Apoptosis markers of circulating leukocytes are associated with the clinical course of inflammatory bowel disease
Here we aimed at evaluating whether the apoptosis status of circulating leukocytes of inflammatory bowel diseases (IBD) patients is attributed to the diseases clinical status. Defects in the programmed cell death of inflammatory cells is known as to play a major role in the pathogenesis of IBD, and...
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Veröffentlicht in: | Gastroenterology and hepatology from bed to bench 2018, Vol.11 (Suppl 1), p.S53-S58 |
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Zusammenfassung: | Here we aimed at evaluating whether the apoptosis status of circulating leukocytes of inflammatory bowel diseases (IBD) patients is attributed to the diseases clinical status.
Defects in the programmed cell death of inflammatory cells is known as to play a major role in the pathogenesis of IBD, and has been associated with the clinical efficacy of therapeutic agents.
A total of 50 IBD patients, 25 with remission and 25 with flare-up phase of the disease, who their disease was confirmed by colonoscopy, were included in this cross-sectional study. Pro-apoptotic Bax and anti-apoptotic Bcl-2 mRNA expression, along with Bax/Bcl-2 ratio, as measures of apoptotic status, were assessed in the Peripheral blood mononuclear cell (PBMC) of the patients using semi-quantitative Real-time PCR method.
The mean Bax mRNA expression level was 0.54±0.12 in flare-up group and 0.53±0.13 in remission group (p=0.8). The mean Bcl-2 mRNA expression level was 0.63±0.13 in flare-up group and 0.55±0.12 in remission group (p=0.03). The mean Bax/Bcl-2 ratio was 0.88±0.17 in flare-up group and 1±21 in remission group (p=0.05). The mean Bax/Bcl-2 ratio was not statistically significant between different disease types (p=0.54) or therapeutic agents (p=0.7).
According to our results, alteration in markers of apoptosis could be traced in the circulating leukocytes of IBD patients, which suggest a potential for clinical application of apoptosis markers in disease monitoring and prediction of relapse. |
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ISSN: | 2008-2258 2008-4234 |