DISTURBANCE OF AN APOPTOSIS OF NEUTROPHILS AT A SEPSIS

Cover Page


Cite item

Full Text

Abstract

The sepsis represents life-endangering disturbances of functions of the internals caused by a dizregulyation of a macroorganism to the  infectious agent and is difficult interaction of pro-inflammatory and  antiinflammatory processes that not seldom defines the fate of  patients. The predetermining factor of a sepsis is the originator. The  immunosupression caused by the originator promotes generalization  of an infection, and the intensive bacteriemia caused by generalization leads to the accruing endotoxinemia that aggravates  immunosupression even more and leads finally to systemic inflammatory reaction — the main and most dangerous implication  of a sepsis. The syndrome of systemic inflammation with  uncontrollable emission of cytokines is the cornerstone of a sepsis.  The pathophysiology of a sepsis begins with impassioned inflammatory reaction which can last several days, and then passes  into more lingering immunosupressivny period where the outcome  depends on the immune system of the patient. Cellular apoptosis is  one of leaders in sepsis immunosupression development. In article  mechanisms of disturbance of an apoptosis of neutrophils are  described that, undoubtedly, affects weighting of a current of a  sepsis and as a result, a failure. Migration of neutrophils under  natural conditions includes four various phases which during a sepsis  are broken. The mechanisms worsening migration of  neutrophils, contributing to the development of a sepsis were  investigated in numerous scientific works. Authors of Peking  University offered schemes of a way of disturbance of an apoptosis  of neutrophils and migration of neutrophils at a sepsis. Despite the  extensive accumulated experience on studying of a pathogenesis of  septic states, there are no effective and specific remedies of fight  from a sepsis now. Perhaps, by prevention of disturbance of the  programmed death of a cell the cytokines developed anti-apoptotic,  caspase inhibitors will be. 

About the authors

X.-F. Shen

Nanjing University Medical School

Email: fake@neicon.ru

Department of General Surgery, Nanjing Medical University, Nanjing, China

Китай

W.-X. Guan

General Military Hospital

Email: fake@neicon.ru

Department of General Surgery, Nanjing Medical University, Nanjing, China

Китай

J.-F. Du

General Military Hospital

Email: fake@neicon.ru

Department of General Surgery, PLA Army General Hospital, Beijing, China

Китай

L. V. Puzyryova

Omsk State Medical University

Author for correspondence.
Email: puzirevalv@mail.ru

PhD (Medicine), Assistant Professor, Department of Infectious Diseases, Omsk State Medical University, Omsk, Russian Federation

