RESUMO
The aim of this study was to evaluate the effects of an environment change and the age at which mating pairs were formed on the lifetime reproductive performance of BALB/c mice. We assigned 60 monogamous pairs to a randomized design in a 2 × 3 factorial arrangement (with or without an environmental modification and with 3 mating ages: 28, 45, or 60 d). Autoclaved cardboard tubes (length, 10 cm; diameter, 4 cm) were used as the environmental modification. Data were collected from a total of 456 litters over a period of 10 mo. The mice tore the cardboard tube and used its parts both as shelters and as nesting material. The presence of a cardboard tube decreased the preweaning litter mortality rate in the first 6 reproductive cycles. Mating at 28 or 45 d of age also decreased the preweaning mortality rate in the first 6 reproductive cycles, compared with monogamous pairs formed at 60 d of age. Treatments did not affect age at first parturition, number of litters, time between litters, or litter size and weight at birth and weaning. In addition to contributing to animal wellbeing, providing a cardboard tube improved productivity by decreasing the preweaning mortality rate. BALB/c siblings should be paired for mating when no older than 28 d, to reduce preweaning mortality of the offspring.
Assuntos
Abrigo para Animais , Camundongos Endogâmicos BALB C/fisiologia , Animais , Peso Corporal , Feminino , Tamanho da Ninhada de Vivíparos , Masculino , Camundongos , Reprodução , DesmameRESUMO
The role of innate immune response in protection against leptospirosis is poorly understood. We examined the expression of the chemokine CXCL2/MIP-2 and the cytokine TNF-α in experimental resistant and susceptible mice models, C3H/HeJ, C3H/HePas and BALB/c strains, using a virulent strain of Leptospira interrogans serovar Copenhageni. Animals were infected intraperitoneally with 10(7) cells and the development of the disease was followed. Mortality of C3H/HeJ mice was observed whereas C3H/HePas presented jaundice and BALB/c mice remained asymptomatic. The infection was confirmed by the presence of leptospiral DNA in the organs of the animals, demonstrated by PCR. Sections of the organs were analyzed, after H&E stain. The relative expression of mRNA of chemokine CXCL2/MIP-2 and cytokine TNF-α was measured in lung, kidney and liver of the mice by qPCR. The concentrations of these proteins were measured in extracts of tissues and in serum of the animals, by ELISA. Increasing levels of transcripts and protein CXCL2/MIP-2 were detected since the first day of infection. The highest expression was observed at third day of infection in kidney, liver and lung of BALB/c mice. In C3H/HeJ the expression of CXCL2/MIP-2 was delayed, showing highest protein concentration in lung and kidney at the 5th day. Increasing in TNF-α transcripts were detected after infection, in kidney and liver of animals from the three mice strains. The expression of TNF-α protein in C3H/HeJ was also delayed, being detected in kidney and lung. Our data demonstrated that Leptospira infection stimulates early expression of CXCL2/MIP-2 and TNF-α in the resistant strain of mice. Histological analysis suggests that the expression of those molecules may be related to the influx of distinct immune cells and plays a role in the naturally acquired protective immunity.