Experience of investigation the microflora and ejaculate proteins with different ultrasound picture of prostate

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Abstract

At present, there are practically no studies deciphering the mechanisms of the possible influence of opportunistic pathogens on the morphological changes in the prostate gland. Many authors doubt that bacteria are the cause of chronic prostatitis. In clinical practice with prostate diseases preference is given to ultrasound examination as a reliable and time-consuming diagnostic test. At the same time, many authors note that for the diagnosis of inflammatory diseases of reproductive organs, the study of relevant secrets is an actual and promising scientific direction.

The aim of the study was the investigation of qualitative and quantitative composition of microflora, a number of ejaculate proteins against the background of a different echoscopic picture of prostate.

Materials and methods. The study included 18 men was in infertile couples for more than 3 years with a previously diagnosed chronic prostatitis (N41.1, observation group), and 28 healthy volunteers (comparison group). All participants in the study performed transrectal ultrasound. In the ejaculate, the concentrations of immunoglobulins of the main classes, total protein and albumin, as well as the level of oxidative modification of proteins were determined. Microbiological examination of the ejaculate was performed according to generally accepted methods. For statistical evaluation of the data obtained, an unpaired version of Student's t-test was used. Differences were considered statistically significant at p<0.05.

Results. Microflora of the ejaculate in observation group was represented mainly by gram-positive cocci. In 39% of cases, the growth of Gram-negative microflora was established, from which Escherichia coli was isolated in 71% of the samples. In most samples, microorganisms were in the association, which is more typical for diffuse changes in prostate tissue. In cases with fibrosis, a noticeable narrowing of the spectrum of the released microflora was recorded: from Gram-negative bacteria only E. coli was isolated, and Gram-positive microorganisms were absent altogether. It was shown that the development of fibrosis in the prostate gland tissue is accompanied by an increase in the concentration of total protein and albumin in the ejaculate. When the process goes to the calcification stage, the levels of these indicators decrease. It was found that in all cases, with the exception of severe fibrosis, the concentration of IgG increases and IgA decreases. The development of fibrosis is accompanied by a decrease in the level of IgG. In the present study, in determining the level of oxidative modification of proteins, a decrease in the concentration of such molecules was found in patients of observation group.

Discussion. In general, chronic inflammation in prostate of men of reproductive age in more than 60% of cases was characterized by fibrosis of the organ tissue and/or the formation of calcifications. In such situation, conditions are created for the persistence of opportunistic pathogenic microflora in fibro-modified tissue beyond the reach of immune system factors. In addition, there are phenomena of secondary immunodeficiency at the local level, manifested in a decrease in the number of leukocytes and their radical-producing function. That is why we consider the detection of conditionally pathogenic microorganisms as an essential fact of the pathogenesis of prostatitis, especially in the case of fibrosis and the formation of calcifications. Thus, the qualitative and quantitative study of microflora, the presence and degree of modification of the main protein components of the ejaculate, to a greater or lesser extent reacting to infectious inflammation, is primarily an asymptomatic one, broadens the concept of the pathogenesis of chronic prostatitis. As an addition to the ultrasound, its results allow us to clarify the duration of the inflammatory process, and to significantly decipher the echographic changes recorded at different stages of the development of the disease.

About the authors

A. P. Godovalov

Perm State Medical University named after academician E.A. Wagner

Author for correspondence.
Email: AGodovalov@gmail.com
ORCID iD: 0000-0002-5112-2003

PhD (Medicine), Leading Researcher of the Central Scientific Laboratory; Associate Professor, Department of Microbiology and Virology

SPIN-код: 4482-4378, AuthorID: 632987

Contacts: Anatoliy P. Godovalov 614990, Russian Federation, Perm, Ekaterininskaya str., 85, Perm State Medical University named after academician E.A. Wagner. Phone: +7 (342) 236-44-85, +7 (912) 981-51-00

