Vertical Helicobacter pylori transmission from Mongolian gerbil mothers to pups.

To identify the time frame and route of mother-to-child Helicobacter pylori infection, a Mongolian gerbil model was used. Four-week-old female Mongolian gerbils were infected with H. pylori, and then mated with uninfected males 2 months after infection. The offspring were sacrificed weekly after birth, and then serum, mother's milk from the stomach and gastric tissues were obtained from pups. Anti-H. pylori antibody titres were measured in sera and maternal milk using an ELISA. The stomach was cut in two in the sagittal plane, and then H. pylori colonization in mucosa was confirmed by culture and real-time RT-PCR in one specimen and by immunochemical staining in the other. Faeces and oral swabs were obtained from infected mothers, and H. pylori 16S rRNA was measured using real-time RT-PCR. H. pylori was not identified in cultures from the gastric mucosa of pups delivered by infected mothers, but H. pylori 16S rRNA was detected from 4 weeks after birth, suggesting that Mongolian gerbil pups become infected via maternal H. pylori transmission from 4 weeks of age. The anti-H. pylori antibody titre in sera of pups from infected mothers was maximum at 3 weeks of age and then rapidly decreased from 4 weeks of age. High antibody titres in mother's milk were detected during the suckling period, and GlcNAcalpha was detectable at 2-4 weeks of age, but disappeared as the offspring aged. Thus H. pylori seems to infect Mongolian gerbil pups from 4 weeks of age, in parallel with decreasing GlcNAcalpha expression in the gastric mucosa. These results suggested that H. pylori infection of Mongolian gerbil pups occurs via faecal-oral transmission from an infected mother.

Development of diabetes in non-obese diabetic mice promotes Chlamydia pneumoniae dissemination from lung to peripheral blood.

We examined a possible association between development of diabetes in non-obese diabetic (NOD) mice and dissemination of Chlamydia (Chlamydophila) pneumoniae from lung to peripheral blood. By real-time reverse transcription-polymerase chain reaction (RT-PCR) with primers for C. pneumoniae 16S rRNA, following multiple intranasal inoculations, we detected bacteria in lung in NOD mice with diabetes (38.5%) as well as Institute of Cancer Research, USA (ICR) mice (40%), but prevalence of bacteria in NOD mice without diabetes (pre-diabetic NOD mice and non-diabetic retired NOD mice) was very low (4.8%). The bacteria were only detected in peripheral blood mononuclear cells (PBMCs) cultured with hydrocortisone of the NOD mice with diabetes (53.8%). Results of immunostaining with fluorescein isothiocyanate-conjugated antichlamydia monoclonal antibody also showed the presence of bacterial antigens in the lungs and the PBMCs judged as positive by the RT-PCR. However, C. pneumoniae from cultured PBMCs of all NOD mice was undetected by cultivation method with inclusion-forming units assay. In addition, no influence of C. pneumoniae intranasal inoculation on development of diabetes in NOD mice was confirmed. Thus, the development of diabetes in NOD mouse appears to be one of critical factors for promoting the dissemination of C. pneumoniae from lung to peripheral blood.