644010, Russian Federation, Omsk, Sergey Lazo str., 2

Phone: +7 (3812) 53-26-66

Россия

References

  1. Бабаев М.А., Тарасова Н.Ю., Бирг Т.М., Дымова О.В. Сепсис — терминология и критерии диагностики: эволюция взглядов на проблему // Клиническая и экспериментальная хирургия. Журнал имени академика Б.В. Петровского. 2016. № 2. С. 35–46. [Babayev M.A., Tarasova N.Yu., Birg T.M., Dymov O.V. Sepsis — terminology and criteria of diagnostics: evolution of views on a problem. Klinicheskaya i eksperimental’naya khirurgiya. Zhurnal imeni akademika B.V. Petrovskogo = Clinical and Experimental Surgery. Journal of Academician B.V. Petrovsky, 2016, no. 2, pp. 35–46. (In Russ.)]
  2. Богданова И.М. Иммунологические механизмы сепсиса и новые походы к его терапии // Клиническая и экспериментальная морфология. 2014. № 3. С. 52–58. [Bogdanova I.M. Immunologic mechanisms of a sepsis and new campaigns to its therapy. Klinicheskaya i eksperimental’naya morfologiya = Clinical and Experimental Morphology, 2014, no. 3. pp. 52–58. (In Russ.)]
  3. Булава Г.В. Иммунологические аспекты сепсиса (обзор литературы) // Неотложная медицинская помощь. 2013. № 2. С. 47–56. [Bulava G.V. Immunologic aspects of a sepsis (review of literature). Neotlozhnaya meditsinskaya pomoshch’ = Emergency Medical Care, 2013, no. 2, pp. 47–56. (In Russ.)]
  4. Винокуров М.Г., Юринская М.М. Регуляция апоптоза нейтрофилов при действии липополисахаридов // Биологические мембраны. 2010. Т. 27, № 1. С. 18–27. [Vinokurov M.G., Yurinskaya M.M. A regulation of an apoptosis of neutrophils at action of lipopolisakharid. Biologicheskie membrany = Biological Membranes, 2010, vol. 27, no. 1, pp. 18–27. (In Russ.)]
  5. Гариб Ф.Ю., Ризопулу А.П. Взаимодействия патогенных бактерий с врожденными иммунными реакциями хозяина // Инфекция и иммунитет. 2012. Т. 2. № 3. С. 581–596. [Garib F.Yu., Rizopulu A.P. Interactions of pathogenic bacteria with congenital immune reactions of the owner. Infektsiya i immunitet = Russian Journal of Infection and Immunity, 2012, vol. 2, no. 3, pp. 581–596. doi: 10.15789/2220-7619-2012-3-581-596 (In Russ.)]
  6. Грачев С.В., Юринская М.М., Тихоненко С.А., Винокуров М.Г. Механизмы регуляции апоптоза нейтрофилов человека при действии эндотоксинов и индукторов апоптоза // Вестник новых медицинских технологий. 2013. Т. 20, № 2. С. 18–20. [Grachev S.V., Yurinskaya M.M., Tikhonenko S.A., Vinokurov M.G. Mechanisms of a regulation of an apoptosis of neutrophils of the person at action of endotoxins and inductors of an apoptosis. Vestnik novykh meditsinskikh tekhnologii = Herald of New Medical Technologies, 2013, vol. 20, no. 2, pp. 18–20. (In Russ.)]
  7. Ермак И.М., Давыдова В.Н. Взаимодействие бактериальных липополисахаридов с растворимыми белками микроорганизма и поликатионами // Биологические мембраны. 2008. Т. 25, № 5. С. 323–342. [Yermak I.M., Davydova V.N. Interaction of bacteriemic lipopolisakharid with soluble proteins of a microorganism and polycations. Biologicheskie membrany = Biological Membranes, 2008, vol. 25, no. 5, pp. 323–342. (In Russ.)]
  8. Игнатов П.Е. Иммунитет и инфекция. М.: Время, 2002. 352 с. [Ignatov P.E. Immunitet i infektsiya [Immunity and infection]. Moscow: Vremja, 2002. 352 p.]