Russian Federation

T Yu. Danielyan

"Medical Studio” LLC

Email: perm-med@mail.ru
MD, PhD, Chief Medical Officer Russian Federation

T I. Karpunina

Perm State Medical University named after academician E.A. Wagner

Email: karpuninapsma@mail.ru
ORCID iD: 0000-0003-2511-4656

PhD, MD (Biology), Professor, Professor of the Department of Microbiology and Virology y

SPIN-код: 2542-8015, AuthorID: 148127

Russian Federation

N V. Vavilov

Perm State Medical University named after academician E.A. Wagner

Email: nikione@yandex.ru

Resident Physician, Department of Microbiology and Virology

SPIN-код: 9689-6946, AuthorID: 995599

Russian Federation

References

  1. Бобков Ю.А., Аль-Шукри С.Х., Горбачев А.Г., Галкина О.В., Козлов В.В., Тотолян А.А. Информативность показателей местного иммунитета при хроническом простатите // Медицинская иммунология. 2000. Т. 2, № 4. С. 401–408.
  2. Вавилов Н.В., Шилов Ю.И. Модификация метода оценки окислительной модификации белков // Медицинская иммунология. 2017. Т. 19, Спец. вып. С. 254.
  3. Годовалов А.П., Карпунина Т.И. Микробиота эякулята мужчин с бесплодием в условиях крупного промышленного города // Известия Самарского научного центра Российской академии наук. Социальные, гуманитарные, медикобиологические науки. 2015. № 17 (5–2). С. 338–343.
  4. Годовалов А.П., Карпунина Т.И. Опыт изучения образцов эякулята инфертильных мужчин с бессимптомной бактериоспермией // Здоровье и образование в XXI веке. 2015. Т. 17, № 11. С. 19–24.
  5. Горпинченко И.И., Мигов В.Г. Ударно-волновая терапия больных хроническим калькулезным простатитом // Здоровье мужчины. 2012. № 4. С. 75–78.
  6. Дубинина Е.Е., Бурмистров С.О., Ходов Д.А., Поротов Г.Е. Окислительная модификация белков сыворотки крови человека, метод ее определения // Биомедицинская химия. 1995. Т. 41. № 1. С. 24–26.
  7. Евдокимов В.В., Раков С.С., Липатова Н.А. Комплексное лабораторное исследование эякулята при заболеваниях мужской репродуктивной системы // Клиническая лабораторная диагностика. 1995. № 6. С. 114–116.
  8. Копытова Т.В., Пантелеева Г.А., Дмитриева О.Н., Коткова Е.В. Оценка окислительной модификации белков у больных хроническими распространенными дерматозами // Клиническая лабораторная диагностика. 2014. № 2. С. 41–44.
  9. Тер-Аванесов Г.В. Андрологические аспекты бесплодного брака // Качество жизни. Медицина. 2004. № 3. С. 60.
  10. Тотолян А.А. Современные подходы к диагностике иммунопатологических состояний // Медицинская иммунология. 1999. Т. 1, № 1–2. С. 75–108.
  11. Тюзиков И.А. Окислительный стресс как ключевой механизм старения: патофизиологические механизмы и SMART-диагностика // Вопросы диетологии. 2017. T. 7, № 1. С. 47–54.
  12. Choi Y.S., Kim K.S., Choi S.W., Kim S., Bae W.J., Cho H.J., Hong S.H., Kim S.W., Hwang T.K., Lee J.Y. Microbiological etiology of bacterial prostatitis in general hospital and primary care clinic in Korea. Prostate Int., 2013, vol. 1, no. 3, pp. 133–138. doi: 10.12954/PI.13023
  13. Elkahwaji J.E., Zhong W., Hopkins W.J., Bushman W. Chronic bacterial infection and inflammation incite reactive hyperplasia in a mouse model of chronic prostatitis. Prostate, 2007, vol. 67, no. 1, pp. 14–21. doi: 10.1002/pros.20445
