GASTROESOPHAGEAL REFLUX DISEASE AND BRONCHIAL ASTHMA: MECHANISMS OF COMORBID FORMATION AND COURSE.

Aleksey Oparin, Givi Akhvlediani, Anatoliy Oparin, Sergei Pavlov

Abstract


The aim of the study: To estimate the level of Galectin-3 with the parallel tracing of the content of pro- and anti-inflammatory cytokines Interleukin-6 (IL-6) and Interleukin-4 (IL-4) for patients with GERD and BA both in case of separate nosologies, and in case of their combined course during the period of exacerbation of the diseases.

Methods. The study was conducted in three groups of patients, homogeneous by gender and age. The first group included 18 patients with GERD. The second group included 19 patients with intermittent or persistent-mild bronchial asthma. The third group included 22 patients suffering from GERD with concomitant BA intermittent or persistent-mild severity. Determination of the level of galectin-3 and interleukins (IL-4 and IL-6) in the blood serum was carried out by enzyme-linked immunosorbent assay.

Results. Analyzing the results of the study, we found that the level of galectin - 3 was increased on average in both groups of patients with isolated GERD (and in patients with BA). In patients of the third group with comorbid pathology, the level of galectin-3 was statistically significantly higher than not only the norm, but also the average of patients with isolated BA and GERD. At the same time, we found the rise in the level of pro-inflammatory (IL-6) and anti-inflammatory (IL-4) cytokines. Moreover, in patients with GERD, the level of IL-6 was increased with a higher degree of reliability, and the level of IL-4 was increased with a lower degree of reliability. In patients with BA, on the contrary, the level of IL-4 was determined more often and higher, and the level of IL-6 was lower.

Conclusions. Analyzing result of the study, a clear correlation and features of changes in the level of galectin-3, IL-4, IL-6 in patients with isolated GERD, BA, as well as with the comorbidity of these diseases, were revealed.

In patients with BA, the level of galectin-3 increases with the same degree of certainty as in the group of patients with GERD. In the cytokine system, on the contrary, the level of anti-inflammatory (IL-4) cytokines increases with a greater degree of certainty than the level of pro-inflammatory (IL-6) cytokines.

In patients with GERD with concomitant BA, the level of galectin-3 increases with a greater degree of certainty. It is observed also a higher rising of pro-inflammatory (IL-6) cytokines and a slightly pronounced increasing of the level of anti-inflammatory (IL-4) cytokines in comparison with the group of patients with isolated GERD.


Keywords


GERD; BA; galectin-3; interleukins; comorbidity

Full Text:

PDF

References


Oparin, A. G., Oparin, A. A., Titkova, A. V. (2013). Rol soputstviushchei gastroezofagealnoi refliuksnoi bolezni v mekhanizme formirovaniia vospalitelnogo gomeostaza u bolnykh khronicheskoi obstruktivnoi bolezniu legkikh. Nauchnaia vzaimosviaz. Farmatsiia, 1 (154), 83–85.

Paleev, N. R., Isakov, V. A,, Ivanova, O. V. (2005). Bronkhialaia astma i gastroezofagealnaia refliuksnaia bolezn: sluchaina li vzaimosviaz? Klinicheskaia meditsina, 1, 9–14.

Panfilova, E. F. (2008). Novye biomarkery serdechnoi nedostatochnosti. Aktualnye voprosy. Farmateka, 12, 14.

Fadeenko, G. D., Gridnev, A. E. (2014). Gastroezofagealnaia refliuksnaia bolezn: pishchevodnye i vnepishchevodnye proiavleniia i komorbidnost. Kyiv, 367.

Fucumori, T., Takenoka, V., Yoshii, T., Kim, H. R., Hogan, V., Inohara, H. et. al. (2003). CD29 and CD7 mediate galectin-3 – induced type II T-cell apoptosis. Cancer Research, 63, 831.

Christenson, R. H., Duh, S.-H., Wu, A. H. B., Smith, A., Abel, G., deFilippi, C. R. et. al. (2010). Multi-center determination of galectin-3 assay performance characteristics: Clinical Biochemistry, 43 (7-8), 683–690. doi: http://doi.org/10.1016/j.clinbiochem.2010.02.001

Gehlken, C., Suthahar, N., Meijers, W. C., de Boer, R. A. (2018). Galectin-3 in Heart Failure. Heart Failure Clinics, 14 (1), 75–92. doi: http://doi.org/10.1016/j.hfc.2017.08.009

Arutiunov, A. G., Burkov, S. G., Shcherba, E. P. (2004). Mekhanizmy vzaimosviazi gastroezofagealnoi refliuksnoi bolezni i bronkhialnoi astmy i taktika vedeniia bolnykh. Klinicheskie perspektivy gastroenterologii i gepatologii, 2 (204), 5–9.

