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Extracellular DNA is increased in dextran sulphate sodium-induced colitis in mice

M. Maronek, B. Gromova, R. Liptak, D. Klimova, B. Cechova, R. Gardlik

. 2018 ; 64 (5-6) : 167-172. [pub] -

Jazyk angličtina Země Česko

Typ dokumentu časopisecké články

Perzistentní odkaz   https://www.medvik.cz/link/bmc19026303

Ulcerative colitis and Crohn's disease constitute the two main forms of inflammatory bowel disease. Prevalence of these diseases increases. In the present day, inadequate and inefficient therapy causes complications and frequent relapse. Extracellular DNA (ecDNA) is the DNA that is outside of cells and may be responsible for activation of the inflammatory response. To determine whether colitis is associated with higher concentration of ecDNA we used male mice of the C57BL/6 strain. Colitis was induced by 2% dextran sulphate sodium (DSS). After 7 days, mice exhibited considerable weight loss compared to the control group. Also, there was a higher stool consistency score and the colon was significantly shorter in comparison to the control group. Higher concentration of ecDNA was found in the DSS group. Interestingly, deoxyribonuclease activity was lower in the colon of the DSS group compared with the negative control. These findings may point to ecDNA as a potential pathogenetic factor and marker of inflammation.

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$a Ulcerative colitis and Crohn's disease constitute the two main forms of inflammatory bowel disease. Prevalence of these diseases increases. In the present day, inadequate and inefficient therapy causes complications and frequent relapse. Extracellular DNA (ecDNA) is the DNA that is outside of cells and may be responsible for activation of the inflammatory response. To determine whether colitis is associated with higher concentration of ecDNA we used male mice of the C57BL/6 strain. Colitis was induced by 2% dextran sulphate sodium (DSS). After 7 days, mice exhibited considerable weight loss compared to the control group. Also, there was a higher stool consistency score and the colon was significantly shorter in comparison to the control group. Higher concentration of ecDNA was found in the DSS group. Interestingly, deoxyribonuclease activity was lower in the colon of the DSS group compared with the negative control. These findings may point to ecDNA as a potential pathogenetic factor and marker of inflammation.
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