The dynamics of soluble apoptosis markers during diet therapy in infants with atopic dermatitis



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Abstract

Background. To estimate the dynamics of soluble apoptosis markers in infants with atopic dermatitis for updating mechanisms of immunopathogenesis and improvement of diet therapy. Methods. We observed 66 bottle-fed infants aged 1,5—12 months old (boys -47, girls — 19) with atopic dermatitis (AD). The sensibilization to cow milk protein was revealed in all 66 infants. Detected allergen-specific IgG and IgE antibodies to cow milk protein, its fraction and goat milk protein were the reason to include infants into the 1st group and feed with hydrolyzed formula (27 infants). 39 infants in the 2nd group, who were not sensibilized to goat milk protein, were fed by goat milk based formula. Serum levels of soluble apoptosis markers (sCD153, caspase-8, sFas-L, caspase-9 and annexin-5) were measured by immunoenzyme method (ELISA). Results. The activation of signal apoptosis systems in infants with AD with increased levels of sFas-L и sCD153 was revealed. Levels of caspase-8 and caspase-9 were significantly lower than in control group, and reflected the impaired elimination of modified immmunocompetent cells. The level of annexin-5 was significantly lower in infants with AD than in control group. The estimation of the dynamics of investigated parameters during diet therapy showed significant increase of caspase-9 level in both groups. The level of caspase-8 was increased only in infants who were fed by goat milk formula. Levels of sFas-L, sCD153 and annexin-5 during diet treatment did not differ significantly between groups. Conclusion. The results showed that sCD153, caspase-8, sFas-L, caspase-9 and annexin-5 play a role in the realization of allergic inflammation in infants with AD. The diet therapy with goat milk formula promotes more physiological repair of the effectory component of the apoptosis.

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About the authors

T B Sentsova

Research Institute of Nutrition, Russian Academy of Medical Sciences

Email: bio45@inbox.ru
Moscow, Russia

V A Revyakina

Research Institute of Nutrition, Russian Academy of Medical Sciences

Moscow, Russia

B S Kaganov

Research Institute of Nutrition, Russian Academy of Medical Sciences

Moscow, Russia

S N Denisova

G.N. Speransky Municipal Children's Clinical Hospital No. 9

Moscow, Russia

I V Vorozhko

Research Institute of Nutrition, Russian Academy of Medical Sciences

Moscow, Russia

O YU Monosova

Research Institute of Nutrition, Russian Academy of Medical Sciences

Moscow, Russia

O O Kirillova

Research Institute of Nutrition, Russian Academy of Medical Sciences

Moscow, Russia

References

  1. Susan Elmore. Apoptosis: A Review of Programmed Cell Death.Toxicol Pathol. 2007, v 35 (4), p. 495-516.
  2. Ream R.M., Sun J., Braciale TJ. Stimulation of naive CD8+ T-cells by a variant viral epitope induces activation and enhanced apoptosis. J. Immunol. 2010, v. 1, 184 (5), p. 2401-2409.
  3. Eisenberg-Lerner A., Bialik S., Simon H.U. Life and death partners: apoptosis, autophagy and the cross-talk between them. Cell Death and Differentiation. 2009, v. 16, p. 966—975.
  4. Janni T.S., Gobejishvili L., Hote.P.T. Inhibition of methionin adenosyltransferase II induces FasL expression? Fas-DISC formation and caspase-8-dependent apoptopic death in T- leukemic cells. Cel/res. 2009, v. 19 (3), p. 358-369.
  5. Kroemer G., Galluzzi L.,Vandenabeele P. Cell Death classification of cell death: recommendations of the Nomen-clature Commmittee on Cell Death. Cell Death and Differentiation. 2009, v. 16, p. 3-11.
  6. Kroemer G., Galluzzi L., Brenner C. Mitochondrial membrane permeabilization in cell death. Physiol. Rev. 2007, v. 87 (1), p. 99-163.
  7. Wilson N.S., Dixit V., Ashkenazi A. Death receptor signal transducers: nodes of coordination in immune signalimg networks. Nat. Immunol. 2009, v. 10, p. 348-335.
  8. Kurokawa M., Kornbluth S. Caspase and kinases in a death grip. Cell. 2009, v. 4, 138 (5), p. 838-854.
  9. Manzo F., Nebbioso A., Miceli M. et al. TNF — relative apap-tosis-inducing ligand: signaling of a ‘smart’ molecule. Int. J. Biol. 2009, v. 41 (3), p. 460-466.
  10. Петрищев Н.Н., Васина Л.В., Луговая А.В. Содержание растворимых маркеров апоптоза и циркулирующих аннексин v-связанных апоптотических клеток в крови больных острым коронарным синдромом. Вестн. С.-Пб. У-та. 2008, т. 11 (1), c. 14-23.
  11. Eisenberg-Lerner A., Bialik S., Simon H.U. Life and death partners: apoptosis, autophagy and the cross-talk between them. Cell Death and Differentiation. 2009, v. 16, p. 966-975.
  12. Булгакова В.А. Научное обснование и эффективность иммунопрофилактики и иммунотерапии вирусной и бактериальной инфекции у детей с бронхиальной астмой. Автореферат диссертации д-ра мед. наук. М., 2009, 42 с.
  13. Luckey Ulrike, Maurer Marcus, Schmidt Talkea et al. T-cell killing by tolerogenic dendritic cells protects mice from allergy. Journal of clinical investigation. 2011, v. 121 (10), p. 3860-3871.
  14. Carsten Flohr. Atopic Dermatitis Diagnostic Criteria and Outcome Measures for Clinical Trials: Still a Mess. Journal of Investigative Dermatology. 2011, v. 131, p. 557-559.
  15. Kunz B., Oranje A.P., Labreze L. et al. Clinical validation and guidelines for the SCORAD index: consensus report of the European Task Force on atopic dermatitis. Dermatology. 1997, v. 195, p. 1019.

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