Characterization of the Maternally Derived Antibody Immunity against Rhdv-2 after Administration in Breeding Does of an Inactivated Vaccine

Inactivated strain-specific vaccines have been successfully used to control rabbit haemorrhagic disease (RHD) caused by RHDV-2 in the rabbit industry. It is unknown whether and how vaccination of breeding does contributed to protect the population of young susceptible rabbit kits. The present study investigates whether the immunity against RHDV-2 produced by vaccination of breeding does is transmitted to their progeny and its dynamic once inherited by kits. For this purpose, New Zealand female rabbits of 8–9 weeks of age were allocated into 2 groups of 40 subjects each and bred during 6 reproductive cycles. The first experimental group was vaccinated with a commercially available inactivated vaccine against RHDV-2 whereas the second group was inoculated with PBS. Moreover, the present study was also meant to identify the mechanisms of transmission of that maternal immunity. For this reason, rabbit kits of vaccinated and non-vaccinated breeding does were cross-fostered before milk uptake. The RHDV-2 antibody response was monitored in the blood serum of breeding does and of their kits by competition ELISA (cELISA) and solid-phase ELISA (spELISA). Since it has been clearly demonstrated that cELISA positive rabbits are protected from RHD, we avoided the resorting of the challenge of the kits with RHDV-2. Results showed that RHDV-2 antibodies were inherited by kits up to one year from vaccination of breeding does. Once inherited, the maternally derived antibody response against RHDV-2 lasted at least until 28 days of life. Finally, the study also elucidated that the major contribution to the maternal derived immunity against RHDV-2 in kits was provided during gestation and probably transmitted through transplacental mechanisms although lactation provided a little contribution to it. The present study contributed to elucidate the characteristics of the maternal antibody immunity produced by vaccination and its mechanisms of transmission.

Transplantation of Dental Pulp Stem Cells in Experimental Bone Defect

This is preliminary study in order to investigate the effect of dental pulp stem cells (DPSCs) on bone regeneration in an animal model. New Zealand rabbits were used as animal model. The critical defect was created in femoral bone and transplantation of DPSCs applied into bone defect. A colorimetric assay was used to detect ALP level in rabbit’s serum. Bone tissue regeneration was evaluated by histological analysis. In the 2nd week, the treated rabbit show increasing in the activity of ALP (157,925 μU) compared to control rabbit (155,361 μU). This increasing trend continues significantly in DPSCs rabbit (169.750 μU) compared to control rabbit (160.406) after 4 weeks. Histological evaluation revealed that the amount of bone lamellae and osteocytes were filled the defect area of DPSCs treated rabbit. Conclusions: Transplantation of DPSCs accelerating bone regeneration by raising ALP level and forming new bone tissue.

Role of hypothalamic interleukin-1β in fever induced by cecal ligation and puncture in rats

Bacterial endotoxin induces fever by causing the release of interleukin (IL)-1β into the circulation or the brain. IL-1β is believed to mediate fever via triggering the production and/or release of IL-6 in the hypothalamus. The present study examined whether IL-1β and IL-6 in the hypothalamus of the rat are also involved in fever during bacterial sepsis caused by cecal ligation and puncture (CLP). CLP induces fever for 2 days. Polyclonal rabbit antibody against rat IL-1β (anti-IL-1β, 2 μg/μl) or control rabbit IgG (2 μg/μl) was unilaterally microinjected into the hypothalamus of rats immediately after or 24 h after CLP or sham-CLP surgery. Anti-IL-1β injected 24 h after CLP (when fever was already present) or sham-CLP surgery did not affect fever. Microinjection of anti-IL-1β into the hypothalamus immediately after surgery caused a significant decrease in body temperature during the night after CLP surgery and a 48% reduction of fever on the following day. Although blood plasma levels of IL-6 were significantly elevated 1.5, 6, 24, and 48 h after CLP surgery, there were no differences in IL-6 concentrations in the extracellular fluid of the anterior hypothalamus (collected by push-pull perfusion). These data suggest that fever due to bacterial sepsis is initiated by IL-1β within the hypothalamus, and this febrile response, unlike endotoxin-induced fever, is not accompanied by elevation in the hypothalamic concentration of IL-6.

Comparative metabolism of plasminogen glycoforms I and II in the alloxan-diabetic rabbit

The metabolism of plasminogen glycoforms I and II was measured in alloxan-induced diabetic and in age-matched control rabbits. Radiolabeled plasminogen I and II were degraded significantly more slowly in diabetic compared with control rabbits; plasminogen II [half-time (T1/2), 1.31 days] was degraded faster than plasminogen I (T1/2), 1.86 days) in diabetic rabbits and in control rabbits (T1/2, 1.18 and 1.58 days, respectively). From the catabolic rates and relative quantities in plasma, we calculated that approximately four molecules of plasminogen II were degraded for one molecule of plasminogen I in the diabetic and control rabbits. To verify this later observation, plasminogen I and II production by diabetic rabbit livers was compared with that by the control livers in vitro. During perfusion with [3H]leucine, 3H-labeled protein was released more slowly from diabetic than from control livers, but no quantitative difference in total plasminogen yield between diabetic and control livers was found. Nevertheless, plasminogen II was produced 0.7 +/- 0.4 and 4.3 +/- 0.3 times faster than plasminogen I by diabetic and control livers, respectively. Plasminogen metabolism in the diabetic rabbit did not differ qualitatively from that in the control rabbit except that catabolism was slowed.