ABSTRACT
Helicobacter pylori infection is one of the most common chronic bacterial infections in humans. The association of other Helicobacter spp. with extragastric diseases in animals is well established, and a role of these bacteria in human liver disease is becoming clearer. Several case-control studies have reported possible associations of Helicobacter spp. with various liver diseases, including hepatocellular carcinoma, which is the fifth most common type of carcinoma among men worldwide, and the eighth most common among women. Thus, it is important to understand molecular mechanisms that may lead to hepatotoxicity or hepatocellular dysfunction in which Helicobacter spp. may play a role in inducing malignant transformation of liver cells.
Subject(s)
Carcinoma, Hepatocellular/epidemiology , Carcinoma, Hepatocellular/microbiology , Helicobacter Infections/complications , Helicobacter pylori/pathogenicity , Animals , Humans , Models, Biological , PrevalenceABSTRACT
Campylobacter jejuni is the main cause of bacterial acute gastroenteritis worldwide. In its colonization of the host intestinal tract, it encounters secreted mucins in the mucus layer and surface mucins in the epithelial cells. Mucins are complex glycoproteins that comprise the major component of mucus and give mucus its viscous consistency. MUC2 is the most abundant secreted mucin in the human intestine; it is a major chemoattractant for C. jejuni, and the bacterium binds to it. There are no studies on the transcriptional response of the bacterium to this mucin. Here, cell-culture techniques and quantitative RT-PCR were used to characterize in vitro the effects of MUC2 on C. jejuni growth and the changes in expression of 20 C. jejuni genes related to various functions. The genes encoding cytolethal distending toxin protein (cdtABC), vacuolating cytotoxin (vacB), C. jejuni lipoprotein (jlpA), Campylobacter invasion antigen (ciaB), the multidrug efflux system (cmeAB), putative mucin-degrading enzymes (cj1344c, cj0843c, cj0256 and cj1055c), flagellin A (flaA) and putative rod-shape-determining proteins (mreB and mreC) were upregulated, whereas those encoding Campylobacter adhesion fibronectin-binding protein (cadF) and sialic acid synthase (neuB1) were downregulated. These results showed that C. jejuni utilizes MUC2 as an environmental cue for the modulation of expression of genes with various functions including colonization and pathogenicity.
Subject(s)
Bacterial Proteins/metabolism , Campylobacter jejuni/growth & development , Campylobacter jejuni/genetics , Gene Expression Regulation, Bacterial , Mucins/metabolism , Bacterial Proteins/genetics , Bacteriological Techniques , Campylobacter jejuni/metabolism , Campylobacter jejuni/pathogenicity , Culture Media , Gene Expression Profiling , Humans , Mucin-2 , Reverse Transcriptase Polymerase Chain Reaction , Virulence/geneticsABSTRACT
The bacterium Wolinella succinogenes is the only known species of its genus. It was first isolated from cow ruminal fluid, and in cattle, it dwells in the reticulum and rumen compartments of the stomach. The global protein response of W. succinogenes to ox-bile was investigated with the aim to understand bile-tolerance mechanisms of the bacterium. Bacteria were grown in liquid media supplemented with different bile concentrations to determine its effects on growth and morphology. Proteomic analyses served to identify 14 proteins whose expression was modulated by the presence of 0.2% bile. Quantitative real-time PCR analyses of the expression of selected genes were employed to obtain independent confirmation of the proteomics data. Proteins differentially expressed revealed metabolic pathways involved in the adaptation of W. succinogenes to bile. The data suggested that bile stress elicited complex physiological responses rather than just specific pathways, and identified proteins previously unknown to be involved in the adaptation of bacteria to bile.
