Hiromoto Mizoguchi

Impaired immune responses occur frequently in cancer patients or in tumor-bearing mice, but the mechanisms of the tumor-induced immune defects remain poorly understood. In an in vivo murine colon carcinoma model (MCA-38), animals bearing a tumor longer than 26 days develop CD8+ T cells with impaired cytotoxic function, decreased expression of the tumor necrosis factor-alpha and granzyme B genes, and decreased ability to mediate an antitumor response in vivo. T lymphocytes from tumor-bearing mice expressed T cell antigen receptors that contained low amounts of CD3 gamma and completely lacked CD3 zeta, which was replaced by the Fc epsilon gamma-chain. Expression of the tyrosine kinases p56lck and p59fyn was also reduced. These changes could be the basis of immune defects in tumor-bearing hosts.

The viability of the coccoid forms of Helicobacter pylori was evaluated by assessing protein synthesis. Metabolic labeling studies showed the synthesis of proteins and the specific protein profiles of H. pylori coccoids produced under various conditions. Harsh conditions such as aerobiosis and starvation (lack of horse serum) in the culture did not affect the synthesis of proteins in the coccoids. Lowering of the pH to that of gastric secretions induced expression of several proteins in the coccoids. However, the coccoids produced under prolonged microaerobic conditions exhibited a profile of acid stress-induced protein expression different from that induced by aerobiosis or starvation. Our data suggest that coccoid H. pylori exhibits diversity in viability following exposure to different stresses and that the response to acid stress of coccoid H. pylori could be involved in infection of the host stomach.