  9. Козлов В.К. Сепсис, тяжелый сепсис, септический шок: патогенетическое обоснование диагноза, клиническая интерпретация, принципы и методы диагностики // Клинико-лабораторный консилиум. 2014. № 2 (49). С. 20–40. [Cozlov V.K. Sepsis, serious sepsis, septic shock: pathogenetic justification of the diagnosis, clinical interpreting, principles and diagnostic methods. Kliniko-laboratornyi konsilium = Clinical Laboratory Consilium, 2014, no. 2 (49), pp. 20–40. (In Russ.)]
  10. Коротина О.Л., Генералов И.И. Нейтрофильные внеклеточные ловушки: механизмы образования, функции // Иммунопатология, алергология, инфектология. 2012. № 4. С. 23–32. [Korotina O.L., Generalov I.I. Neutrophylic extracellular traps: mechanisms of education, function. Immunopatologiya, alergologiya, infektologiya = Immunopathology, Alergology, Infectology, 2012, no. 4, pp. 23–32. (In Russ.)]
  11. Норкин М.Н., Леплина О.Ю., Тихонова М.А., Тюрин И.Н., Останин А.А., Черных Е.Р. Роль апоптоза и анергии Т-клеток в патогенезе гнойно-септических заболеваний // Медицинская иммунология. 2000. Т. 2, № 1. С. 35–42. [Norkin M.N., Leplina O.Yu., Tikhonova M.A., Tyurin I.N., Ostanin A.A., Chernykh E.R. Role of an apoptosis and an anergy of T-cells in a pathogenesis of purulent-septic diseases. Meditsinskaya immunologiya = Medical Immunology (Russia), 2000, vol. 2, no. 1, pp. 35–42. (In Russ.)]
  12. Потапнев М.П. Аутофагия, апоптоз, некроз клеток и иммунное распознавание своего и чужого // Иммунология. 2014. № 2. С. 95–102. [Potapnev M.P. Autophagy, apoptosis, necrosis of cells and immune recognition of self and nonself. Immunologiya = Immunology, 2014, no. 2, pp. 95–102. (In Russ.)]
  13. Хаертынов Х.С., Анохин В.А., Бойчук С.В. Патофизиология неонатального сепсиса // Вестник современной клинической медицины. 2014. Т. 7, № 6. С. 97–104. [Hayertynov H.S., Anokhin V.A., Boychuk S.V. Patofiziologiya of a neonatal sepsis. Vestnik sovremennoi klinicheskoi meditsiny = Herald of Modern Clinical Medicine, 2014, vol. 7, no. 6, pp. 97–104. (In Russ.)]
  14. Хаертынов Х.С., Анохин В.А., Бойчук С.В., Ризванов А.А. Сепсис и апоптоз // Гены и клетки. 2016. Т. 11, № 4. С. 18–21. [Hayertynov H.S., Anokhin V.A., Boychuk S.V., Rizvanov A.A. Sepsis and apoptosis. Geny i kletki = Genes and Cells, 2016, vol. 11, no. 4, pp. 18–21. (In Russ.)]
  15. Юринская М.М., Винокуров М.Г., Зацепина О.Г., Гарбуз Д.Г., Гужова И.В., Рожкова Е.А., Сусликов А.В., Карпов В.Л., Евгеньев М.Б. Экзогенные белки теплового шока БТШ70 подавляют эндотоксин-индуцированную активацию нейтрофилов человека // Доклады академии наук. 2009. Т. 426, № 3. С. 406–409. [Yurinskaya M.M., Vinokurov M.G., Zatsepina O.G., Garbuz D.G., Guzhova I.V., Rozhkova E.A., Suslikov A.V., Karpov V.L., Evgenyev M.B. Exogenous proteins of thermal shock Btsh70 supresses an endotoxin-induced activation of neutrophils of the person. Doklady akademii nauk = Reports of the Academy of Sciences, 2009, vol. 426, no. 3, pp. 406–409. (In Russ.)]
  16. Ahmed N.A., McGill S., Yee J., Hu F., Michel R.P., Christou N.V. Mechanisms for the diminished neutrophil exudation to secondary inflammatory sites in infected patients with a systemic inflammatory response (sepsis). Crit. Care Med., 1999, vol. 27, pp. 2459–2468.
  17. Brade L., Hoist O., Brade H. An artificial glycoconjugate containing the bisphosphorylated glucosamine disaccharide backbone of lipid A binds monoclonal antibodies. Infect. Immun., 1993, vol. 61, no. 10, pp. 4514–4517.
  18. Brandenburg K., Wiese A. Endotoxin: relationships between structure, function and activity. Curr. Top. Med. Chem., 2004, vol. 4, iss. 11, pp. 1127–1146. doi: 10.2174/1568026043388213
