Development of Immunopathobiogenesis on SIRS-Sepsis

A Guntur Hermawan


Over the past decade, sepsis has been diagnosed according to consensus guidelines established in 1991 as an infection in addition to the symptoms of systemic inflammatory response syndrome (SIRS). In addition to the previous criteria, the 2001 conference added several new diagnostic criteria for sepsis. Of particular interest was the inclusion of the biomarkers procalcitonin (PCT) and C-reactive protein (CRP), despite the overall conclusion that it was premature to use biomarkers for sepsis diagnosis. The primary recommendation of the panel was the implementation of the Predisposition, insult Infection, Response, and Organ dysfunction (PIRO).

The immune system has traditionally been devided into innate and adaptive components, each of which has a different role and function in defending the host against infectious agents. Stimulation of different TLRs induces distinct patterns of gene expression, which not only leads to the activation of innate immunity but also increasing evidence supports an additional critical role for TLRs in orchestrating the development of adaptive immune responses.

The superantigens are able to induce toxic shock syndrome and can sometimes cause multiple organ failure via adaptive immune system. The superantigenic activity of the bacterial exotoxins can be attributed to their ability to cross-link major histocompatibility complex class II molecules on antigen-presenting cells outside the peptide groove with T-cell receptors to form a trimolecular complex. This trimolecular interaction leads to uncontrolled release of a number of proinflammatory cytokines. Proinflammatory cytokines especially IFN-γ and TNF-α, the key cytokines causing toxic shock syndrome.

KEYWORDS: sepsis, innate immunity, adaptive

Full Text:



Adelbert EA, Jawetz E, Melnick JL. Review of medical microbiology. 14th ed. Frederick: Lange Medical; 1980, NLMID.

Cotran RS, Kumar V, Collins T, Robbins SL. Pathologic basis of disease. 6th ed. Philadelphia: Saunders; 1999, NLMID.

Whitnack E. Sepsis. In: Schaechter M, Madoff G, Eisenstein BI. Mechanisms of microbial disease. 2nd ed. Baltimore: Williams & Wilkins; 1993, NLMID.

Thijs LG. Introduction to mediators of sepsis. 5th Symposium. Shock & Critical Care. 1998; [n.vol]: 67-70.

Bone RC, Balk RA, Cerra FB, Dellinger RP, Fein AM, Kraus WA, et al. Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. The ACCP/SCCM Consensus Conference Committee. American College of Chest Physicians/Society of Critical Care Medicine. Chest. 1992; 101: 1644-55, CrossRef.

Carrigan SD, Scott G, Tabrizian M. Toward resolving the challenges of sepsis diagnosis. Clinical Chemistry. 2004; 50: 1301-14, CrossRef.

Levy MM, Fink MP, Marshall JC, Abraham E, Angus D, Cook D, et al. 2001 SCCM/ESICM/ACCP/ATS/SIS International Sepsis Definitions Conference. Crit Care Med. 2003. 31: 1560-6, CrossRef.

Liew FY, Damo X, Brint EK, O’Neill LAJ. Negative regulator of toll-like receptor-mediated immune response. Nat Rev Immunol. 2005; 5: 446-8, CrossRef.

Akira S, Takeda K. Toll-like receptor signalling. Nat Rev Immunol. 2004; 4: 499-511, CrossRef.

Van Amersfoort ES, Van Berkel TJC, Kuiper J. Receptors, mediator, and mechanisms involved in bacterial sepsis and setic shock. Clin Microbiol Rev. 2003; 16: 379-414, CrossRef.

Guntur. Perbedaan respon imun yang berperan pada sepsis dan syok septik [dissertation]. Surabaya: Universitas Arilangga; 2001.

Hamblin, Anne S. Cytokines and cytokine receptor. New York: Oxford; 1993, NLMID.

Hoeprich MC, Miyajima A, Coffman R. Cytokines. In: Paul WE, Editor. Fundamental Immunology. 3th ed. New York: Raven Press; 1993. p.763-90, NLMID.

Srikadan S, Cohen J. The pathogenesis of septic shock. Journal of Infection. 1995; 30: 201-6, CrossRef.

Cohen J. Sepsis syndrom. Journal of Med Int Infection. 1996; [n.vol]: 31-4.

Bone RC. The pathogenesis of sepsis. Ann Intern Med. 1991; 115: 457-69, CrossRef.

Werdan K, Pilz G. Supplement immunoglobulin in sepsis: a critical apprasial. Clin Exp Immunol. 1996; 104: 83-90, PMID.

Israels LG, Israels ED. Mechanisms in hematology. 2nd ed. Concord: Core Health Services, Inc; 1997.

Unenue ER. Macrophages, antigen-presenting cell and the phenomena of antigen handling and presentation. In: Fundamental Immunology. 3rd ed. Norris: Raven Press; 1993. p.111-8, NLMID.

Sivasubramanaian N, Carabello BA, et al. Cardiac inflammation and innate immunity in septic shock. Chest. 2002; 121: 1329-36, CrossRef.

Barron RL. Patophysiology of septic shock and implications for therapy. Clinical Pharmacy. 1993; 12: 829-45, PMID.

Yoshida M. Human response in endotoxemia, endotoxin pathophysiology and clinical aspects. Jakarta: One Day Symposium on Endotoxin; 1994.

Dale DC. Septic Shock. In: Isselbacher KJ, Harrison TR. Harrison's principles of internal medicine. New York: McGraw-Hill: 1995. p.232-8, NLMID

Belanti J. Immunologi III. Yogyakarta: Gadjah Mada University Press; 1993.

Muraille E, Leo O. Resiviting the Th1/Th2 paradigm. Scandinavian Journal of Immunology. 1998; 47: 1-9, CrossRef.

Abbas AK . Cells and of The Immune System. Short course Human Immunology. [n.p]: [n.p]; 1994.



Indexed by:






The Prodia Education and Research Institute