IMMUNODIAGNOSIS OF PERITONEAL SEPSIS

Authors

  • O. V. Plytka I. Horbachevsky Ternopil National Medical University
  • V. V. Hnativ I. Horbachevsky Ternopil National Medical University

DOI:

https://doi.org/10.11603/1811-2471.2022.v.i4.13493

Keywords:

immunodiagnostics, sepsis, peritoneal sepsis

Abstract

SUMMARY. The work provides an overview of scientific sources related to immunodiagnostics of peritoneal sepsis. As a result of the progression of the inflammatory process caused by microorganisms, there is a massive production of inflammatory mediators, activation of specific and non-specific links of immune protection.

Material and Methods. The work uses bibliographic and analytical methods of searching and analyzing scientific information obtained from scientific publications with an impact factor. The search was carried out in the databases Pubmed, medLine, ClinicalKey, and included publications over the last 10 years.

Results. Sepsis can be viewed as a competition between pathogens and the host's immune response; pathogens seek advantage by disrupting various aspects of the body's defenses. For example, sepsis induces apoptotic deletion of immune effector cells, suppresses the expression of major histocompatibility complex class II molecules, increases the expression of negative costimulatory molecules, increases the number of anti-inflammatory cytokines, and increases the number of regulatory T cells and myeloid cells. In patients with sepsis, monocytes have a reduced ability to release proinflammatory cytokines in response to endotoxin. In sepsis, T cells become insensitive to proliferation and revert to a type 2 profile with increased production of IL-4 and IL-10 and suppression of IL-12 and IFN-γ.

Conclusions. T-cell depletion has been shown in patients with sepsis. The prolonged duration of sepsis is characterized by a high antigenic load and a high level of pro-inflammatory and anti-inflammatory cytokines, which causes exhaustion of T cells. A link between T cell depletion and mortality in sepsis has been established by studies showing that increased expression of PD-1 in circulating T cells in patients with sepsis correlated with decreased T cell proliferative capacity and mortality. The main lever is that the first line of defense against infection – innate immunity – can be a double-edged sword, since the same cells, molecules and mechanisms that participate in the protective process can also participate in pathological inflammatory processes. Therefore, in the diagnosis, it is necessary to find subtle differences between SZR and sepsis, and in its treatment – to maintain a balance between an adequate immune response and an inflammatory reaction, which will allow to effectively fight pathogens, limiting inflammation that can harm the body.

References

Davies, M.G., & Hagen, P.O. (1997). Systemic inflammatory response syndrome. Br. J. Surg., 84, 920-935.

Singer, M., Deutschman, C.S., & Seymour, C.W. (2016). The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA, 8, 801-810.

Kumar, A., Roberts, D., Wood, K.E., Light, B., Parrillo, J.E., Sharma, S., Suppes, R., … Cheang, M. (2006). Duration of hypotension before initiation of effective antimicrobial therapy is the critical determinant of survival in human septic shock. Crit. Care Med., 34(6), 1589-1596.

Sydorchuk, R.I. (2006). Abdominalnyi sepsis – Abdominal sepsis. Chernivtsi: Vyd-vo BDMU, 462 [in Ukrainian].

Mandell, G., Bennett, J., & Dolin, R. (2009). Principles and Practice of Infectious Diseases, 7th ed. Philadelphia: Churchill Livingstone, 1320.

Kryvoruchko, I.A. (2009). Diaghnostyka ta kompleksne likuvannja khvorykh na abdominalnyi sepsis [Diagnosis and comprehensive treatment of patients with abdominal sepsis]. Ukr. zhurnal khirurhiyi – Ukr. Journal of Surgery, 1 77-80 [in Ukrainian].

Dronjak, M.M. (2008). Abdominaljnyj sepsis [Abdominal sepsis]. Ukr. zh. khirurhiyi – Ukr. Journal of Surgery, 1, 100-104 [in Ukrainian].

Quartin, A.A., Schein, R.M., Kett, D.H., & Peduzzi, P.N. (1997). Magnitude and duration of the effect of sepsis on survival. Department of Veterans Affairs Systemic Sepsis Cooperative Studies Group. JAMA, 277, 1058-1063.

Cinel I., & Opal S.M. (2009). Molecular biology of inflammation and sepsis: a primer. Crit. Care Med, 37, 291-304.

