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s MadCAM-1 as an immunological marker in the «gut liver axis» at patients with chronic hepatitis C and excess body weight

https://doi.org/10.22625/2072-6732-2019-11-2-63-70

Abstract

Background and aims: to estimate concentration of sMadCAM-1 in peripheral blood at patients with chronic hepatitis C with excess body weight.

Materials and methods: The research included 88 patients (67 men, 21 women 41.4±3.2 years of age) with chronic hepatitis C (CHC) and excess body weight (the index of body mass is ³25 kg/m2, and abdominal circumference more than 94 cm in men, and 80 cm in women) with various morfofunktsionalny changes in a liver and a small bowel. From them men there were 67 people, women – 21, middle age was 41.4±3.2 years.

To all the patients complex clinical, biochemical, virologic, morphological trial was carried out. The functional condition of intestines was estimated by identification of a small intestinal bacterial overgrowth (SIBO) when carrying out the hydrogen respiratory test (HRT) with lactulose and existence of endoscopic signs of inflammation of a mucous membrane of intestines at a fibroezofagogastroduodenoskopiya. The quantitative assessment of a mucosal addressin cell adhesion molecule -1 was carried out by the definition concentration of its soluble form (sMadCAM-1) in a blood plasma by enzyme immunoassay method.

Results: the sMadCAM-1 level of peripheral blood at the patients with excess body weight increased in process of progressing of a stage of chronic hepatitis C (F0 – 349.10 (324.27-373.92) ng/ml; F1/2 – 439.69 (406.43-472.94) ng/ml; F3/4 – 1057.82 (593.38-1522.26) ng/ml; p˂0.05), existence of a syndrome of excess bacterial growth and endoscopic signsof a duodenitis. Besides, patients had its concentration more with the biochemical signs characterizing cytolytic (at ALT˃N: 502.54 (432.04-573.03) ng/ml against 381.04(345.49-416.58) at the ALT normal values), cholestatic (at GGTP˃N: 550.59 (453.31-647.88) ng/ml against 400.86(365.13-436.59) atnormal GGTP, p values 0.05; at ALP N: 572.2 (353.7-790.8) ng/ml against 468.7 (408.5-528.9) ng/ml at normal ALP, p values 0.05) and metabolic syndromes (at glucose of blood, TG, VLDL N: 562.93 (369.59-756.27) ng/ml, 681.15 (387.81-974.49) ng/ml, 809.65(124.04-1495.28) against (438.34(391.36-485.31) ng/ml), (421.69(379.41-463.97) ng/ml), 434.47(389.45-479.48), p values 0.05 at normal values of these indicators respectively).

Conclusion: Progressing of fibrosis and functional disturbances in intestines are interconnected with increase in concentration of MadCAM-1 in blood that allows to consider pathological changes in intestines of various genesis as the accessory factor promoting progressing of СHC at patients with excess body weight. Besides, definition of concentration of sMadCAM-1 in peripheral blood can be used as one of markers of noninvasive diagnostics of a stage of fibrosis at the patients with СHC and excess body weight.

About the Authors

K. V. Zhdanov
Military Medical Academy named after S.M. Kirov
Russian Federation
Saint-Petersburg


A. V. Semenov
Science Research Institute of Epidemiology and Microbiology named after Pasteur
Russian Federation
Saint-Petersburg


S. S. Karyakin
Military Medical Academy named after S.M. Kirov
Russian Federation
Saint-Petersburg


K. V. Kozlov
Military Medical Academy named after S.M. Kirov
Russian Federation
Saint-Petersburg


V. S. Sukachev
Military Medical Academy named after S.M. Kirov
Russian Federation
Saint-Petersburg


Yu. V. Ostankova
Science Research Institute of Epidemiology and Microbiology named after Pasteur
Russian Federation
Saint-Petersburg


D. E. Valutite
Science Research Institute of Epidemiology and Microbiology named after Pasteur
Russian Federation
Saint-Petersburg


E. B. Zueva
Science Research Institute of Epidemiology and Microbiology named after Pasteur
Russian Federation
Saint-Petersburg


R. S. Sidorov
Center for Prevention and Control of AIDS and Infectious Diseases
Russian Federation
Saint-Petersburg


A. V. Saulevich
Military Medical Academy named after S.M. Kirov
Russian Federation
Saint-Petersburg


Yu. I. Bulan’kov
Military Medical Academy named after S.M. Kirov
Russian Federation
Saint-Petersburg


Yu. I. Lyashenko
Military Medical Academy named after S.M. Kirov
Russian Federation
Saint-Petersburg


K. S. Ivanov
Military Medical Academy named after S.M. Kirov
Russian Federation
Saint-Petersburg


References

1. Global hepatitis report. WHO 2017.

2. ZHdanov K. V., Lobzin YU.V, Gusev D.A., Kozlov K.V. Viral hepatitis .SPb.;Foliant, 2011. 304 p (in Russian)

3. Lauer G.M., Walker B.D. Hepatitis C virus infection. N Engl J Med 2001;345:41–52.

4. Webster D.P, Klenerman P, Dusheiko GM. Hepatitis C. Lancet Lond Engl 2015;385:1124–35.

5. Denisov N.L., Grinevich V.B., Kravchuk YU.A., Kornouhov L.A. Medicinskij Alfavit. 2016;3:46–51. (in Russian).

6. Volta U., Bonazzi C., Bianchi F.B., Baldoni A.M., Zoli M., Pisi E. IgA antibodies to dietary antigens in liver cirrhosis. Ric Clin Lab 1987;17:235–42.

