KEMAMPUAN DARI Lactobacillus plantarum GALUR IS-10506 DAN IS-20506 DALAM MENGHAMBAT AKTIVASI NFkB, MEREGULASI TURUN TNF-RECEPTOR 1 (TNF-R1) DAN OPOPTOSIS PADA BRUSH SEL EPITEL BORDER Rattus novergicus YANG DIINDUKSI LPS

Authors

  • Titis Sari Kusuma Jurusan Ilmu Gizi Kesehatan Fakultas Kedokteran Universitas Brawijaya
  • Wibi Riawan Laboratorium Biokimia Biomolekuler Fakultas Kedokteran Universitas Brawijaya
  • I Gusti Made Reza Gunadi Ranuh Departemen Ilmu Kesehatan Anak Fakultas Kedokteran Universitas Airlangga
  • Ingrid S. Surono SEAMEO TROPMED, Universitas Indonesia

DOI:

https://doi.org/10.21776/ub.jkb.2008.024.01.3

Abstract

Probiotic bacteria have a beneficial effect on diarrhea. In this study, we have examined effect of Lactobacillus plantarum Strain IS-10506 (LIS-10506) and IS-20506  (LIS-20506) on inhibition of NFκB activation, downregulation TNF Receptor-1 (TNF-R1) and Apoptosis in Epithelial Brush Border of Rattus novergicus induced with LPS. On the first day, LPS was inducedto Rattus novergicus per oral. At the 3rdday, Lactobacillus plantarum Strain IS-10506 and LIS20506 separately were supplemented for 7 days (the 3rdday up to the 9thday). Rat was sacrificed after anaesthetizing with ether to assess NFκB activation, TNFR1 and apoptosis. Result showed the decreases of activation NFκB in LIS-10506 group as well as in LIS-20506 group, significantly different, in NFκB activation at group with only LPS (average 14.33+4.509) compared to group with LIS-10506 induction (average 2.00+1.732)and LIS-20506 induction (average 1.33+1.528), at p( p<0.000). Downregulation of TNF-R1 was significant  at LPS group compared to LIS-10506 induction as well as LIS-20506 induction. The index of apoptosis showed significant of degradation (p<0.000) after induced by LIS, where LPS group (14.67+2.517), LIS-10506 induction (6.33+2.309) and LIS-20506 induction (6.00+3.000). As a conclusion, supplementation of LIS-10506 and LIS-20506 separately will inhibit theNFκB activation, and although the mechanism was not sure, what by significant degrade the expression TNF-R1( as ekuivalen of activity TNFα), and the mentioned give the implication that happened by the degradation of occurence apoptosis at cell of epitel bush border intestine.

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References

Le Luyer, B., C. L. Morin, et al. Crohn's disease in children and adolescents. Arch Fr Pediatr 1985; 42(8): 677-82.

Saavedra, J.M., A. Abi-Hanna, et al. Long-term consumption of infant formulas containinglive probiotic bacteria: tolerance and safety. Am J Clin Nutr 2004; 79(2): 261-7.

Ahmed, M., A. G. Billoo, et al. Risk factors of persistent diarrhoea in children below five years of age. J Pak Med Assoc 1995; 45(11): 290-2.

Vanderhoof, J. A. and R. J. Young. Use of probiotics in childhood gastrointestinal disorders. J Pediatr Gastroenterol Nutr 1998; 27(3): 323-32.

Mack, D. R., S. Michail, et al. Probiotics inhibit enteropathogenic E. coli adherence in vitro by inducing intestinal mucin gene expression. Am J Physiol 1999; 276(4 Pt 1): G941-50.

Van Neil, C. W., C. Feudtner, et al. Lactobacillus Therapy for Acute Infectious Diarrheain Children:A Meta-analysis.Pediatrics 2002; 109: 678-684.

Marteau, P. and F. Shanahan. Basic aspects and pharmacology of probiotics: an overview of pharmacokinetics, mechanisms of action and side-effects. Best Pract Res Clin Gastroenterol 2003; 17(5): 725-40.

Bibiloni, R., R.N. Fedorak, et al. VSL#3 probiotic-mixture induces remission in patients with active ulcerative colitis. Am J Gastroenterol 2005; 100(7): 1539-46.

Perdigon, G., S. Alvarez, et al. Immune system stimulation by probiotics. J Dairy Sci 1995; 78(7): 1597-606.

Mettienen, M., S. Matikainen, et al. Lactobacilli and Streptococci Induce Interleukin-12(IL-12), IL-18, and Gamma Interferon Production in Human Peripheral Blood Mononuclear Cells. Infect Immun 1998; 66: 6058-52.

Matsuzaki, T. and J. Chin. Modulating immune responses with probiotic bacteria.Immunol Cell Biol 2000; 78(1): 67-73.

