion by Stimulating the Bcl10-NF-κB Pathway in HT-29 Cells and AggravatesC.freundii-Induced Inflammation in Mice

Zhen

Niu

et al. 2017

Mediators of Inflammation

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Background. The dietary usage of carrageenan as common food additive has increased observably over the last 50 years. But there is substantial controversy about its safety. Methods. We investigated whether the κ-carrageenan could enhance lipopolysaccharide-induced IL-8 expression by studying its actions on the TLR4-NF-κB pathway. The aggravating effect of κ-carrageenan on Citrobacter freundii DBS100-induced intestinal inflammation was also investigated in a mouse model. Results. Our data show that κ-carrageenan pretreatment promoted LPS-induced IL-8 expression in HT-29 cells. Although CD14, MD-2, and TLR4 were upregulated, the binding of LPS was not enhanced. However, the pathway of Bcl10-NF-κB was triggered. Interestingly, κ-carrageenan competitively blocked the binding of FITC-LPS. Furthermore, pretreatment with κ-carrageenan for one week previous to gavage with C. freundii DBS100 markedly aggravated weight loss, mortality, and colonic damage. The secretion of cytokines was unbalanced and the ratio of Tregs was decreased significantly. In addition, κ-carrageenan, together with C. freundii DBS100, enhanced the transcription and secretion of TLR4 and NF-κB. Conclusions. κ-Carrageenan can synergistically activate LPS-induced inflammatory through the Bcl10-NF-κB pathway, as indicated by its aggravation of C. freundii DBS100-induced colitis in mice. General Significance. Our results suggest that κ-carrageenan serves as a potential inflammatory agent that magnifies existing intestinal inflammation.

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“…It has been noted in previous studies ~'5 that cecal ulcers were easily induced in guinea pigs by carrageenan. According to Maillet et al 6 …”

Section: Introductionmentioning

confidence: 99%

Morphological analysis of acute ulcerative colitis experimentally induced by dextran sulfate sodium in the guinea pig: Some possible mechanisms of cecal ulceration

et al. 1994

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This study in the guinea pig demonstrated that ulcerative colitis-like lesions were induced more rapidly and effectively than in other laboratory animals by the oral administration of dextran sulfate sodium (DSS). In all guinea pigs receiving 3% DSS solution, diarrhea was noted within 48h, and bleeding at 48-72h. Light microscopically, hemorrhagic and ulcerative lesions were observed in the cecum and proximal colon as early as 72h after administration. Lamina propria macrophages, gather in the subepithelial region under normal conditions, were markedly increased in number after DSS administration; by 96 h, they were approximately three times as many as in the control specimens. The cecal mucosa was also characterized, in earlier stages, by the obliteration of virtually all cryptal lumina because of the accumulation of mucous secretions, leading to the subsequent disappearance of the crypts. The obliteration of crypts, which preceded the increase of macrophages, is suggested to play a leading part in this ulceration.

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Carrageenan: Effects in Animals

Cited by 33 publications

References 3 publications

Degraded Carrageenan-Induced Colitis in CF<sub>1</sub> Mice

Degraded Carrageenan-Induced Colitis in CF<sub>1</sub> Mice

κ-Carrageenan Enhances Lipopolysaccharide-Induced Interleukin-8 Secretion by Stimulating the Bcl10-NF-κB Pathway in HT-29 Cells and AggravatesC.freundii-Induced Inflammation in Mice

Morphological analysis of acute ulcerative colitis experimentally induced by dextran sulfate sodium in the guinea pig: Some possible mechanisms of cecal ulceration

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