ABSTRACT
Schistosomiasis is an inflammatory disease that occurs when schistosome species eggs are deposited in the liver, resulting in fibrosis and portal hypertension. Schistosomes can interact with host inflammasomes to elicit host immune responses, leading to mitochondrial damage, generation of high levels of reactive oxygen species (ROS) and activation of apoptosis during inflammation. This study aims to examine whether ROS and NF-κB (p65) expression elicited other types of inflammasome activation in Schistosoma mansoni-infected mouse livers. We examine the relationship between inflammasome activation, mitochondrial damage and ROS production in mouse livers infected with S. mansoni. We demonstrate a significant release of ROS and superoxides and increased NF-κB (p65) in S. mansoni-infected mouse livers. Moreover, activation of the NLRP3 and AIM2 inflammasomes was triggered by S. mansoni infection. Stimulation of HuH-7 hepatocellular carcinoma cells with soluble egg antigen induced activation of the AIM2 inflammasome pathway. In this study, we demonstrate that S. mansoni infection promotes both NLRP3 and AIM2 inflammasome activation.
Subject(s)
DNA-Binding Proteins/genetics , Inflammasomes/genetics , NLR Family, Pyrin Domain-Containing 3 Protein/genetics , Schistosomiasis mansoni/immunology , Animals , Apoptosis , Cell Line, Tumor , DNA-Binding Proteins/immunology , Disease Models, Animal , Inflammasomes/immunology , Inflammation , Liver/parasitology , Liver/pathology , Male , Mice , Mice, Inbred BALB C , NLR Family, Pyrin Domain-Containing 3 Protein/immunology , Reactive Oxygen Species/immunology , Transcription Factor RelA/genetics , Transcription Factor RelA/immunologyABSTRACT
Giardia duodenalis is a zoonotic protozoan parasite that causes diarrhea through waterborne transmission or fecal-oral infection. The cysts are chlorine-resistant and, therefore, can pollute drinking water and induce a pandemic disease. In this study, we aimed to detect G. duodenalis infection in stray dogs in Hualien, Taiwan. We collected faecal samples from 118 dogs and amplified DNA sequences of the ß-giardin gene by nested polymerase chain reactions (nested PCR). Eleven of the 118 faecal samples tested positive for the parasite. The genotype analysis of the 11 samples indicated that 7 samples belonged to assemblage C and four samples belonged to assemblage D. Our study provided a better understanding of the infection rate and genotypes of G. duodenalis in dogs from Hualien City, and human infection could not be induced by this zoonotic infection pathway in Hualien City.
