Mice with asthma are more resistant to influenza virus infection and NK cells activated by the induction of asthma have potentially protective effects.

PURPOSE: This study was conducted in order to investigate whether the virulence of the influenza virus infection is affected by asthma in mice. METHODS: Mice with asthma or control mice were infected with influenza virus. The survival rate, body weight, virus titer, cytokine profile, and cell infiltration in bronchoalveolar lavage fluid (BALF) were measured. The NK cell cytotoxicity was determined by a co-culture system with YAC-1 cells, and the effects of NK cells were observed by depletion of NK cells using anti-asialoGM1 serum. The virus-specific CD8(+) T cell killing assay was also performed. RESULTS: When asthmatic or control mice were infected with non- and sub-lethal doses of influenza virus, the asthmatic mice were more resistant to the virus than control mice with regard to the survival rate, the remission of body weight loss, and the virus burden. Anti-viral cytokines and the NK cell number were increased in the BALF of asthmatic mice before the infection. The NK cell cytotoxicity in the asthmatic mice was significantly enhanced compared to that in control mice, and the depletion of NK cells in asthmatic mice was abrogated both the improved survival rate and the recovery of the body weight loss. The antigen-specific CD8(+) T cell killing activity in asthmatic mice was also significantly increased following the infection compared to that in control mice. CONCLUSION: NK cell activated by the induction of asthma and the subsequently activated antigen-specific CD8(+) T cells could promptly eliminate the viral-infected cells, thus leading to improvements in the morbidity and mortality of influenza virus infection.

The performance of the BD geneOhm MRSA™ assay for MRSA isolated from clinical patients in Japan, including the effects of specimen contamination and ways to improve it.

The BD geneOhm MRSA™ assay has been increasingly used in recent years, and it is possible to use it to screen and detect methicillin-resistant Staphylococcus aureus (MRSA) from a specimen within 2 h. The purpose of the present study was to evaluate the performance, i.e., the specificity and sensitivity, of the BD geneOhm MRSA™ assay to detect MRSA. Its specificity was assessed to be 100% compared to bacterial culture methods, which are commonly used in medical laboratories. Its bacterial limit of detection was over 10 colony-forming units (cfu) per reaction, although MRSA was detected at a cfu below 10 per reaction in a few samples. Additionally, the effect of MRSA isolate contamination was examined. While contamination with protein or other bacteria did not affect the outcome, contamination with a high concentration of blood resulted in an unresolved outcome. To inactivate polymerase chain reaction (PCR) inhibitors, the DNA samples were freeze-thawed prior to the BD geneOhm MRSA™ assay, which led to the sensitivity of the assay increasing. In summary, the BD geneOhm MRSA™ assay is rapid and shows high specificity and sensitivity of cultured MRSA isolates. It will, therefore, be a valuable diagnostic tool for detecting MRSA in specimens from clinical patients.

Oral administration of heat-killed Lactobacillus plantarum strain b240 protected mice against Salmonella enterica Serovar Typhimurium.

The purpose of this study was to investigate the effects of heat-killed Lactobacillus plantarum strain b240 (b240) on systemic infection by Salmonella enterica serovar Typhimurium (S. Typhimurium) and to determine the mechanism by which b240 protects against infection. Mice were administered either b240 or saline orally for 3 weeks, and then inoculated with S. Typhimurium. The mice treated with b240 were significantly protected against S. Typhimurium as compared to those fed saline. Moreover, translocation of S. Typhimurium into each organ tested in the mice that received b240 tended to be less than in the control mice. An important mechanism of protection against infection was demonstrated by the ability of b240 to inhibit both binding by and invasion of S. Typhimurium into cells. These results indicate that nonviable lactic acid bacteria also play important roles in preventing infection by enteric pathogens.

IFN-γ production downstream of NKT cell activation in mice infected with influenza virus enhances the cytolytic activities of both NK cells and viral antigen-specific CD8+ T cells.

Natural killer T (NKT) cell activation is responsible for eliminating pathogens. However, the biological functions of NKT cells against influenza virus are not fully understood. We therefore investigated the effects of NKT cells in viral infection using CD1d knockout (KO) mice. When CD1d KO or wild-type (WT) mice were infected with a sub-lethal dosage of the influenza virus, the survival rate of CD1d KO mice was significantly lower than for WT mice in association with delayed viral clearance in the lungs. Consistently, IFN-γ production in bronchoalveolar lavage fluid of CD1d KO mice was largely reduced compared to WT mice during infection. Moreover, the cytotoxic activities of NK cells and viral antigen-specific CD8(+) T cells were impaired in CD1d KO mice. It was concluded that activated NKT cell-induced IFN-γ release enhances both NK-cell activity and antigen-specific CD8(+) T cells to eliminate the influenza virus, thus leading to an enhanced survival.