Apoptosis markers of circulating leukocytes are associated with the clinical course of inflammatory bowel disease
Gastroenterology and Hepatology from Bed to Bench,
Vol. 11 No. Supplement 1 (2018),
11 December 2018
,
Page s53-s58
https://doi.org/10.22037/ghfbb.v0i0.1453
Abstract
Aim: 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.
Background: 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.
Methods: 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.
Results: 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).
Conclusion: 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.
Keywords: Inflammatory bowel diseases, Apoptosis, Remission, Flare-up, Biomarker.
(Please cite as: Amini Kadijani A, Javadinia F, Mirzaei AR, Khazaei koohpar Z, Balaii H, Baradaran Ghavami SH, et al. Apoptosis markers of circulating leukocytes are associated with the clinical course of inflammatory bowel disease Gastroenterol Hepatol Bed Bench 2018;11(Suppl. 1):S53-S58).
- Inflammatory bowel diseases
- Apoptosis
- Remission
- Flare-up
- Biomarker.
How to Cite
References
ZhangY-Z,LiY-Y. Inflammatory bowel disease: pathogenesis. World J Gastroenterol 2014;20:91.
Taghipour N, Molaei M, Mosaffa N, Rostami-Nejad M, Asadzadeh Aghdaei H, Anissian A, et al. An experimental model of colitis induced by dextran sulfate sodium from acute progresses to chronicity in C57BL/6: correlation between conditions of mice and the environment. Gastroenterol Hepatol Bed Bench. 2016;9:45-52.
Karbalaei R, Piran M, Rezaei-Tavirani M, Asadzadeh-Aghdaei H, Heidari MH. A systems biology analysis protein-protein interaction of NASH and IBD based on comprehensive gene information. Gastroenterol Hepatol Bed Bench. 2017;10:194-201.
Xavier R, Podolsky D. Unravelling the pathogenesis of inflammatory bowel disease. Nature 2007;448:427-34.
Peppelenbosch M, Van Deventer S. T cell apoptosis and inflammatory bowel disease. Gut 2004;53:1556-8.
Sturm A. What is the role of apoptosis in the normal and inflamed intestine? Inflam Bowel Dis 2008;14:S113-4.
Smythies LE, Sellers M, Clements RH, Mosteller-Barnum M, Meng G, Benjamin WH, et al. Human intestinal macrophages display profound inflammatory anergy despite avid phagocytic and bacteriocidal activity.J Clin Invest 2005;115:66.
Lügering A, Lebiedz P, Koch S, Kucharzik T. Apoptosis as a therapeutic tool in IBD? Ann N Y Acad Sci 2006;1072:62-77.
Aghdaei HA, Kadijani AA, Sorrentino D, Mirzaei A, Shahrokh S, Balaii H, et al. An increased Bax/Bcl-2 ratio in circulating inflammatory cells predicts primary response to infliximab in inflammatory bowel disease patients. United European Gastroenterol J 2018:2050640618774637.
Liverani E, Scaioli E, Digby RJ, Bellanova M, Belluzzi A. How to predict clinical relapse in inflammatory bowel disease patients. World J Gastroenterol 2016;22:1017.
Hanauer SB. Combination Therapy for Inflammatory Bowel Disease. Gastroenterol Hepatol 2017;13.
Mary J-Y, Modigliani R. Development and validation of an endoscopic index of the severity for Crohn's disease: a prospective multicentre study. Groupe d'Etudes Therapeutiques des Affections Inflammatoires du Tube Digestif (GETAID). Gut 1989;30:983-9.
Schroeder KW, Tremaine WJ, Ilstrup DM. Coated oral 5-aminosalicylic acid therapy for mildly to moderately active ulcerative colitis. N Engl J Med 1987;317:1625-9.
Schmittgen TD, Livak KJ. Analyzing real-time PCR data by the comparative CT method. Nat Protoc 2008;3:1101.
Mudter J, Neurath MF. Apoptosis of T cells and the control of inflammatory bowel disease: therapeutic implications. Gut 2007;56:293-303.
Kiesslich R, Duckworth CA, Moussata D, Gloeckner A, Lim LG, Goetz M, et al. Local barrier dysfunction identified by confocal laser endomicroscopy predicts relapse in inflammatory bowel disease. Gut 2012;61:1146-53.
Hagiwara C, Tanaka M, Kudo H. Increase in colorectal epithelial apoptotic cells in patients with ulcerative colitis ultimately requiring surgery. J Gastroenterol Hepatol 2002;17:758-64.
Di Sabatino A, Ciccocioppo R, Luinetti O, Ricevuti L, Morera R, Cifone MG, et al. Increased enterocyte apoptosis in inflamed areas of Crohn’s disease. Dis Colon Rectum 2003;46:1498-507.
Amini KA, Asadzadeh AH, Sorrentino D, Mirzaei A, Shahrokh S, Balaii H, et al. Transmembrane TNF-α Density, but not Soluble TNF-α Level, is Associated with Primary Response to Infliximab in Inflammatory Bowel Disease. Clin Translat Gastroenterol 2017;8:e117.
Bantel H, Berg C, Vieth M, Stolte M, Kruis W, Schulze-Osthoff K. Mesalazine inhibits activation of transcription factor NF-κB in inflamed mucosa of patients with ulcerative colitis. Am J Gastroenterol 2000;95:3452-7.
Taghipour N, Aghdaei HA, Haghighi A, Mossafa N, Tabaei SJ, Rostami-Nejad M. Potential treatment of inflammatory bowel disease: a review of helminths therapy. Gastroenterol Hepatol Bed Bench. 2014;7:9-16.
Di Sabatino A, Ciccocioppo R, Cinque B, Millimaggi D, Morera R, Ricevuti L, et al. Defective mucosal T cell death is sustainably reverted by infliximab in a caspase dependent pathway in Crohn’s disease. Gut 2004;53:70-7.
Danese S, Sans M, Scaldaferri F, Sgambato A, Rutella S, Cittadini A, et al. TNF-α blockade down-regulates the CD40/CD40L pathway in the mucosal microcirculation: a novel anti-inflammatory mechanism of infliximab in Crohn’s disease. J Immunol 2006;176:2617-24.
Lügering A, Schmidt M, Lügering N, Pauels H-G, Domschke W, Kucharzik T. Infliximab induces apoptosis in monocytes from patients with chronic active Crohn's disease by using a caspase-dependent pathway. Gastroenterology 2001;121:1145-57.
Coury F, Ferraro-Peyret C, Le Cam S, Guerin S, Tebib J, Sibilia J, et al. Peripheral blood lymphocytes from patients with rheumatoid arthritis are differentially sensitive to apoptosis induced by anti-tumour necrosis factor-alpha therapy. Clin Experiment Rheumatol 2008;26:234.
El-Hodhod M, Aly R, Youssef S, Mohamed S. Enhanced blood lymphocytes apoptosis in children with inflammatory bowel disease. ISRN gastroenterol 2013;2013:415417.
- Abstract Viewed: 146 times
- PDF Downloaded: 121 times