Ulcerogenic Helicobacter pylori Strains Isolated from Children: A Contribution to Get Insight into the Virulence of the Bacteria

Infection with Helicobacter pylori is the major cause for the development of peptic ulcer disease (PUD). In children, with no other etiology for the disease, this rare event occurs shortly after infection. In these young patients, habits of smoking, diet, consumption of alcohol and non-steroid anti-inflammatory drugs and stress, in addition to the genetic susceptibility of the patient, represent a minor influence. Accordingly, the virulence of the implicated H. pylori strain should play a crucial role in the development of PUD. Corroborating this, our in vitro infection assays comparing a pool of five H. pylori strains isolated from children with PUD to a pool of five other pediatric clinical isolates associated with non-ulcer dyspepsia (NUD) showed the greater ability of PUD strains to induce a marked decrease in the viability of gastric cells and to cause severe damage in the cells cytoskeleton as well as an impairment in the production/secretion of mucins. To uncover virulence features, we compared the proteome of these two groups of H. pylori strains. Two-dimensional gel electrophoresis followed by mass-spectrometry allowed us to detect 27 differentially expressed proteins between them. In addition to the presence of genes encoding well established virulence factors, namely cagA, vacAs1, oipA “on” status, homB and jhp562 genes, the pediatric ulcerogenic strains shared a proteome profile characterized by changes in the abundance of: motility-associated proteins, accounting for higher motility; antioxidant proteins, which may confer increased resistance to inflammation; and enzymes involved in key steps in the metabolism of glucose, amino acids and urea, which may be advantageous to face fluctuations of nutrients. In conclusion, the enhanced virulence of the pediatric ulcerogenic H. pylori strains may result from a synergy between their natural ability to better adapt to the hostile human stomach and the expression of the established virulence factors

Putative mechanisms and biological role of coccoid form formation in Campylobacter jejuni.

In certain conditions Campylobacter jejuni cells are capable of changing their cell shape from a typically spiral to a coccoid form (CF). By similarity to other bacteria, the latter was initially considered to be a viable but non-culturable form capable of survival in unfavourable conditions. However, subsequent studies with C. jejuni and closely related bacteria Helicobacter pylori suggested that CF represents a non-viable, degenerative form. Until now, the issue on whether the CF of C. jejuni is viable and infective is highly controversial. Despite some preliminary experiments on characterization of CF cells, neither biochemical mechanisms nor genetic determinants involved in C. jejuni cell shape changes have been characterized. In this review, we highlight known molecular mechanisms and genes involved in CF formation in other bacteria. Since orthologous genes are also present in C. jejuni, we suggest that CF formation in these bacteria is also a regulated and genetically determined process. A possible significance of CF in the lifestyle of this important bacterial pathogen is discussed