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DSS colitis - Dextran sulfate sodium (DSS for colitis)

DSS Colitis

, Photo - distal colon H&E staining when given mice 3% DSS in drinking water for 7 days

DSS colitis

CAS no. 9011-18-1

The DSS is supplied as the sodium salt and is stabilised by a small addition of phosphate salts. DSS is stable indefinitely when stored in well sealed containers at room temperature. A certificate of analysis is supplied with each batch. The molecular weight range, sulfur content, moisture etc are carefully controlled.

Dextran sulfate sodium (DSS) with a mol. wt. of approx. 40000 when administered orally in the drinking water has been found to induce colitis in experimental animals. Concentrations from 2 to 5% have been used and symptoms develop within one week. The recommended concentrations of DSS for mice are 2.5-3.5% and this will depend, eg. on the strain, age and sex of the animals. For rats somewhat higher concentrations may be required 3.5-5%. It will also depend on whether your study requires a milder onset of colitis or a more aggresive response.

Reference: A-C. Bylund-Fellenius, E.Landström, L-G.Axelsson and T.Midtvedt,Microb.Ecol.,1994:7;207.

Read our brief advice on using DSS for Colitis

A new large batch of DB001 is now available. Full details on recommended dosage will also be supplied.

If you need larger quantities please contact us for a bulk quotation.

References

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2019

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2018

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2017

56. Do, A. et al. An HDAC6 Inhibitor Confers Protection and Selectively Inhibits B-Cell Infiltration in DSS-Induced Colitis in Mice. J. Pharmacol. Exp. Ther. 360, 140–151 (2017).

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62. Berlec, A. et al. Dextran sulphate sodium colitis in C57BL/6J mice is alleviated by Lactococcus lactis and worsened by the neutralization of Tumor necrosis Factor α. Int. Immunopharmacol. 43, 219–226 (2017).

63. Matsuzawa-Ishimoto, Y. et al. Autophagy protein ATG16L1 prevents necroptosis in the intestinal epithelium. J. Exp. Med. 214, 3687–3705 (2017).

64. Constante, M., Fragoso, G., Calvé, A., Samba-Mondonga, M. & Santos, M. M. Dietary Heme Induces Gut Dysbiosis, Aggravates Colitis, and Potentiates the Development of Adenomas in Mice. Front. Microbiol. 8, (2017).

65. Markovic, B. S. et al. Bacterial Flora Play Important Roles in Acute Dextran Sulphate Sodium-Induced Colitis But Are Not Involved in Gal-3 Dependent Modulation of Colon Inflammation. Serbian J. Exp. Clin. Res. 18, 213–220 (2017).

66. Fugmann, T., Sofron, A., Ritz, D., Bootz, F. & Neri, D. The MHC Class II Immunopeptidome of Lymph Nodes in Health and in Chemically Induced Colitis. J. Immunol. Baltim. Md 1950 198, 1357–1364 (2017).

67. Menghini, P. et al. A novel model of colitis-associated cancer in SAMP1/YitFc mice with Crohn’s disease-like ileitis. PloS One 12, e0174121 (2017).

68. Udden, S. M. N. et al. NOD2 Suppresses Colorectal Tumorigenesis via Downregulation of the TLR Pathways. Cell Rep. 19, 2756–2770 (2017).

69. Khelifi, L., Soufli, I., Labsi, M. & Touil-Boukoffa, C. Immune-protective effect of echinococcosis on colitis experimental model is dependent of down regulation of TNF-α and NO production. Acta Trop. 166, 7–15 (2017).

70. Constante, M., Fragoso, G., Lupien-Meilleur, J., Calvé, A. & Santos, M. M. Iron Supplements Modulate Colon Microbiota Composition and Potentiate the Protective Effects of Probiotics in Dextran Sodium Sulfate-induced Colitis. Inflamm. Bowel Dis. 23, 753–766 (2017).

71. Štofilová, J. et al. Cytokine production in vitro and in rat model of colitis in response to Lactobacillus plantarum LS/07. Biomed. Pharmacother. 94, 1176–1185 (2017).

72. Pagel, R. et al. Circadian rhythm disruption impairs tissue homeostasis and exacerbates chronic inflammation in the intestine. FASEB J. 31, 4707–4719 (2017).

73. Carvajal, A. E. et al. Reelin protects from colon pathology by maintaining the intestinal barrier integrity and repressing tumorigenic genes. Biochim. Biophys. Acta BBA - Mol. Basis Dis. 1863, 2126–2134 (2017).