7. Kirpich I.A., Marsano L.S., McClain C.J. Gut-liver axis, nutrition, and non-alcoholic fatty liver disease. Clin Biochem 2015;48:923–30.

8. Trivedi P.J., Adams D.H. Gut-liver immunity. J Hepatol 2016;64:1187–9.

9. Talanceva M.S., ZHdanov K.V., SHustov S.B, Barsukov A.V., Kozlov K.V., Sveklina T.S. Arterial’naya gipertenziya. 2012; 1 (18): 62-66.

10. Brandl K., Kumar V., Eckmann L. Gut-liver axis at the frontier of host-microbial interactions. Am J Physiol-Gastrointest Liver Physiol 2017;312:G413–9.

11. Inagaki T, Moschetta A, Lee Y-K, Peng L, Zhao G, Downes M, et al. Regulation of antibacterial defense in the small intestine by the nuclear bile acid receptor. Proc Natl Acad Sci U S A 2006;103:3920–5.

12. Hylemon P.B., Zhou H., Pandak W.M., Ren S., Gil G., Dent P. Bile acids as regulatory molecules. J Lipid Res 2009;50:1509–20.

13. Balmer M.L., Slack E., de Gottardi A., Lawson M.A.E., Hapfelmeier S., Miele L. et al. The liver may act as a firewall mediating mutualism between the host and its gut commensal microbiota. Sci Transl Med 2014;6:237 -66.

14. Cani P.D., Delzenne N.M. Interplay between obesity and associated metabolic disorders: new insights into the gut microbiota. Curr Opin Pharmacol 2009;9:737–43.

15. ZHdanov K.V., Zaharenko S.M., Kozlov K.V., Gusev D.A., Sukachev V.S., Kurtukov M.V. Lechenie I Profilaktika 2014:18–26 (in Russian).

16. Salmi M., Jalkanen S. Ectoenzymes in leukocyte migration and their therapeutic potential. Semin Immunopathol 2014;36:163–76.

17. Burmester G.-R., Pecutto A. Evident immunology .M.: BINOM. Laboratoriya znanij, 2014. 320 p (in Russian).

18. Alford S.K., Longmore G.D., Stenson W.F., Kemper C. CD46-induced immunomodulatory CD4+ T cells express the adhesion molecule and chemokine receptor pattern of intestinal T cells. J Immunol Baltim Md 1950 2008;181:2544–55.

19. Trivedi P.J., Bruns T., Ward S., Mai M., Schmidt C., Hirschfield G.M. et al. Intestinal CCL25 expression is increased in colitis and correlates with inflammatory activity. J Autoimmun 2016;68:98–104.

20. Trivedi P.J., Adams D.H. Mucosal immunity in liver autoimmunity: a comprehensive review. J Autoimmun 2013;46:97–111.

21. Ala A., Brown D., Khan K., Standish R., Odin JA, Fiel MI. et al. Mucosal addressin cell adhesion molecule (MAdCAM-1) expression is upregulated in the cirrhotic liver and immunolocalises to the peribiliary plexus and lymphoid aggregates. Dig Dis Sci 2013;58:2528–41.

22. Drescher H.K., Schippers A., Clahsen T., Sahin H., Noels H., Hornef M. et al. β7-Integrin and MAdCAM-1 play opposing roles during the development of non-alcoholic steatohepatitis. J Hepatol 2017;66:1251–64.

23. Grant A.J., Lalor P.F., Hübscher S.G., Briskin M., Adams D.H. MAdCAM-1 expressed in chronic inflammatory liver disease supports mucosal lymphocyte adhesion to hepatic endothelium (MAdCAM-1 in chronic inflammatory liver disease). Hepatol Baltim Md 2001;33:1065–72.

24. Ogawa H., Binion D.G., Heidemann J., Theriot M., Fisher P.J., Johnson N.A. et al. Mechanisms of MAdCAM-1 gene expression in human intestinal microvascular endothelial cells. Am J Physiol Cell Physiol 2005;288:C272-281.

25. Tanida S., Mizoshita T., Mizushima T., Sasaki M., Shimura T., Kamiya T. et al. Involvement of oxidative stress and mucosal addressin cell adhesion molecule-1 (MAdCAM-1) in inflammatory bowel disease. J Clin Biochem Nutr 2011;48:112–6.

26. Currò D., Pugliese D., Armuzzi A. Frontiers in Drug Research and Development for Inflammatory Bowel Disease. Front Pharmacol 2017;8:400.

27. Eaton J.E., Talwalkar J.A., Lazaridis K.N., Gores G.J., Lindor K.D. Pathogenesis of primary sclerosing cholangitis and advances in diagnosis and management. Gastroenterology 2013;145:521–36.

28. Hillan K.J., Hagler K.E., MacSween R.N., Ryan A.M., Renz M.E., Chiu H.H. et al. Expression of the mucosal vascular addressin, MAdCAM-1, in inflammatory liver disease. Liver 1999;19:509–18.

29. Borovikov V. P. Popular introduction to the modern analysis of data in the STATISTICA system. Moscow.: Goryachaya liniya – Telekom, 2016. 288 p ( in Russian).


Review

For citations:


Zhdanov K.V., Semenov A.V., Karyakin S.S., Kozlov K.V., Sukachev V.S., Ostankova Yu.V., Valutite D.E., Zueva E.B., Sidorov R.S., Saulevich A.V., Bulan’kov Yu.I., Lyashenko Yu.I., Ivanov K.S. s MadCAM-1 as an immunological marker in the «gut liver axis» at patients with chronic hepatitis C and excess body weight. Journal Infectology. 2019;11(2):63-70. (In Russ.) https://doi.org/10.22625/2072-6732-2019-11-2-63-70

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