  14. Fabre V., Wu H., PondTor S., Coutinho H., Acosta L., Jiz M., Olveda R., Cheng L., White E.S., Jarilla B. Tissue inhibitor of matrixmetalloprotease1 predicts risk of hepatic fibrosis in human schistosoma japonicum infection. J. Infect. Dis., 2011, vol. 203, pp. 707–714. doi: 10.1093/infdis/jiq099
  15. Karsdal M.A., Genovese F., Madsen E.A., Manon-Jensen T., Schuppan D. Collagen and tissue turnover as a function of age: Implications for fibrosis. J. Hepatol., 2016, vol. 64, pp. 103–109. doi: 10.1016/j.jhep.2015.08.014
  16. Khan F.U., Ihsan A.U., Khan H.U., Jana R., Wazir J., Khongorzul P., Waqar M., Zhou X. Comprehensive overview of prostatitis. Biomed. Pharmacother., 2017, vol. 94, pp. 1064–1076. doi: 10.1016/j.biopha.2017.08.016
  17. Krieger J.N., Lee S.W., Jeon J., Cheah P.Y., Liong M.L., Riley D.E. Epidemiology of prostatitis. Int. J. Antimicrob. Agents., 2008, vol. 31 (suppl. 1), pp. S85–S90. doi: 10.1016/j.ijantimicag.2007.08.028
  18. Nagy E., Szoke I., Torok L., Pajor L. The role of anaerobic bacteria in prostatitis. Adv. Exp. Med. Biol., 2000, vol. 485, pp. 289–299. doi: 10.1007/0-306-46840-9_38 1
  19. Nickel J.C. Chronic prostatitis: current concepts and antimicrobial chemotherapy. Infect. Urol., 2000, vol. 13, no. 5, pp. 22–28.
  20. Palapattu G.S., Sutcliffe S., Bastian P.J. Prostate carcinogenesis and inflammation: emerging insights. Carcinogenesis, 2005, vol. 26, no. 7, pp. 1170–1181. doi: 10.1093/carcin/bgh317
  21. Reznick A.Z., Packer L. Oxidative damage to proteins: spectrophotometric method for carbonyl assay. Methods Enzym., 1994, vol. 233, pp. 357–363. doi: 10.1016/S0076-6879(94)33041-7
  22. Stamatiou K. The undefined role of Gram positive bacteria in chronic prostatitis development. Infez. Med., 2013, vol. 21 (1), pp. 85–87.
  23. Thurmond P., Yang J.-H., Li Y., Lerner L.B., Azadzoi K.M. Structural modifications of the prostate in hypoxia, oxidative stress, and chronic ischemia. Korean J. Urol., 2015, vol. 56, no. 3, pp. 187–196. doi: 10.4111/kju.2015.56.3.187
  24. Tinkel J., Hassanain H., Khouri S.J. Cardiovascular antioxidant therapy: a review of supplements, pharmacotherapies, and mechanisms. Cardiol. Rev., 2012, vol. 20, no. 2, pp. 77–83. doi: 10.1097/CRD.0b013e31823dbbad
  25. Trujillo K.A., Heaphy C.M., Mai M., Vargas K.M., Jones A.C., Vo P., Butler K.S., Joste N.E., Bisoffi M., Griffith J.K. Markers of fibrosis and epithelial to mesenchymal transition demonstrate field cancerization in histologically normal tissue adjacent to breast tumors. Int. J. Cancer., 2011, vol. 129, pp. 1310–1321. doi: 10.1002/ijc.25788
  26. WHO laboratory manual for the examination and processing of human semen. 5th ed. WHO, 2010. 271 p.
  27. Wong L., Hutson P.R., Bushman W. Prostatic inflammation induces fibrosis in a mouse model of chronic bacterial infection. PLoS One, 2014, vol. 9, no. 6: e100770. doi: 10.1371/journal.pone.0100770
  28. Wong L., Hutson P.R., Bushman W. Resolution of chronic bacterialinduced prostatic inflammation reverses established fibrosis. Prostate, 2015, vol. 75, no. 1, pp. 23–32. doi: 10.1002/pros.22886

Copyright (c) 2019 Godovalov A.P., Danielyan T.Y., Karpunina T.I., Vavilov N.V.

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