74. Li, X. et al. Myeloid-derived cullin 3 promotes STAT3 phosphorylation by inhibiting OGT expression and protects against intestinal inflammation. J. Exp. Med. 214, 1093–1109 (2017).

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76. Zhdanov, A. V. et al. Quantitative analysis of mucosal oxygenation using ex vivo imaging of healthy and inflamed mammalian colon tissue. Cell. Mol. Life Sci. 74, 141–151 (2017).

77. Hardbower, D. M. et al. EGFR-mediated macrophage activation promotes colitis-associated tumorigenesis. Oncogene 36, 3807–3819 (2017).

78. O’Sullivan, S. et al. Inhibition of matrix metalloproteinase-9 by a barbiturate-nitrate hybrid ameliorates dextran sulphate sodium-induced colitis: effect on inflammation-related genes: Nitrate inhibition of MMP-9 in DSS-induced colitis. Br. J. Pharmacol. 174, 512–524 (2017).

79. Carvajal, A. E. et al. Reelin expression is up-regulated in mice colon in response to acute colitis and provides resistance against colitis. Biochim. Biophys. Acta BBA - Mol. Basis Dis. 1863, 462–473 (2017).

80. Sünderhauf, A. et al. Regulation of epithelial cell expressed C3 in the intestine – Relevance for the pathophysiology of inflammatory bowel disease? Mol. Immunol. 90, 227–238 (2017).

81. Katlinski, K. V. et al. Inactivation of Interferon Receptor Promotes the Establishment of Immune Privileged Tumor Microenvironment. Cancer Cell 31, 194–207 (2017).

82. Adedara, I. A., Ajayi, B. O., Awogbindin, I. O. & Farombi, E. O. Interactive effects of ethanol on ulcerative colitis and its associated testicular dysfunction in pubertal BALB/c mice. Alcohol 64, 65–75 (2017).

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2016

84. Guada, M. et al. Cyclosporine A-loaded lipid nanoparticles in inflammatory bowel disease. Int. J. Pharm. 503, 196–198 (2016).

85. El-Salhy, M. & Umezawa, K. Treatment with novel AP-1 and NF-κB inhibitors restores the colonic endocrine cells to normal levels in rats with DSS-induced colitis. Int. J. Mol. Med. 37, 556–564 (2016).

86. Kriščiukaitis, A. et al. Elaboration of Optimized Expert Knowledge Based Quantitative Features for Automatic Histological Image Evaluation. Biomed. Eng. 2016 19, (2016).

87. Dolowschiak, T. et al. IFN-γ Hinders Recovery from Mucosal Inflammation during Antibiotic Therapy for Salmonella Gut Infection. Cell Host Microbe 20, 238–249 (2016).

88. Di Martino, L. et al. Protective Role for TWEAK/Fn14 in Regulating Acute Intestinal Inflammation and Colitis-Associated Tumorigenesis. Cancer Res. 76, 6533–6542 (2016).

89. Bootz, F., Ziffels, B. & Neri, D. Antibody-Based Targeted Delivery of Interleukin-22 Promotes Rapid Clinical Recovery in Mice With DSS-Induced Colitis. Inflamm. Bowel Dis. 22, 2098–2105 (2016).

90. Brauer, R. et al. MMP-19 deficiency causes aggravation of colitis due to defects in innate immune cell function. Mucosal Immunol. 9, 974–985 (2016).

91. Ahl, D. et al. Lactobacillus reuteri increases mucus thickness and ameliorates dextran sulphate sodium-induced colitis in mice. Acta Physiol. 217, 300–310 (2016).

92. Chng, S. H. et al. Ablating the aryl hydrocarbon receptor (AhR) in CD11c+ cells perturbs intestinal epithelium development and intestinal immunity. Sci. Rep. 6, 23820 (2016).

93. Heinsbroek, S. E. M. et al. miR-511-3p, embedded in the macrophage mannose receptor gene, contributes to intestinal inflammation. Mucosal Immunol. 9, 960–973 (2016).

94. Das, S. et al. Mice deficient in Muc4 are resistant to experimental colitis and colitis-associated colorectal cancer. Oncogene 35, 2645–2654 (2016).

95. Ohta, T. et al. Crucial roles of XCR1-expressing dendritic cells and the XCR1-XCL1 chemokine axis in intestinal immune homeostasis. Sci. Rep. 6, 23505 (2016).