  19. Buras J.A., Holzmann B., Sitkovsky M. Animal models of sepsis: setting the stage. Nat. Rev. Drug Discov., 2005, vol. 4, pp. 854–865. doi: 10.1038/nrd1854
  20. Delano M.J., Kelly-Scumpia K.M., Thayer T.C., Winfield R.D., Scumpia P.O., Cuenca A.G., Harrington P.B., O’Malley K.A., Warner E., Gabrilovich S., Mathews C.E., Laface D., Heyworth P.G., Ramphal R., Strieter R.M., Moldawer L.L., Efron P.A. Neutrophil mobilization from the bone marrow during polymicrobial sepsis is dependent on CXCL12 signaling. J. Immunol., 2011, vol. 187, pp. 911–918. doi: 10.4049/jimmunol.1100588
  21. Dellinger R.P., Levy M.M., Rhodes A., Annane D., Gerlach H., Opal S.M., Sevransky J.E., Sprung C.L., Douglas I.S., Jaeschke R., Osborn T.M., Nunnally M.E., Townsend S.R., Reinhart K., Kleinpell R.M., Angus D.C., Deutschman C.S., Machado F.R., Rubenfeld G.D., Webb S., Beale R.J., Vincent J.L., Moreno R. Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock. Intensive Care Med., 2013, vol. 39, iss. 2, pp. 165–228. doi: 10.1007/s00134-012-2769-8
  22. Dounousi E., Torino C., Pizzini P., Cutrupi S., Panuccio V., D’Arrigo G., Abd ElHafeez S., Tripepi G., Mallamaci F., Zoccali C. Intact FGF23 and α-Klotho during acute inflammation/sepsis in CKD patients. Eur. J. Clin. Invest., 2017, vol. 47, iss. 6, pp. 440– 472. doi: 10.1111/eci.12765
  23. Eash K.J., Greenbaum A.M., Gopalan P.K., Link D.C. CXCR2 and CXCR4 antagonistically regulate neutrophil trafficking from murine bone marrow. J. Clin. Inves., 2010, vol. 120, no. 7, pp. 2423–2431. doi: 10.1172/JCI41649
  24. Elmore S. Apoptosis: a review of programmed cell death. Toxicol. Pathol., 2007, vol. 35, iss. 4, pp. 495–516. doi: 10.1080/01926230701320337
  25. Geering B., Simon H.U. Peculiarities of cell death mechanisms in neutrophils. Cell Death Differ., 2011, vol. 18, no. 9, pp. 1457–1469. doi: 10.1038/cdd.2011.75
  26. Guo R.F., Sun L., Gao H., Shi K.X., Rittirsch D., Sarma V.J., Zetoune F.S., Ward P.A. In vivo regulation of neutrophil apoptosis by C5a during sepsis. J. Leukoc. Biol., 2006, vol. 80, iss. 6, pp. 1575–1583. doi: 10.1189/jlb.0106065
  27. Ianaro A., Tersigni M., D’Acquisto F. New insight in LPS antagonist. Mini Rev. Med. Chem., 2009, vol. 9, no. 3, pp. 306–317. doi: 10.2174/1389557510909030306
  28. Iba T., Hashiguchi N., Nagaoka I., Tabe Y., Murai M. Neutrophil cell death in response to infection and its relation to coagulation. J. Intensive Care, 2013, vol. 1, pp. 13. doi: 10.1186/2052-0492-1-13
  29. Karampela I., Kandri E., Antonakos G., Vogiatzakis E., Christodoulatos G.S., Nikolaidou A., Dimopoulos G., Armaganidis A., Dalamaga M. Kinetics of circulating fetuin-A may predict mortality independently from adiponectin, high molecular weight adiponectin and prognostic factors in critically ill patients with sepsis: a prospective study. J. Crit. Care, 2017, vol. 41, pp. 78–85. doi: 10.1016/j.jcrc.2017.05.004
  30. Kebir D., Filep J.G. Role of neutrophil apoptosis in the resolution of inflammation. Sci. World J., 2010, vol. 10, pp. 1731–1748. doi: 10.1100/tsw.2010.169
  31. Kovach M.A., Standiford T.J. The function of neutrophils in sepsis. Curr. Opin. Infect. Dis., 2012, vol. 25, no. 3, pp. 321–327. doi: 10.1097/QCO.0b013e3283528c9b