Casey, L.C. (2000). Immunologic response to infection and its role in septic shock. Crit. Care Clin, 16, 193-213.

Angus, D.C. (2011). The search for effective therapy for sepsis: back to the drawing board? JAMA, 306, 2614-2615.

Hotchkiss, R.S., & Opal, S. (2010). Immunotherapy for sepsis – a new approach against an ancient foe. N. Engl. J. Med., 363, 87-89.

Kox, W.J., Volk, T., Kox, S.N., & Volk, H.D. (2000). Immunomodulatory therapies in sepsis. Intensive Care Med., 26 (1), 124-128.

Bone, R.C., & Sir Isaac Newton. (1996). Sepsis, SIRS, and CARS. Crit. Care Med., 24, 1125-1128.

Munford, R.S., & Pugin, J. (2001). Normal responses to injury prevent systemic inflammation and can be immunosuppressive. Am. J. Respir. Crit. Care Med., 163, 316-321.

Boomer, J.S., To, K., & Chang, K.C. (2011). Immunosuppression in patients who die of sepsis and multiple organ failure. JAMA, 306, 2594-2605.

Hotchkiss, R.S., Swanson, P.E., & Freeman, B.D. (1999). Apoptotic cell death in patients with sepsis, shock, and multiple organ dysfunction. Crit. Care Med., 27, 1230-1251.

Unsinger, J., McDonough, J.S., & Shultz, L.D. (2009). Sepsis-induced human lymphocyte apoptosis and cytokine production in “humanized” mice. J. Leukoc. Biol., 86, 219-227.

Hotchkiss, R.S., Strasser, A., McDunn, J.E., & Swanson, P.E. (2009). Cell death. N. Engl. J. Med., 36, 1570-1583.

Hotchkiss, R.S., Schmieg, R.E., & Swanson, P.E. (2000). Rapid onset of intestinal epithelial and lymphocyte apoptotic cell death in patients with trauma and shock. Crit. Care Med., 28, 3207-3217.

Voll, R.E., Herrmann, M., Roth, E.A., Stach, C., Kalden, J.R., & Girkontaite, I. (1997). Immunosuppressive effects of apoptotic cells. Nature, 390, 350-351.

Tsujimoto, H., Ono, S., & Hiraki, S. 2004). Hemoperfusion with polymyxin B-immobilized fibers reduced the number of CD16 + CD14 + monocytes in patients with septic shock. J. Endotoxin. Res., 10, 229-237.

Biswas, S.K., & Lopez-Collaxo, E. (2009). Endotoxin tolerance: new mechanisms, molecules and clinical significance. Trends Immunol., 30, 475-487.

Monneret, G., Finck, M.E., & Venet, F. (2004). The anti-inflammatory response dominates after septic shock: association of low monocyte HLA-DR expression and high interleukin-10 concentration. Immunol. Lett., 95, 193-198.

Hynninen, M., Pettila, V., & Takkunen, O. (2003). Predictive value of monocyte histocompatibility leukocyte antigen-DR expression and plasma interkeukin04 and -10 levels in critically ill patients with sepsis. Shock, 20, 1-4.

Oberholzer, A., Oberholzer, C., & Moldawer, L.L. (2002). Interleukin-10: a complex role in the pathogenesis of sepsis syndromes and its potential as an anti-inflammatory drug. Crit. Care Med., 30, 58-63.

Muehlstedt. S.G., Lyte. M., & Rodriguez. J.L. (2002). Increased IL-10 production and HLA-DR suppression in the lungs of injured patients precede the development of nosocomial pneumonia. Shock, 17, 443-450.

Hiraki, S., Ono, S., & Tsujimoto, H. (2012). Neutralization of interleukin-10 or transforming growth factor-beta decreases the percentages of CD4 + CD25 + Foxp3 + regulatory T cells in septic mice, thereby leading to an improved survival. Surgery, 15, 313-322.

Lukaszewicz, A.C., Grienay, M., & Resche-Rigon, M. (2009). Monocytic HLA-DR expression in intensive care patients: interest for prognosis and secondary infection prediction. Crit. Care Med., 37, 2746-2752.