96. Misiorek, J. O. et al. Keratin 8-deletion induced colitis predisposes to murine colorectal cancer enforced by the inflammasome and IL-22 pathway. Carcinogenesis 37, 777–786 (2016).

97. Yu, C. et al. Platelet-Derived CCL5 Regulates CXC Chemokine Formation and Neutrophil Recruitment in Acute Experimental Colitis. J. Cell. Physiol. 231, 370–376 (2016).

98. Di Giovangiulio, M. et al. Vagotomy Affects the Development of Oral Tolerance and Increases Susceptibility to Develop Colitis Independently of α-7 Nicotinic Receptor. Mol. Med. 22, 464–476 (2016).

99. Farombi, E. O. et al. Dietary protocatechuic acid ameliorates dextran sulphate sodium-induced ulcerative colitis and hepatotoxicity in rats. Food Funct. 7, 913–921 (2016).

100. Simovic Markovic, B. et al. Pharmacological Inhibition of Gal-3 in Mesenchymal Stem Cells Enhances Their Capacity to Promote Alternative Activation of Macrophages in Dextran Sulphate Sodium-Induced Colitis. Stem Cells International (2016). doi:10.1155/2016/2640746

101. Matthis, A. L. et al. Importance of the Evaluation of N-Acetyltransferase Enzyme Activity Prior to 5-Aminosalicylic Acid Medication for Ulcerative Colitis. Inflamm. Bowel Dis. 22, 1793–1802 (2016).

102. El-Salhy, M. & Umezawa, K. Anti-inflammatory effects of novel AP-1 and NF-κB inhibitors in dextran-sulfate-sodium-induced colitis in rats. Int. J. Mol. Med. 37, 1457–1464 (2016).

103. Goodman, W. A. et al. KLF6 contributes to myeloid cell plasticity in the pathogenesis of intestinal inflammation. Mucosal Immunol. 9, 1250–1262 (2016).

104. Vázquez-Carretero, M. D. et al. The Synaptojanins in the murine small and large intestine. J. Bioenerg. Biomembr. 48, 569–579 (2016).

105. Martin, J. C. et al. IL-22BP is produced by eosinophils in human gut and blocks IL-22 protective actions during colitis. Mucosal Immunol. 9, 539–549 (2016).

106. Márquez-Flores, Y. K., Villegas, I., Cárdeno, A., Rosillo, M. Á. & Alarcón-de-la-Lastra, C. Apigenin supplementation protects the development of dextran sulfate sodium-induced murine experimental colitis by inhibiting canonical and non-canonical inflammasome signaling pathways. J. Nutr. Biochem. 30, 143–152 (2016).

107. De Fazio, L. et al. Dietary Geraniol by Oral or Enema Administration Strongly Reduces Dysbiosis and Systemic Inflammation in Dextran Sulfate Sodium-Treated Mice. Front. Pharmacol. 7, (2016).

108. Beloqui, A. et al. A comparative study of curcumin-loaded lipid-based nanocarriers in the treatment of inflammatory bowel disease. Colloids Surf. B Biointerfaces 143, 327–335 (2016).

109. Gerling, M. et al. Stromal Hedgehog signalling is downregulated in colon cancer and its restoration restrains tumour growth. Nat. Commun. 7, 12321 (2016).

110. Jia, L.-G. et al. A Novel Role for TL1A/DR3 in Protection against Intestinal Injury and Infection. J. Immunol. Baltim. Md 1950 197, 377–386 (2016).

111. Lee, S. et al. Arhgap17, a RhoGTPase activating protein, regulates mucosal and epithelial barrier function in the mouse colon. Sci. Rep. 6, 26923 (2016).

112. Aden, K. et al. Epithelial IL-23R Signaling Licenses Protective IL-22 Responses in Intestinal Inflammation. Cell Rep. 16, 2208–2218 (2016).

113. Bosma, M. et al. FNDC4 acts as an anti-inflammatory factor on macrophages and improves colitis in mice. Nat. Commun. 7, 11314 (2016).

114. Elmasry, A., Daba, M.-H. & El-Karef, A. Possible Effects of Moringa oleifera versus Ginger (Zingiber officinalis) on Experimental Colitis in Mice. Br. J. Med. Med. Res. 16, 1–19 (2016).

115. Helenius, T. O., Antman, C. A., Asghar, M. N., Nyström, J. H. & Toivola, D. M. Keratins Are Altered in Intestinal Disease-Related Stress Responses. Cells 5, 35 (2016).

