Role of Non-conventional T Lymphocytes in Respiratory Infections: The Case of the Pneumococcus

Non-conventional T lymphocytes constitute a special arm of the immune system and act as sentinels against pathogens at mucosal surfaces. These non-conventional T cells (including mucosal-associated invariant T [MAIT] cells, gamma delta [γδ] T cells, and natural killer T [NKT] cells) display several innate cell-like features and are rapidly activated by the recognition of conserved, stress-induced, self, and microbial ligands. Here, we review the role of non-conventional T cells during respiratory infections, with a particular focus on the encapsulated extracellular pathogen Streptococcus pneumoniae, the leading cause of bacterial pneumonia worldwide. We consider whether MAIT cells, γδ T cells, and NKT cells might offer opportunities for preventing and/or treating human pneumococcus infections.     

Chemotherapeutic Studies of Mycobacterial Infections in Mice

Of six antibiotics investigated, streptovaricin C had the most marked chemotherapeutic effect on Mycobacterium kansasii infections in mice. By the intraperitoneal route this antibiotic caused elimination of the pathogens from all organs. Kanamycin eliminated the pathogens from the lungs of all animals and from the spleens and livers of most of them. Bluensomycin also removed the pathogens from the lungs of all animals, and spectinomycin and lincomycin, from the lungs of the majority of the animals. The three latter antibiotics lowered the bacterial counts in liver and spleen. Streptovaricin C also decreased the bacterial counts in brain, spleen, and liver of mice inoculated intracerebrally with M. kansasii. In one experiment it completely eliminated this pathogen from the spleen and almost completely from the liver. The effect of streptovaricin C on the cerebral infection was more marked than that of streptovaricin complex. Respiratory and cerebral infections of mice with M. avium, serotypes I and II, were limited by streptovaricin C, and marked decreases of the bacterial counts in brain, lungs, spleen, and liver were observed.     

Cellular Changes in Blood Indicate Severe Respiratory Disease during Influenza Infections in Mice

Influenza A infection is a serious threat to human and animal health. Many of the biological mechanisms of the host-pathogen-interactions are still not well understood and reliable biomarkers indicating the course of the disease are missing. The mouse is a valuable model system enabling us to study the local inflammatory host response and the influence on blood parameters under controlled circumstances. Here, we compared the lung and peripheral changes after PR8 (H1N1) influenza A virus infection in C57BL/6J and DBA/2J mice using virus variants of different pathogenicity resulting in non-lethal and lethal disease. We monitored hematological and immunological parameters revealing that the granulocyte to lymphocyte ratio in the blood represents an early indicator of severe disease progression already two days after influenza A infection in mice. These findings might be relevant to optimize early diagnostic options of severe influenza disease and to monitor successful therapeutic treatment in humans.     

Measurement of Respiratory Volume for Virus Retention Studies in Mice

A pressure plethysmograph for measuring respiratory volume in mice during exposure to virus aerosols is described. The respiratory frequency and tidal volume were measured, and from these data the minute ventilation was calculated. The mean respiratory frequency of adult, male mice was 255 per min; the mean tidal volume of 0.18 ml was inversely related to respiratory frequency. The standardized mean minute ventilation rate was 1.46 ml per g of body weight. The respiratory frequency and tidal volume of CD-1 and HA/ICR strains of mice of the same age were similar. The respiratory retention rate for a 2.7-mum aerosol of vesicular stomatitis virus was 41%, and 58% of the virus retained was found in the trachea and lung.     

The Pathology of Vinyl Chloride Exposed Mice

Outbred albino laboratory mice were exposed to 50 p.p.m. and 500 p.p.m. vinyl chloride by inhalation 6 hrs./day, 5 days/week during 52 and 26 weeks, respectively. Pathologic examination showed the presence of histologically benign alveologenic lung adenomas, haem-angiosarcomas in fat tissue as well as a few benign and malignant tumours at various sites. Only one liver haemangiosarcoma was noted. All animals exposed to 500 p.p.m. developed tumours; 71 % of the animals given 50 p.p.m. were tumour bearing. The frequency of all tumours, number of tumour foci and size of foci in both groups suggest a dose-dependent carcinogenic effect of vinyl chloride. Haemocoelia due to blood vessel rupture was a common cause of death. Telangiectasis of the liver was also observed in a few animals. The role of fat tissue as well as blood vessel involvement in the pathology of vinyl chloride is discussed.