Role of Immune System against Sepsis

Document Type : Original Article


Student of Microbiology / Member of Iranian Society of Microbiology


Sepsis, which is a highly heterogeneous syndrome, can result in death as a consequence of a systemic inflammatory response syndrome. The activation and regulation of the immune system play a key role in the initiation, development and prognosis of sepsis.[1]
The roles of inflammation and coagulation in the pathophysiology of sepsis are described. Sepsis results when an infectious insult triggers a localized inflammatory reaction that then spills over to cause systemic symptoms of fever or hypothermia, tachycardia, tachypnea, and either leukocytosis or leukopenia. These clinical symptoms are called the systemic inflammatory response syndrome. Severe sepsis is defined by dysfunction of one of the major organ systems or unexplained metabolic acidosis. The inflammatory reaction is mediated by the release of cytokines, including tumor necrosis factor-alpha, interleukins, and prostaglandins, from neutrophils and macrophages. The cytokines activate the extrinsic coagulation cascade and inhibit fibrinolysis. Monocyte-macrophage cells and dendritic cells play a key role in the innate immune response. These cells have the ability to phagocytosis bacteria and interact with their products through an interaction with their pattern-recognition receptors.[13]
These overlapping processes result in microvascular thrombosis; thrombosis is one potential factor producing organ dysfunction. Activation of the coagulation system leads to consumption of endogenous anticoagulants (e.g., protein C and Anti-thrombin); this may be an important factor in the development of microvascular coagulation. Anti-inflammatory mediators as well as inflammatory mediators have a role in sepsis, and an excess of either can result in poor patient outcomes. Sepsis is a complex syndrome involving activation of a variety of systems.[2]
In this article, we try to further investigate
The role of the Human Immune System against various infections mostly Blood infection (Sepsis).


[1] Qiu, Yue, et al. "The Immune System Regulation in Sepsis: From Innate to Adaptive." Current Protein and Peptide Science 20.8 (2019): 799-816.
[2] Jacobi, Judith. "Pathophysiology of sepsis." American Journal of Health-System Pharmacy 59.suppl_1 (2002): S3-S8.
[3] Shen, Xiao‐Fei, et al. "Neu cellular and molecular medicine 21.9 (2017): 1687-1697.
[4] Delano, Matthew J., and Peter A. Ward. "The immune system's role in sepsis progression, resolution, and long‐term outcome." Immunological -353. reviews 274.1 (2016): 330.
[5] Medical News Today/Written by Jennifer Huizen on January 10, 2020
[6] van Rees, Dieke J., et al. "Immune receptors on neutrophils." Seminars in immunology. Vol. 28. No. 2. Academic Press, 2016.
[7] Shen, Xiao‐Fei, et al. "Neu cellular and molecular medicine 21.9 (2017): 1687-1697.
[8] Cecconi, Maurizio, et al. "Sepsis and septic shock." The Lancet 392.10141 (2018): 75-87.
[9] Horeczko, Timothy, Jeffrey P. Green, and Edward A. Panacek. "Epidemiology of the systemic inflammatory response syndrome (SIRS) in the emergency department." Western Journal of Emergency Medicine 15.3 (2014): 329.
[10] Galli, Stephen J., Niels Borregaard, and Thomas A. Wynn. "Phenotypic and functional plasticity of cells of innate immunity: macrophages, mast cells and neutrophils." Nature immunology 12.11 (2011): 1035.
[11] National Human Genome Research Institute/Lawrence C. Brody, Ph.D.
[12] Medical News Today/Written by Joana Cavaco Silva on January 13, 2020
[13] de Pablo, Raul, et al. "Role of circulating lymphocytes in patients with sepsis." BioMed research international 2014 (2014).
[14] Kantari, Chahrazade, Magali Pederzoli-Ribeil, and Véronique Witko-Sarsat. "The role of neutrophils and monocytes in innate immunity." Trends in Innate Immunity. Vol. 15. Karger Publishers, 2008. 118-146.