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Innate Immune Response in Non Alcoholic Fatty Liver Disease: An Overview of Alterations in TLR9, Macrophages, and TNFα Supriatna, Novianti; Siregar, Nurjati Chairani
Proceedings Book of International Conference and Exhibition on The Indonesian Medical Education Research Institute Vol. 6 No. - (2022): Proceedings Book of International Conference and Exhibition on The Indonesian M
Publisher : Writing Center IMERI FMUI

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.69951/proceedingsbookoficeonimeri.v6i-.131

Abstract

Non-Alcoholic Fatty Liver Disease (NAFLD) and Alcoholic Liver Disease (ALD) are two causes of chronic liver disease. In Indonesia, NAFLD is the most common case of hepatic disease for Indonesian people. Risk factors such as obesity, diabetes mellitus, and metabolic syndrome increase the risk of developing NAFLD. About 1.5 billion people worldwide suffer from fatty liver, with a prevalence of 25-30%. Hence, it will continue to increase sharply if risk factors or diseases are not mitigated with pharmacological treatment and diet. The innate immune response induces abnormalities in fatty liver, mediated by Kupffer cells and TLR9 (Toll-Like Receptor 9), leading to inflammation via proinflammatory cytokines, like TNFα. Hepatocyte injury releases signals in the form of mitochondrial DNA enclosed in microparticles, which travels into the plasma, and are then captured by TLR9. Activation of TLR9 on Kupffer cells is the starting point of the inflammatory process in the pathogenesis of NAFLD, and it triggers other immune responses that encourage the development of steatohepatitis until a more severe liver injury occurs. The latest study found that analysis is needed to determine the immunological mechanisms and therapeutic targets associated with inflammation in fatty liver disease as evidenced by various immunological approaches.
Effect of the modified Atkins diet on NLRP3, caspase-1, IL-1β, and IL-10 in patients with tetralogy of Fallot undergoing open-heart surgery: A randomized controlled trial Yanuarso, Piprim B.; Djer, Mulyadi M.; Hendarto, Aryono; Pudjiadi, Antonius H.; Rachmadi, Lisnawati; Wibowo, Heri; Advani, Najib; Murni, Indah K.; Kekalih, Aria; Sukardi, Rubiana; Dilawar, Ismail; Susanti, Dhama S.; Supriatna, Novianti
Narra J Vol. 5 No. 1 (2025): April 2025
Publisher : Narra Sains Indonesia

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.52225/narra.v5i1.2138

Abstract

Cardiopulmonary bypass in tetralogy of Fallot (TOF) corrective surgery induces hyperinflammation by activating NLRP3, caspase-1, and interleukin-1β (IL-1β), subsequently triggering an interleukin-10 (IL-10) response. Despite its known metabolic and anti-inflammatory effects, the impact of the modified Atkins diet (MAD) in pediatric cardiac surgery remains unexplored, with no studies on its use in TOF patients undergoing open-heart surgery. The aim of this study was to assess the effect of MAD on the expression of NLRP3, caspase-1, IL-1β, and IL-10, in TOF patients undergoing open-heart surgery. A double-arm, randomized-controlled trial was conducted with 44 TOF patients. The treatment group (n=22) received the MAD, a low-carbohydrate, high-fat regimen with unrestricted fat and protein intake for at least 14 days preoperatively, while the control group (n=22) followed a standard diet without carbohydrate restriction. Blood plasma and infundibulum heart tissues were collected for analysis. Whole blood samples were collected using a winged infusion needle before the intervention, an Abbocath infusion needle after 14 days of intervention, and a syringe without a needle connected to an arterial line in patients undergoing open-heart surgery at 6, 24, and 48 hours post-surgical correction. Infundibulum heart tissues were collected during the open-heart surgery. This study demonstrated significant differences in NLRP3 protein expression (p=0.015), caspase-1 protein expression (p=0.001), and IL-10 levels between before intervention and 6-, 24-, and 48-hours post-surgery in the MAD group compared to the control group. In contrast, no significant differences in IL-10 levels were observed in the control group between before intervention and 48 hours post-surgery (p=0.654). In conclusion, MAD may modulate perioperative inflammation in TOF patients undergoing open-heart surgery by downregulating NLRP3 and caspase-1 expression while sustaining IL-10 levels. Despite reduced NLRP3 and caspase-1 expression, unchanged IL-1β levels indicate alternative regulatory mechanisms.