PRODUCTION OF CYTOKINES BY VAGINAL EPITHELIOCYTES IN THE PROCESS OF INTERACTION WITH DOMINANT AND ASSOCIATIVE MICROSYMBIONTS


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Abstract

Aim. Study the expression of cytokines by vaginal epitheliocytes in the process of interaction
with dominant and associative microsymbionts. Materials and methods. IL-8, IL-6, IL-1ƒ and
TNFƒ expression in response to interaction with heat inactivated Lactobacillus spp., Staphylococcus
aureus, Escherichia coli, Corynebacterium spp. or their secretory products in comparison with
basal expression of cytokines by vaginal epitheliocytes was studied. Results. Lactobacilli secretory
products were shown not to influence the expression of IL-8 and IL-1ƒ and moderately stimulated
IL-6 and TNFƒ expression. Contact of epitheliocytes with heat inactivated lactobacilli increased
secretion of IL-8, IL-6 and IL-1ƒ and reduced TNFƒ production. Secretory products of
S. aureus and E. coli caused stimulation of IL-6, IL-1ƒ production and practically did not change
the expression of IL-8 and TNFƒ. Contact of epitheliocytes with heat inactivated S. aureus suppressed
TNFƒ production and had no influence on IL-8, IL-6 and IL-1ƒ expression, contact with
E. coli stimulated TNFƒ and IL-1ƒ expression and suppressed IL-6 expression. Changes in cytokine
expression during interaction of epitheliocytes with corynebacteria were largely similar to the
results of interaction with lactobacilli except IL-6 production that was markedly stimulated by
corynebacteria secretory products. Conclusion. In epithelial-bacterial interactions dominant
and associative microorganisms have a differential effect on functional status of mucosal epitheliocytes
manifesting in production of cytokines that could be the basis of mucosal immunity
regulation.

About the authors

E A Kremleva

S V Cherkasov

References

  1. Бухарин О.В., Сгибнев А.В., Черкасов С.В., Иванов Ю.Б. Изменение активности каталазы Staphylococcus aureus ATCC 6538Р под влиянием метаболитов микроорга низмов, выделенных из различных экотопов. Микробиология. 2002, 71 (2): 183-186.
  2. Дерябин Д.Г. Стафилококки: экология и патогенность. Екатеринбург, УрО РАН, 2000.
  3. Клаус Д. (ред.). Лимфоциты. Методы. М., Мир, 1990.
  4. Лакин Р.Ф. Биометрия. М., Высшая школа, 1990.
  5. Boomsma C.M., Bozkurt N. et. al. Is bacterial vaginosis associated with a proinflammatory cytokine profile in endometrial secretions of women undergoing IVF? Reprod. Biomed. Online. 2010, 21 (1): 133-141.
  6. Cauci S., Culhane J.F. Modulation of vaginal immune response among pregnant women with bacterial vaginosis by Trichomonas vaginalis, Chlamydia trachomatis, Neisseria gonorrhoeae, and yeast. Am. J. Obstet. Gynecol. 2007, 196 (2): 133-137.
  7. Donders G. G., Vereecken A., Bosmans E. et al. Definition of a type of abnormal vaginal flora that is distinct from bacterial vaginosis: aerobic vaginitis. BJOG. 2002, 109 (1): 34-43.
  8. Fichorova R. N., Trifonova R.T., Gilbert R.O. et al. Trichomonas vaginalis lipophosphoglycan triggers a selective upregulation of cytokines by human female reproductive tract epithelial cells. Infect. Immun. 2006, 74 (10): 5773-5779.
  9. Pivarcsi A., Nagy I., Koreck A. et al. Microbial compounds induce the expression of pro-inflammatory cytokines, chemokines and human beta-defensin-2 in vaginal epithelial cells. Microbes Infect. 2005, 7 (9-10): 1117-1127.
  10. Wasiela M., Krzemiński Z., Kalinka J., Brzezińska-Błaszczyk E. Correlation between levels of selected cytokines in cervico-vaginal fluid of women with abnormal vaginal bacterial flora. Med. Dosw. Mikrobiol. 2005, 57 (3): 327-333.

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Copyright (c) 2012 Kremleva E.A., Cherkasov S.V.

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