116. O’Shea, C. J. et al. The effect of algal polysaccharides laminarin and fucoidan on colonic pathology, cytokine gene expression and Enterobacteriaceae in a dextran sodium sulfate-challenged porcine model. J. Nutr. Sci. 5, (2016).

117. Däbritz, J., Judd, L. M., Chalinor, H. V., Menheniott, T. R. & Giraud, A. S. Altered gp130 signalling ameliorates experimental colitis via myeloid cell-specific STAT3 activation and myeloid-derived suppressor cells. Sci. Rep. 6, 20584 (2016).

118. Simovic Markovic, B. et al. Galectin-3 Plays an Important Pro-inflammatory Role in the Induction Phase of Acute Colitis by Promoting Activation of NLRP3 Inflammasome and Production of IL-1β in Macrophages. J. Crohns Colitis 10, 593–606 (2016).

119. Shen, F. et al. Vinegar Treatment Prevents the Development of Murine Experimental Colitis via Inhibition of Inflammation and Apoptosis. J. Agric. Food Chem. 64, 1111–1121 (2016).

2015

120. Heinsbroek, S. E. M. et al. Orally delivered β-glucans aggravate dextran sulfate sodium (DSS)-induced intestinal inflammation. Nutr. Res. 35, 1106–1112 (2015).

121. Sommer, F. & Bäckhed, F. The gut microbiota engages different signaling pathways to induce Duox2 expression in the ileum and colon epithelium. Mucosal Immunol. 8, 372–379 (2015).

122. Moon, C. et al. Vertically transmitted faecal IgA levels determine extra-chromosomal phenotypic variation. Nature 521, 90–93 (2015).

123. Fornasa, G. et al. Dichotomy of short and long thymic stromal lymphopoietin isoforms in inflammatory disorders of the bowel and skin. J. Allergy Clin. Immunol. 136, 413–422 (2015).

124. Elkatary, R. et al. Effect of Different Doses of Sitagliptin in Treatment of Experimentally Induced Colitis in Mice. Br. J. Pharm. Res. 7, 140–151 (2015).

125. Ajayi, B. O., Adedara, I. A. & Farombi, E. O. Pharmacological activity of 6-gingerol in dextran sulphate sodium-induced ulcerative colitis in BALB/c mice. Phytother. Res. PTR 29, 566–572 (2015).

126. Elkatary, R., Abdelrahman, K., Hassanin, A. & Elmasry, A. A Comparative Study between the Effect of Simvastatin and Sitagliptin Combined and the Effect of a Large Dose of Each in an Early Treatment of Experimentally Induced Colitis in Mice. 17

127. Asghar, M. N. et al. The Amount of Keratins Matters for Stress Protection of the Colonic Epithelium. PLOS ONE 10, e0127436 (2015).

128. Petrolis, R. et al. Digital imaging of colon tissue: method for evaluation of inflammation severity by spatial frequency features of the histological images. Diagn. Pathol. 10, 159 (2015).

129. Zwicker, S. et al. Interleukin 34: a new modulator of human and experimental inflammatory bowel disease. Clin. Sci. 129, 281–290 (2015).

130. Banerjee, A. et al. Umbilical cord mesenchymal stem cells modulate dextran sulfate sodium induced acute colitis in immunodeficient mice. Stem Cell Res. Ther. 6, 79 (2015).

131. Talero, E. et al. Inhibition of chronic ulcerative colitis-associated adenocarcinoma development in mice by VSL#3. Inflamm. Bowel Dis. 21, 1027–1037 (2015).

132. Spisni, E. et al. Cyclooxygenase-2 Silencing for the Treatment of Colitis: A Combined In Vivo Strategy Based on RNA Interference and Engineered Escherichia Coli. Mol. Ther. 23, 278–289 (2015).

133. Hu, S. et al. The DNA Sensor AIM2 Maintains Intestinal Homeostasis via Regulation of Epithelial Antimicrobial Host Defense. Cell Rep. 13, 1922–1936 (2015).

134. Forte, D. et al. Human cord blood-derived platelet lysate enhances the therapeutic activity of adipose-derived mesenchymal stromal cells isolated from Crohn’s disease patients in a mouse model of colitis. Stem Cell Res. Ther. 6, 170 (2015).