Berezniakov, V. I., Korzh, A. N. (2015). Soderzhanie prokaltsitonina galektina – 3 v krovi bolnykh s vnebolnichnoi pnevmoniei i soputstvuiushchei serdechnoi nedostatochnostiu i bez nee. Mezhdunarodnii meditsinskii zhurnal, 4, 13–17.

Korabelnikov, D. I., Chuchalin, A. G. (2002). Bronkhialnaia astma i soputstvuiushchiei zabolevaniia organov pishchevareniia. Pulmonologiia, 5, 87–92.

Liamina, S. V., Kruglov, S. V., Vedenikin, T. Iu. (2011). Novaia strategiia upravleniia immunnym otvetom pri zabolevaniiakh legkikh – rol surfaktantnogo belka D kak bivalentnogo faktora reprogrammirovaniia makrofagov. Fundamentalnye issledovaniia, 1, 90–98.

Doehner, W. (2012). Diagnostic biomarkers in cardiovascular disease: the proteomics approach. European Heart Journal, 33 (18), 2249–2251. doi: http://doi.org/10.1093/eurheartj/ehs187

Lok, D. J. A., Van Der Meer, P., de la Porte, P. W. B.-A., Lipsic, E., Van Wijngaarden, J., Hillege, H. L., van Veldhuisen, D. J. (2010). Prognostic value of galectin-3, a novel marker of fibrosis, in patients with chronic heart failure: data from the DEAL-HF study. Clinical Research in Cardiology, 99 (5), 323–328. doi: http://doi.org/10.1007/s00392-010-0125-y

Mueller, T., Leitner, I., Egger, M., Haltmayer, M., Dieplinger, B. (2015). Association of the biomarkers soluble ST2, galectin-3 and growth-differentiation factor-15 with heart failure and other non-cardiac diseases. Clinica Chimica Acta, 445, 155–160. doi: http://doi.org/10.1016/j.cca.2015.03.033

Lakomkin, A. A., Skvortsova, T. V., Gariunova, T. V. (2012). Galektin-3 – novii marker diagnostiki i prognoza serdechnoi nedostatochnosti. Kardiologiia, 3, 45–52.

Maev, I. V., Liamina, S. V., Kalish, S. V., Malysheva, E. V. (2014). Funktsionalnaia aktivnost alveoliarnykh makrofagov u bolnykh bronkhialnoi astmoi i gastroezofagealnoi refliuksnoi bolezniu. Klinicheskaia meditsina, 6, 41–48.

Woodruff, P. G., Modrek, B., Choy, D. F., Jia, G., Abbas, A. R., Ellwanger, A. et. al. (2009). T-helper Type 2–driven Inflammation Defines Major Subphenotypes of Asthma. American Journal of Respiratory and Critical Care Medicine, 180 (5), 388–395. doi: http://doi.org/10.1164/rccm.200903-0392oc

Maev, I. V., Liamina, S. V., Malysheva, E. V., IUrenev, G. L. (2015). Immunnii otvet i fenotip alveoliarnykh makrofagov pri bronkhialnoi astme, gastroezofagealnoi refliuksnoi bolezni i ikh sochetanii. Terapevticheskii arkhiv, 3, 34–41.

Barbas, A. S., Downing, T. E., Balsara, K. R., Tan, H. E., Rubinstein, G. J., Holzknecht, Z. E. et. al. (2008). Chronic aspiration shifts the immune response from Th1 to Th2 in a murine model of asthma. European Journal of Clinical Investigation, 38 (8), 596–602. doi: http://doi.org/10.1111/j.1365-2362.2008.01976.x

Gow, A. J., Guo, C. (2011). Surfactant Protein-D Regulates Alveolar Macrophage Phenotype. American Journal of Respiratory and Critical Care Medicine, 183, 1085. doi: http://doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a1085

Martinez, F. O., Gordon, S., Locati, M., Mantovani, A. (2006). Transcriptional Profiling of the Human Monocyte-to-Macrophage Differentiation and Polarization: New Molecules and Patterns of Gene Expression. The Journal of Immunology, 177 (10), 7303–7311. doi: http://doi.org/10.4049/jimmunol.177.10.7303

Woodruff, P. G., Modrek, B., Choy, D. F., Jia, G., Abbas, A. R., Ellwanger, A. et. al. (2009). T-helper Type 2–driven Inflammation Defines Major Subphenotypes of Asthma. American Journal of Respiratory and Critical Care Medicine, 180 (5), 388–395. doi: http://doi.org/10.1164/rccm.200903-0392oc




DOI: http://dx.doi.org/10.21303/2504-5679.2020.001199

Refbacks

  • There are currently no refbacks.




Copyright (c) 2020 Aleksey Oparin, Givi Akhvlediani, Anatoliy Oparin, Sergei Pavlov

Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 International License.

ISSN 2504-5679 (Online), ISSN 2504-5660 (Print)