  32. Luan Y.Y., Yao Y.M., Xiao X.Z., Sheng Z.Y. Insights into the apoptotic death of immune cells in sepsis. J. Interferon Cytokine Res., 2015, vol. 35, no. 1, pp. 17–22. doi: 10.1089/jir.2014.0069
  33. Martin T. R., Nakamura M., Matute-Bello G. The role of apoptosis in acute lung injury. Crit. Care Med., 2003, vol. 31, suppl. 4, pp. 184–187. doi: 10.1097/01.CCM.0000057841.33876.B1
  34. Milot E., Fotouhi-Ardakani N., Filep J.G. Myeloid nuclear differentiation antigen, neutrophil apoptosis and sepsis. Front. Immunol., 2012, vol. 3: 397, 6 p. doi: 10.3389/fimmu.2012.00397
  35. Perianayagam M.C., Balakrishnan V.S., Pereira B.J., Jaber D.L. C5a delays apoptosis of human neutrophils via an extracellular signal-regulated kinase and Bad-mediated signalling pathway. Eur. J. Clin. Invest., 2004, vol. 34, pp. 50–56.
  36. Plewes K., Kingston H.W.F., Ghose A., Maude R.J., Herdman M.T., Leopold S.J., Ishioka H., Hasan M.M.U., Haider M.S., Alam S., Piera K.A., Charunwatthana P., Silamut K., Yeo T.W., Faiz M.A., Lee S.J., Mukaka M., Turner G.D.H., Anstey N.M., Jackson Roberts L., White N.J., Day N.P.J., Hossain M.A., Dondorp A.M. The glyoxalase system and methylglyoxal-derived carbonyl stress in sepsis: glycotoxic aspects of sepsis pathophysiology. Int. J. Mol. Sci., 2017, vol. 18, iss. 3: 657. doi: 10.3390/ijms18030657
  37. Roger T., Calandra T. Interleukin-33 safeguards neutrophils in sepsis. Nat. Med., 2010, vol. 16, no. 6, pp. 638–639. doi: 10.1038/nm0610-638
  38. Romaschin A.D., Foster D.M., Walker P.M., Marshall J.C. Let the cells speak: neutrophils as biologic markers of the inflammatory response. Sepsis, 1998, vol. 2, iss. 2, pp. 119–125. doi: 10.1023/A:1009769923763
  39. Schulze-Osthoff K., Ferrari D., Los M., Wesselborg S., Peter M.E. Apoptosis signaling by death receptors. Eur. J. Biochem., 1998, vol. 254, iss. 3, pp. 439–459. doi: 10.1046/j.1432-1327.1998.2540439.x
  40. Shen X.-F., Cao K., Jiang J.-P., Guan W.-X., Du J.-F. Neutrophil dysregulation during sepsis: an overview and update. J. Cell. Mol. Med., 2017, vol. 21, no. 9, pp. 1687–1697. doi: 10.1111/jcmm.13112
  41. Simon H.U. Neutrophil apoptosis pathways and their modifications in inflammation. Immunol. Rev., 2003, vol. 193, iss. 1, pp. 101–110. doi: 10.1034/j.1600-065X.2003.00038.x
  42. Wang J.F., Li J.B., Zhao Y.J., Yi W.J., Bian J.J., Wan X.J., Zhu K.M., Deng X.M. Up-regulation of programmed cell death 1 ligand 1 on neutrophils may be involved in sepsis- induced immunosuppression: an animal study and a prospective case-control study. Anesthesiology, 2015, vol. 122, no. 4, pp. 852–863. doi: 10.1097/ALN.0000000000000525
  43. Wang N., Mao L., Yang L., Zou J., Liu K., Liu M., Zhang H., Xiao X., Wang K. Resveratrol protects against early polymicrobial sepsis-induced acute kidney injury through inhibiting endoplasmic reticulum stress-activated NF-κB pathway. Oncotarget, 2017, no. 8, pp. 36449–36461. doi: 10.18632/oncotarget.16860

Supplementary files

Supplementary Files
Action
1. JATS XML
Download

Copyright (c) 2018 Shen X., Guan W., Du J., Puzyryova L.V.

Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 International License.
СМИ зарегистрировано Федеральной службой по надзору в сфере связи, информационных технологий и массовых коммуникаций (Роскомнадзор).
Регистрационный номер и дата принятия решения о регистрации СМИ: серия ПИ № ФС 77 - 64788 от 02.02.2016.


This website uses cookies

You consent to our cookies if you continue to use our website.

About Cookies