DOI QR코드

DOI QR Code

Effects of the Oral Administration of a Probiotic Combination on the Expression of Cytokine and the Histopathology of the Large Intestine in an Animal Model of Enteritis

  • Received : 2011.03.10
  • Accepted : 2012.03.19
  • Published : 2012.04.30

Abstract

It is known that lactic-acid bacteria (LAB) helps keeping the intestine healthy and to enhance its immunologic competence. In addition, it is known to control the composition of the enterobacteria and the intestinal inflammatory reaction by inducing immunological enhancement. This study was performed, in a mouse model, to test the treatment and preventive effects of LAB of inflammatory bowel disease (IBD), which was induced by a blend of LAB-administering trinitrobenzene sulfonic acid (TNBS). To obtain the animal model of IBD, 2% TNBS was rectally administered once to a five-week-old male Balbc/J mouse. A probiotic combination was administered to the prevention group five times a week for eight weeks before the inducement of enteritis, and the mixture was administered to the treatment group five times a week, after the administration of TNBS. The changes in the levels of the cytokines of the lymph nodes and the tissue of the large intestine were observed, both with the naked eye and with a microscope. The observation showed that the levels of inflammatory cells, infiltration, and necrosis were much lower in the LAB-administered groups than in that of the control group. In addition, the inflammatory cytokines (e.g., TNF-${\alpha}$, IL-17A) decreased in the lymph nodes and the tissues of the large intestine. The results indicated that the administration of the combination to the animal model suppressed the inflammatory cytokines in the large intestine and in the lymph nodes, which in turn suppressed the progression of colitis.

Keywords

References

  1. Andreakos, E. T., Foxwell, B. M., Brennan, F. M., Maini, R. N., and Feldmann M. (2002) Cytokines and anti-cytokine biologicals in autoimmunity: present and future. Cytokine Growth Factor Rev. 13, 299-313. https://doi.org/10.1016/S1359-6101(02)00018-7
  2. Bussolino, F., Ziche, M., Wang, J. M., Alessi, D., Morbidelli, L., Cremona, O., Bosia, A., Marchisio, P. C., and Mantovani, A. (1991) In vitro and in vivo activation of endothelial cells by colony-stimulating factors. J. Clin. Invest. 87, 986-995. https://doi.org/10.1172/JCI115107
  3. Fabia, R., Ar'Rajab, A., Johansson, M. L., Andersson, R., Willen, R., Jeppsson, B., Molin, G., and Bengmark, S. (1993) Impairment of bacterial flora in human ulcerative colitis and experimental colitis in the rat. Digestion 54, 248-255. https://doi.org/10.1159/000201045
  4. Favier, C., Neut, C., Mizon, C., Cortot, A., Colombel, J. F., and Mizon, J. (1997) Fecal beta-D-galactosidase production and Bifidobacteria are decreased in Crohn's disease. Dig. Dis. Sci. 42, 817-822. https://doi.org/10.1023/A:1018876400528
  5. Gabay, C. and Kushner, I. (1999) Acute-phase proteins and other systemic responses to inflammation. N. Engl. J. Med. 340, 448-454. https://doi.org/10.1056/NEJM199902113400607
  6. Hoffmann, J. C., Peters, K., Henschke, S., Herrmann B., Pfister, K., Westermann, J., and Zeitz, M. (2001) Role of T lymphocytes in rat 2,4,6-trinitrobenzene sulphonic acid (TNBS) induced colitis: increased mortality after gammadelta T cell depletion and no effect of alphabeta T cell depletion. Gut 48, 489-495. https://doi.org/10.1136/gut.48.4.489
  7. Kim, J. J., Ryu, J. K., Lee, D. H., Song, S. I., Kim, C. Y., and Kim, Y. I. (1996) The effect of anti-inflammatory drugs on colitis induced by trinitrobenzene sulfonic acid in rats. Korean J. Gastroenterol. 28, 224-231.
  8. Morris, G. P., Beck, P. L., Herridge, M. S., Depew, W. T., Szewczuk, M. R., and Wallace, J. L. (1989) Hapten-induced model of chronic inflammation and ulceration in the rat colon. Gastroenterology 96, 795-803. https://doi.org/10.1016/S0016-5085(89)80079-4
  9. Neurath, M., Fuss, I., and Strober, W. (2000) TNBS-colitis. Int. Rev. Immunol. 19, 51-62. https://doi.org/10.3109/08830180009048389
  10. Ott, S. J., Musfeldt, M., Wenderoth, D. F., Hampe, J., Brant, O., Folsch, U. R., Timmis, K. N., and Schreiber, S. (2004) Reduction in diversity of the colonic mucosa associated bacterial microflora in patients with active inflammatory bowel disease. Gut 53, 685-693. https://doi.org/10.1136/gut.2003.025403
  11. Platzer, E. (1989) Human hemopoietic growth factors. Eur. J. Haematol. 42, 1-15.
  12. Rogler, G. and Andus, T. (1998) Cytokines in inflammatory bowel disease. World J. Surg. 22, 382-389. https://doi.org/10.1007/s002689900401
  13. Sartor, R. B. (1997) Pathogenesis and immune mechanisms of chronic inflammatory bowel diseases. Am. J. Gastroenterol. 92, 5S-11S.
  14. Seksik, P., Rigottier-Gois, L., Gramet, G., Sutren, M., Pochart, P., Marteau, P., Jian, R., and Dore, J. (2003) Alterations of the dominant faecal bacterial groups in patients with Crohn's disease of the colon. Gut 52, 237-242. https://doi.org/10.1136/gut.52.2.237
  15. Swidsinski, A., Ladhoff, A., Pernthaler, A., Swidsinski, S., Loening-Baucke, V., Ortner, M., Weber, J., Hoffmann, U., Schreiber, S., Dietel, M., and Lochs, H. (2002) Mucosal flora in inflammatory bowel disease. Gastroenterology 122, 44-54. https://doi.org/10.1053/gast.2002.30294
  16. Weaver, C. T., Hatton, R. D., Mangan, P. R., and Harrington, L. E. (2007) IL-17 family cytokines and the expanding diversity of effector T cell lineages. Annu. Rev. Immunol. 25, 821-852. https://doi.org/10.1146/annurev.immunol.25.022106.141557
  17. Yamada, Y., Marshall, S., Specian, R. D., and Grisham, M. B. (1992) A comparative analysis of two models of colitis in rats. Gastroenterology 102, 1524-1534. https://doi.org/10.1016/0016-5085(92)91710-L
  18. Yeom, M.-J., Choi, B.-H., Han, D.-O., Lee, H.-J., Shim, I., Kim, S.-H., and Hahm, D.-H. (2004) In vitro inhibition of pro-inflammatory mediator mRNA expression by nephrite in lipopolysaccharide-induced mouse macrophage cells. Korean J. Oriental Physiol. Pathol. 18, 1622-1627.