Mycoplasma hominis is an opportunistic human mycoplasma. Two other pathogenic human species, M. genitalium and Ureaplasma parvum, reside within the same natural niche as M. hominis: the urogenital tract. These three species have overlapping, but distinct, pathogenic roles. They have minimal genomes and, thus, reduced metabolic capabilities characterized by distinct energy-generating pathways. Analysis of the M. hominis PG21 genome sequence revealed that it is the second smallest genome among self-replicating free living organisms (665,445 bp, 537 coding sequences (CDSs)). Five clusters of genes were predicted to have undergone horizontal gene transfer (HGT) between M. hominis and the phylogenetically distant U. parvum species. We reconstructed M. hominis metabolic pathways from the predicted genes, with particular emphasis on energy-generating pathways. The Embden–Meyerhoff–Parnas pathway was incomplete, with a single enzyme absent. We identified the three proteins constituting the arginine dihydrolase pathway. This pathway was found essential to promote growth in vivo. The predicted presence of dimethylarginine dimethylaminohydrolase suggested that arginine catabolism is more complex than initially described. This enzyme may have been acquired by HGT from non-mollicute bacteria. Comparison of the three minimal mollicute genomes showed that 247 CDSs were common to all three genomes, whereas 220 CDSs were specific to M. hominis, 172 CDSs were specific to M. genitalium, and 280 CDSs were specific to U. parvum. Within these species-specific genes, two major sets of genes could be identified: one including genes involved in various energy-generating pathways, depending on the energy source used (glucose, urea, or arginine) and another involved in cytadherence and virulence. Therefore, a minimal mycoplasma cell, not including cytadherence and virulence-related genes, could be envisaged containing a core genome (247 genes), plus a set of genes required for providing energy. For M. hominis, this set would include 247+9 genes, resulting in a theoretical minimal genome of 256 genes.

The results presented in this study indicate that Helicobacter species can be present in the liver of patients with primary hepatic carcinoma, but their eventual role in the carcinogenesis process, although it is plausible, remains to be proven. Based on sequence similarity, it seems that Helicobacter species that are related closely to H. pylori but are distinct from it have been found.

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It has been reported that Helicobacter hepaticus infection of mice leads to chronic hepatitis and hepatocarcinoma. Our aim was to monitor a cohort of 80 conventional A/J mice in which half of the mice were infected by H. hepaticus in order to study the evolution of the infection and the pathological changes in comparison to uninfected mice. H. hepaticus was detected by culture only in some colon and cecum specimens after 17 months of age, while PCR detected H. hepaticus in the intestines of all inoculated mice after only 5 months of infection. The percentage of mice in which H. hepaticus was detected in the gallbladder, bile ducts, and liver by PCR, as well as the number of bacteria present in the liver, tended to increase with increasing age and longer infection time. Anti-H. hepaticus immunoglobulin G antibodies were positive by enzyme-linked immunosorbent assay only in inoculated mice. Pathological findings were also more frequent as the mice grew older: fibrosis was present (especially in the peripheral part of the liver), and significant portal inflammation including lymphoid nodules was present in almost all infected animals. Biliary lesions of neutrophilic acute cholangitis or lymphocytic cholangitis were noted. However, lesions were also observed in uninfected animals, although at a significantly lower level, and the only hepatocellular carcinoma occurred in an uninfected mouse. The evolution towards hepatocarcinoma is not always the endpoint and may depend on the bacterial strain and on the environmental conditions.Helicobacter species are responsible for chronic infections. In humans, Helicobacter pylori induces gastritis, which may last for decades and may be a lifelong condition. This infection is the first bacterial infection found to be involved in the development of a carcinogenic process in humans (8).After the occurrence of an unexpected and high level of hepatocellular tumors in mice with chronic active hepatitis, H. hepaticus was cultured from the liver and identified as a new species of Helicobacter that induces carcinoma (5). This bacterium has been the topic of extensive research since then. There have been studies on diagnostic methods (4, 13, 16, 17), pathogenic properties (2, 18), and the process of carcinogenesis (3, 9, 15) but few prospective studies of the natural history of H. hepaticus infection and liver pathology in mice. Therefore, our aim was to study the natural history of this infection for 17 months and to use the LightCycler methodology to quantitate the bacteria present in the liver.Study design. Eighty male A/J mice (3 to 4 weeks old) (not specific pathogen free), obtained from Jackson Laboratory (Bar Harbor, Maine), were maintained in microisolator cages and fed conventional food (Usine d'Alimentation Rabonnelle, Villemoisson-sur-Orge, France). The mice were cared for in accordance with the National Institutes of Health guidelines. Half of the mice were orally inoculated with H. hepaticus (group I), and the other half (group II) were used as controls. H. hepaticus type st...