Dokumen Artikel Penelitian ini milik penulis/penelliti yang diserahkan sebagian (judul dan Abstrak) hak ciptanya kepada Universitas Airlangga untukdigunakan referensi dalam penulisan artikel ilmiah.

Penulis : SUHARTONO TAAT PUTRAFakultas : Kedokteran

Tim Peneliti : A. GUNTUR HERMAWAN,

PERBEDAAN RESPONS IMUN YANG BERPERAN PADA SEPSIS DANSYOK SEPTIK SUATU PENDEKATAN IMUNOPATOBIOLOGIK SEPSIS

DAN SYOK SEPTIK PADA IMMUNOCOMPROMISE DAN NONIMMUNOCOMPROMISE

Abstrak :

The purpose of this study was intended to explain a shock septic mechanism in immunocompromise (IC)and Non immuno-compromise (NIC). This study contains two phases of observational analysis. First phaseapplied cross sectional design to differentiate iznmune response for IC and NIC in non-sepsis condition.Second phase applied Cohort design to differentiate immune response for IC and NIC in sepsis and septicshock condition. First and second phases of this study used a separate sample. The variables of immuneresponse were determined by analyzing IgG, C3, C4, IL-10, IFNg. TNF-a and IL-1b. A multivariateanalysis (Manova) was applied in this study for statistical analysis.Result of this study showed that there was a significant difference (p<0.05) in immune response towardan IC and NIC non-sepsis condition marked by increasing on IL-10, TNF-a, IgG and decreasing on C3 variable. However, there was no significant (p>0.05)difference on the result for IC and NIC in sepsis condition. No significant difference also found for IC andNIC in septic shock condition (p>0.05). Then it is concluded that IC and NIC groups showed nodifference in septic and shock condition. Therefore, those two groups together are considered into onegroup to analyse the difference between IC-NIC in septic shock and IC-NIC in non-septic shock thatshowed a significant difference (p<0.05).Furthermore, due to immune response differences above, the study was continued with discriminantanalysis (discriminator). For IC-N1C septic shock and IC-NIC sepsis, there were four variables asdiscriminators, IL-10, IL-b, IgG and C3.To explain the immunopathobiogenesis, a narration of conceptual framework has been done usingdiscriminant pattern. Based on such method, immunogene stimulation to macrophage (APC) couldinfluence Th2, inducing the increase of IL-10 contribution that accelerating B lymphocyte maturity tobecome IgG-producing plasma cells. IgG with toxin fortned a toxin complex which precipitated on the wallof endothelial cells in blood vessels, and activated C3 complement, leading to endothelial destructionthrough a process called antibody dependent cellular cytotoxicity (ADCC). Thl stimulation increased IFNg.IFNg stimulated macrophage, inducing the increase of IL 1b which stimulated endothelial cells to induce1CAM-l. As an adhesive substance, ICAM-1 would be bound with neutrophyl, leading to endothelialdestruction in blood vessels through DTH process. Both processes caused leakage of the wall of blo vessel,leading to produce the occurrence of septic shock.In conclusion, the immunopathobiogenesis of septic shock c be caused by the mechanisms of ADCC andDTH.

Keyword :

Immunocompromise (IC), Non-Immunocompromise (NIC), Sepsis, Septic Shock, ADCC, DTH

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