Efficacy of three innovative bacterin vaccines against experimental infection with Mycoplasma hyopneumoniae

International audienceAbstractNew vaccine formulations that include novel strains of Mycoplasma hyopneumoniae and innovative adjuvants designed to induce cellular immunity could improve vaccine efficacy against this pathogen. The aim of this experimental study was to assess the efficacy of three experimental bacterin formulations based on M. hyopneumoniae field strain F7.2C which were able to induce cellular immunity. The formulations included a cationic liposome formulation with the Mincle receptor ligand trehalose 6,6-dibehenate (Lipo_DDA:TDB), a squalene-in-water emulsion with Toll-like receptor (TLR) ligands targeting TLR1/2, TLR7/8 and TLR9 (SWE_TLR), and a poly(lactic-co-glycolic acid) micro-particle formulation with the same TLR ligands (PLGA_TLR). Four groups of 12 M. hyopneumoniae-free piglets were primo- (day (D) 0; 39 days of age) and booster vaccinated (D14) intramuscularly with either one of the three experimental bacterin formulations or PBS. The pigs were endotracheally inoculated with a highly and low virulent M. hyopneumoniae strain on D28 and D29, respectively, and euthanized on D56. The main efficacy parameters were: respiratory disease score (RDS; daily), macroscopic lung lesion score (D56) and log copies M. hyopneumoniae DNA determined with qPCR on bronchoalveolar lavage (BAL) fluid (D42, D56). All formulations were able to reduce clinical symptoms, lung lesions and the M. hyopneumoniae DNA load in the lung, with formulation SWE_TLR being the most effective (RDSD28–D56 −61.90%, macroscopic lung lesions −88.38%, M. hyopneumoniae DNA load in BAL fluid (D42) −67.28%). Further experiments raised under field conditions are needed to confirm these results and to assess the effect of the vaccines on performance parameters

ECOLIVE: Training for the Production of Organic Olive Oil

The Book is a training manual on organic olive and olive oil production released through the ERASMUS+ Project (2015-1-TR01-KA202-022526) funded by the EU between 01.09.2015 and 31.08.2018. The Project is coordinated by İzmir ABİGEM (Turkey) with partnership MAKRO Consultancy(Turkey), Action Synergy (Greece), Kefalonia and Ithaca Agricultural Cooperative (EASKI/Greece), SVIMED ONLUS (Italy) and G.G. Eurosuccess Consulting Ltd. (South Cyprus)

Evaluation of disc degeneration adjacent to AOspine A fractures: pre- and post-operative MRI analysis

Introduction: The management of type A thoracolumbar fractures varies from conservative treatment to multiple level fusion. Indeed, although Magerl defined the type A fracture as a strictly bone injury, several authors suggested associated disc lesions or degeneration after trauma. However, the preservation of mobility of the adjacent discs should be a major issue. This study was conducted to analyze the presence of immediate post-traumatic disc injuries and to know if discs degenerate after receiving treatment. Methods: We retrospectively reviewed the files of 27 patients with an AOspine A fracture, corresponding to 34 fractures (64 discs) with pre and post-operative MRI (mean follow-up: 32.4 months). Based on Pfirrmann’s and Oner’s classifications of disc injuries, two observers analyzed independently the type of lesion in the discs adjacent to the fractured vertebra in immediate post-trauma and at the last follow-up. Results: The immediate post-traumatic analysis according to Pfirrmann’s classification found 97% of the cranial adjacent discs and 100% of the caudal discs classified Pfirrmann 3 or less. The analysis on the secondary MRI revealed that 78% of cranial adjacent discs and 88% of caudal adjacent discs still were classified Pfirrmann 3 or less. Conclusions: Since, the great majority of type A fractures does not cause immediate disc injuries, these fractures are, as described by Magerl, strictly bony injuries. The quality of the body reduction seems to prevent secondary degeneration. These results may encourage surgeons not to perform arthrodesis on type A fractures even for A3 and A4

Pulmonary mesenchymal stem cells are engaged in distinct steps of host response to respiratory syncytial virus infection

International audienceLung-resident (LR) mesenchymal stem and stromal cells (MSCs) are key elements of the alveolar niche and fundamental regulators of homeostasis and regeneration. We interrogated their function during virus-induced lung injury using the highly prevalent respiratory syncytial virus (RSV) which causes severe outcomes in infants. We applied complementary approaches with primary pediatric LR-MSCs and a state-of-the-art model of human RSV infection in lamb. Remarkably, RSV-infection of pediatric LR-MSCs led to a robust activation, characterized by a strong antiviral and pro-inflammatory phenotype combined with mediators related to T cell function. In line with this, following in vivo infection, RSV invades and activates LR-MSCs, resulting in the expansion of the pulmonary MSC pool. Moreover, the global transcriptional response of LR-MSCs appears to follow RSV disease, switching from an early antiviral signature to repair mechanisms including differentiation, tissue remodeling, and angiogenesis. These findings demonstrate the involvement of LR-MSCs during virus-mediated acute lung injury and may have therapeutic implications

Pulmonary mesenchymal stem cells are engaged in distinct steps of host response to respiratory syncytial virus infection

Lung-resident (LR) mesenchymal stem and stromal cells (MSCs) are key elements of the alveolar niche and fundamental regulators of homeostasis and regeneration. We interrogated their function during virus-induced lung injury using the highly prevalent respiratory syncytial virus (RSV) which causes severe outcomes in infants. We applied complementary approaches with primary pediatric LR-MSCs and a state-of-the-art model of human RSV infection in lamb. Remarkably, RSV-infection of pediatric LR-MSCs led to a robust activation, characterized by a strong antiviral and pro-inflammatory phenotype combined with mediators related to T cell function. In line with this, following in vivo infection, RSV invades and activates LR-MSCs, resulting in the expansion of the pulmonary MSC pool. Moreover, the global transcriptional response of LR-MSCs appears to follow RSV disease, switching from an early antiviral signature to repair mechanisms including differentiation, tissue remodeling, and angiogenesis. These findings demonstrate the involvement of LR-MSCs during virus-mediated acute lung injury and may have therapeutic implications