135. Helenius, T. O. et al. Keratin 8 absence down-regulates colonocyte HMGCS2 and modulates colonic ketogenesis and energy metabolism. Mol. Biol. Cell 26, 2298–2310 (2015).

136. Soufli, I. et al. Crude extract of hydatid laminated layer from Echinococcus granulosus cyst attenuates mucosal intestinal damage and inflammatory responses in Dextran Sulfate Sodium induced colitis in mice. J. Inflamm. 12, 19 (2015).

137. Bootz, F., Schmid, A. S. & Neri, D. Alternatively Spliced EDA Domain of Fibronectin Is a Target for Pharmacodelivery Applications in Inflammatory Bowel Disease. Inflamm. Bowel Dis. 21, 1908–1917 (2015).

138. Te Velde, A. A. et al. Effects of Dietary Plant Sterols and Stanol Esters with Low- and High-Fat Diets in Chronic and Acute Models for Experimental Colitis. Nutrients 7, 8518–8531 (2015).

139. Zhdanov, A. V., Okkelman, I. A., Collins, F. W. J., Melgar, S. & Papkovsky, D. B. A novel effect of DMOG on cell metabolism: direct inhibition of mitochondrial function precedes HIF target gene expression. Biochim. Biophys. Acta BBA - Bioenerg. 1847, 1254–1266 (2015).

140. Speca, S. et al. Novel PPARγ Modulator GED-0507-34 Levo Ameliorates Inflammation-driven Intestinal Fibrosis. Inflamm. Bowel Dis. 22, 279–292 (2016).

141. Gouyer, V. et al. Delivery of a mucin domain enriched in cysteine residues strengthens the intestinal mucous barrier. Sci. Rep. 5, 9577 (2015).

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SELECTED OLDER PUBLICATIONS

143. Sommer, F. et al. Altered Mucus Glycosylation in Core 1 O-Glycan-Deficient Mice Affects Microbiota Composition and Intestinal Architecture. PLOS ONE 9, e85254 (2014).

144. Wagner, A. E. et al. DSS-induced acute colitis in C57BL/6 mice is mitigated by sulforaphane pre-treatment. J. Nutr. Biochem. 24, 2085–2091 (2013).

145. Beloqui, A. et al. Budesonide-loaded nanostructured lipid carriers reduce inflammation in murine DSS-induced colitis. Int. J. Pharm. 454, 775–783 (2013).

146. Thaker, A. I., Shaker, A., Rao, M. S. & Ciorba, M. A. Modeling Colitis-Associated Cancer with Azoxymethane (AOM) and Dextran Sulfate Sodium (DSS). JoVE J. Vis. Exp. e4100 (2012). doi:10.3791/410

147. Van Crombruggen, K. et al. Influence of soluble guanylate cyclase inhibition on inflammation and motility disturbances in DSS-induced colitis. Eur. J. Pharmacol. 579, 337–349 (2008).

148. Ten Hove, T., Drillenburg, P., Wijnholds, J., te Velde, A. A. & van Deventer, S. J. H. Differential Susceptibility of Multidrug Resistance Protein-1 Deficient Mice to DSS and TNBS-Induced Colitis. Dig. Dis. Sci. 47, 2056–2063 (2002).

149. Dieleman et al. Chronic experimental colitis induced by dextran sulphate sodium (DSS) is characterized by Th1 and Th2 cytokines. Clin. Exp. Immunol. 114, 385–391 (1998).

Products


A word of advice using DSS for Colitis

TdB Consultancy has marketed DSS since 1980s and had participated in its development for colitis research. During these years we have had very few complaints from customers and these were evaluated carefully and, in most cases, the problems were traced to variations in batches of the animals used.

It should be stressed that the nature of the colitis (severe or mild) induced is determined by the concentration of DSS used, although the strain of animals, age and sex may also influence the results. For those starting a study for the first time, we have recommended that a trial run with two or three concentrations (e.g. 2, 2.5 and 3% DSS) be performed to obtain the symptoms required.

We have noted that one supplier of DSS has recently included on its web-site, an absurd comparison of samples of DSS from different suppliers. The dose used appears to be 2%, the number of animals used not stated and presumably the single line is a mean value.

It should first be understood that manufacture of dextran derivatives (or any polymer product) inevitably leads to small differences between batches. It is standard practice to set ranges for each of the analytical parameters.  Has a study with one batch any value? - one needs to compare at least five batches. We suggest the time be spent on research.

Not an expert or wanting a general description, read up on the basics about colitis on wikipedia