Ono, S., Tsujimoto, H., Matsumoto, A., Ikuta, S., Kinoshita, M., & Mochizuki, H. (2004). Modulation of human leukocyte antigen-DR on monocytes and CD16 on granulocytes in patients with septic shock using hemoperfusion with polymyxin B-immobilized fiber. Am. J. Surg., 188, 150-156.

Seki, S., Osada, S., & Ono, S. (1998). Role of liver NK cells and peritoneal macrophages in IFN- gamma and IL-10 production in experimental bacterial peritonitis in mice. Infect. Immun., 66, 5286-5294.

Hiraki, S., Ono, S., Kinoshita, M., Tsujimoto, H., Seki, S., & Mochizuki, H. (2007). Interleukin-18 restores immune suppression in patients with nonseptic surgery, but not with sepsis. Am. J. Surg., 193, 676-680.

Takabayashi, A., Kanai, M., & Kawai, Y. (2003). Change in mitochondrial membrane potential in peripheral blood lymphocytes, especially in natural killer cells, is a possible marker for surgical stress on the immune system. World J. Surg., 27, 659-665.

Ikuta, S., Ono, S., Kinoshita, M., Tsujimoto, H., Yamauchi, A., & Mochizuki, H. (2003). Interleukin-18 concentration in the peritoneal fluid correlates with the severity of peritonitis. Am. J. Surg., 185, 550-555.

Sakaguchi, S., Sakaguchi, N., Asano, M., Itoh, M., & Toda, M. (1995). Immunologic self-tolerance maintained by activated T cells expressing IL-2 receptor alpha-chains (CD25). Breakdown of a single mechanism of self-tolerance causes various autoimmune diseases. J. Immunol., 155, 1151-1164.

Shevach, E.M. (2001). Certified professionals: CD4(+)CD25(+) suppressor T cells. J. Exp. Med., 193, 41-46.

Shevach, E.M., DiPaolo, R.A., Andersson, J., Zhao D.M., Stephens, G.L., & Thornton, A.M. (2006). The lifestyle of naturally occurring CD4 + CD25 + Foxp3 + regulatory T cells. Immunol. Rev., 212, 60-73.

Sakaguchi, S., Ono, M., & Setoguchi, R. (2006). Foxp3 + CD25 + CD4 + natural regulatory T cells in dominant self-tolerance and autoimmune disease. Immunol. Rev., 212, 8-27.

Monneret, G., Debard, A.L., & Venet, F. (2003). Marked elevation of human circulating CD4 + CD25 + regulatory T cells in sepsis-induced immunoparalysis. Crit. Care Med., 3, 2068-2071.

Ono, S., Kimura, A., & Hiraki, S. (2013). Removal of increased circulating CD4 + CD25 + Foxp3 + regulatory T cells in patients with septic shock using hemopefusion with polymyxin B-immobilized fibers. Surgery, 153, 262-271.

Venet, F., Chung, C.S., & Kherouf, H. (2009). Increased circulating regulatory T cells (CD4(+)CD25 (+)CD127 (-)) contribute to lymphocyte anergy in septic shock patients. Intensive Care Med., 5, 678-686.

Venet, F., Chung, C.S., & Kherouf, H. (2006). Human CD4 + CD25 + regulatory T lymphocytes inhibit lipopolysaccharide-induced monocyte survival through a Fas/Fas ligand-dependent mechanism. J. Immunol., 177, 6540-6547.

Tiemessen, M.M., Jagger, A.L., & Evan, H.G. (2007). CD4 + CD25 + Foxp3 + regulatory T cells induce alternative activation of human monocytes/macrophages. Proc. Natl. Acad. Sci. USA., 104, 19446-19451.

Guignant, C., Lepape, A., & Huang, X. (2011). Programmed death-1 levels correlate with increased mortality, nasocomial infection and immune dysfunctions in septic shock patients. Crit. Care, 15, 99.

Si-Tahar, M., Touqui, L., & Chignard, M. 2009). Innate immunity and inflammation - two facets of the same anti-infectious reaction. Clin. Exp. Immunol., 156, 194-198.

Published

2023-01-26

How to Cite

Plytka, O. V., & Hnativ, V. V. (2023). IMMUNODIAGNOSIS OF PERITONEAL SEPSIS. Achievements of Clinical and Experimental Medicine, (4), 18–25. https://doi.org/10.11603/1811-2471.2022.v.i4.13493

Issue

Section

Огляд літератури