Blackwell, T., S. and J. Christman, W. The Role of Nuclear Factor-kB in Cytokine Gene Regulation. Am.J.Respir.Cell Mol.Biol 1997; 17: 3-9.

Collins T, Cybulsky M. NF-kB: pivotal mediator or innocent bystander in atherogenesis?.J Clin Invest 2001;107:255-265.

Worns, M. A., A. W. Lohse, et al. Five cases of de novo inflammatory bowel disease after orthotopic liver transplantation. Am J Gastroenterol 2006; 101(8): 1931-7.

Palinski, W and Sotirios T. Immunomodulatory Effects of Statins: Mechanisms andPotential Impact on Arteriosclerosis. J Am Soc Nephrol 2002; 13:1673-1681

Husada, J.J. The Role of Apoptosis in Brain Injury. Simposium Neuro Intensif Quality Hotel, Solo. 9-10 Oktober 2004.

Boatright, K.M dan Guy S. Salvesen. Mechanism of Caspase Activation. Current Opinion in Cell Biology 2003; 15 : 725-731.

Soini Y, Paakko P, and Lehto V.P. Histopathological Evaluation of Apoptosis in Cancer. American Journal of Pathology 1998; 153(4): 1041-1048

Pizem, J. and Cor A. Detection of Apoptosis Cells in Tumour Paraffin Section, Radiol. Onco 2003; 37(4): 225-232

Evans, T J. Moyes D, Carpenter A et al. Protective effect of 55- but not 75-kD soluble tumor necrosis factor receptor-immunoglobulin G fusion protein in an animal model of gram-negative sepsis. J Exp Med 1994; 180: 2173–2179

Bowen, R. The Gastrointestinal Barrier. 2006, 1-7.

Just, I., G. Fritz, et al. Clostridium difficle Toxin B acts on the GTP-binding protein Rho. J Biol Chem 1994; 269: 10706-12.

Dilon,S., E. Rubin, et al. Involvement of Ras-related Rho proteins in the mechanisms of action Clostridium difficile Toxin A and Toxin B. Infect Immun 1995; 63: 1421-6.

Just, I., J. Selzer, et al. Glucosylation of Rho proteins by Clostridium difficle Toxin B. Nature 1995; 375: 500-3.

Moore, J., H. Garner, et al. Intracecal endotoxin and lactate during the onset of equine laminitis: a preliminary report. Am J Vet Res 1979; 40: 722–723.

Ruemmele, F. M. Chronic enteropathy: molecular basis. Nestle Nutr Workshop Ser Pediatr Program 2007; (59): 73-85; discussion 85-8.

Aderem, A. and R. Ulevitch. Toll-like receptors in the induction of the innate immune response. Nature 2000; 406: 782–787.

Abreu, M., E. Arnold, et al. TLR4 and MD-2 expression is regulated by immune-mediated signals in human intestinal epithelial cells. J Biol Chem 2002; 277: 20431–20437.

Antal-Szalmas, P. Evaluation of CD14 in host defense. Eur J Clin Invest 2000; 30: 167–179.

Libby, P. Inflammation in atherosclerosis, Nature 2002; Dec 19-26;420(6917):868-74.

Palinski, W and Sotirios T. Immunomodulatory Effects of Statins: Mechanisms and Potential Impact on Arteriosclerosis, J Am Soc Nephrol 2002; 13:1673-1681.

Szmitko, PE. Chao-Hung W, Richard D. W, Greg A. J, Todd J. A, Subodh V. Biomarkers of Vascular Disease Linking Inflammation to Endothelial Activation. Circulation 2003; 108:2041-2048.

Hansson, G. Regulation of Immune Mechanisms in Atherosclerosis. Annals of the New York Academy of Sciences 2001; 947:157-166.

Montalto, M., F. Arancio, et al. Probiotics: history, definition, requirements and possible therapeutic applications.Ann Ital Med Int 2002;17(3): 157-65.

Cataloluk, O. and B. Gogebakan. Presence of drug resistance in intestinal Lactobacilli of diary and human origin in Turkey. FEMS Microbiol Lett 2004; 236(1): 7-12.

Surono, I. and A. Harsono. Antimutagenicity of milk cultured with lactic acid bacteria from dadih against mutagenic terassi. Milchwissenschaft 1996; 51: 493-497.

Surono, I. In vitro probiotic properties of indigenous dadih lactic acid bacteria. Asian-Aus. J.Anim.Sci 2003;16: 726-731.

Neurath, M. F., I. Fuss, et al. Antibodies to interleukin 12 abrogate established experimental colitis in mice. J Exp Med 1995; 182(5): 1281-90.

Menard, S., C Candalh, J C Bambou, et al. Lactic acid bacteria secrete metabolites retaining anti-inflammatory properties after intestinal transport. Gut 2004; 53:821–828

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Published

2013-04-29

Issue

Vol. 24 No. 1 (2008)

Section

Research Article

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