Immunosuppression abrogates resistance of young rabbits to Rabbit Haemorrhagic Disease (RHD).

Rabbit Haemorrhagic Disease (RHD) is caused by a calicivirus (RHDV) that kills 90% of infected adult European rabbits within 3 days. Remarkably, young rabbits are resistant to RHD. We induced immunosuppression in young rabbits by treatment with methylprednisolone acetate (MPA) and challenged the animals with RHDV by intramuscular injection. All of these young rabbits died within 3 days of infection due to fulminant hepatitis, presenting a large number of RHDV-positive dead or apoptotic hepatocytes, and a significant seric increase in cytokines, features that are similar to those of naïve adult rabbits infected by RHDV. We conclude that MPA-induced immunosuppression abrogates the resistance of young rabbits to RHD, indicating that there are differences in the innate immune system between young and adult rabbits that contribute to their distinct resistance/susceptibility to RHDV infection.

Early acute depletion of lymphocytes in calicivirus-infected adult rabbits.

Rabbit Haemorrhagic Disease (RHD) is a lethal infection caused by calicivirus that kills 90% of the infected adult rabbits within 3 days. The calicivirus replicates in the liver and causes a fulminant hepatitis. Most studies on the pathology of RHD have been focused on the fulminant liver disease. This may not be the only mechanism in the pathogenesis of RHD: calicivirus infection may also induce leukopenia in the infected adult rabbits. We show now by flow cytometry analysis that the calicivirus induces an early decrease in B and T cells, in both spleen and liver. The depletion of B and T cells was associated with apoptosis labelled by annexin V. These changes occurred in rabbits before they showed enzymatic evidence of liver damage and persisted after liver transaminase values were very high. We conclude that depletion of lymphocytes caused by the calicivirus infection precedes or attends liver damage. The relative contribution of this lymphocyte depletion for the pathogenesis of the fatal calicivirus infection of rabbits remains to be investigated.

Respiratory epithelia in Wistar rats.

Morphofunctional changes of respiratory epithelia became the object of intense study in Wistar rats after previous research showed that occupationally-simulated exposure to low frequency noise (500 Hz, including infrasound) induced irreversible lesions in these tissues. Aspects of normal respiratory epithelia in rats are lacking in the literature, and are the object of this report. Ten Wistar rats were kept in silence, fed standard rat food, and had unrestrained access to water (treated in accordance with 86/609/CE). The animals were sacrificed at 3.5 months of age, and respiratory epithelial fragments were excised and prepared for scanning (SEM) and transmission (TEM) electron microscopy. Brush cells (BC) were frequently observed with TEM, but with SEM they were often covered by the cilia of neighbouring cells. BC were always observed at the center of a ring of secretory cells (SC), in a rosetta-shaped formation. In TEM, the microvilli of SC surrounding the BC were uniform, and had the same density and shape in all cells. Multivesicular bodies were identified in areas within the BC. Formation and budding of vesicles from ciliary plasma membranes and from BC microvilli were frequently observed in both TEM and SEM. These data contribute to the understanding of the BC function.

[Respiratory epithelia in Wistar rats after 48 hours of continuous exposure to low frequency noise]. / O epitélio respiratório em ratos Wistar após 48 horas de exposição contínua ao ruído de baixa frequência.

Previous studies show that exposure to low frequency noise (LFN) (< or =500 Hz, including infrasound) produces irreversible lesions in Wistar rat respiratory epithelia. Recovery periods for LFN-induced lesions have thus become an object of interest. Changes in the respiratory epithelia of Wistar rats after continuous short-term exposure to LFN are described. Twelve rats were exposed to continuous LFN for 48 hrs, and 10 age-matched rats were kept in silence. Animals were treated in accordance with 86/609/CE. After exposure ceased, two rodents were sacrificed immediately, and another two after 6, 12, 24, 48 hrs, and 7 days of post-exposure silence. Respiratory epithelial fragments were prepared for light and scanning/transmission electron microscopy. Six hours after exposure, intense and irregular cellular tumefaction was visible and rosetta structures, formed by secretory cells (SC) centered on a brush cell (BC), were identifiable. Cilia were shorter and shaggy. BC microvilli tended to group, losing the uniform distribution seen in controls. Twelve hours after exposure, cell ballooning was still present, BC shape was highly irregular and microvilli were grouped. SC microvilli were still shorter than controls. Seven days after exposure, controls and exposed were indistinguishable. LFN-induced epithelial lesions seem to be reversible if recovery periods are respected.

[Respiratory epithelia in Wistar rats born in low frequency noise plus varying amounts of additional exposure]. / O epitélio respiratório em ratos Wistar nascidos em ruído de baixa frequência e expostos a ruído adicional.

Earlier studies of Wistar rat respiratory epithelia exposed to low frequency noise (LFN) (< or =500 Hz, including infrasound) showed that LFN effects trauma on the respiratory tract. In rats gestated and born in LFN environments, trauma was still treated in accordance with 86/609/EC. Respiratory epithelial fragments were prepared for light and scanning/transmission electron microscopy. Group A brush cell (BC) microvilli tended to group together; in Group B they were clearly clustered together, and in Groups C-F they became fused. Rosetta structures (rings of secretory cells centered on a BC) were visible in Groups A-D and difficult to identify in Groups E,F. The amount of sheared cilia increased with exposure time, as did the images of cellular de-differentiation. LFN exposure induces severe trauma on the respiratory epithelial cells in these rats.