Bronquite infecciosa (BI) é causada por um vírus que afeta o sistema respiratório de aves comerciais e de vida livre, ocasionando grandes perdas econômicas na indústria avícola no mundo. O presente estudo objetivou avaliar a presença de anticorpos contra o vírus da bronquite infecciosa (VBI), em galpões de frangos de corte nunca vacinados. Um total de 1000 amostras de soro foram coletados de duas regiões (R1 considerada associada à indústria e R2 considerada independente). A quantificação dos anticorpos contra VBI foi realizada pelo kit comercial de ELISA indireto. Positividade de anticorpos para VBI foi observada em 34% das amostras, com valores altos na R1 (41.51%) e R2 (52,63%). Este estudo demonstrou o risco de não vacinar para o VBI, uma vez que o VBI afeta a produção e a susceptibilidade dos galpões à infecção pelo VBI.

Apoptosis, a programmed suicidal cell death characterized by chromatin condensation, DNA fragmentation, membrane blebbing, and cell shrinkage, can be induced through intrinsic and extrinsic pathways (Best 2008). In the mitochondriamediated pathway, mitochondria release several apoptotic factors, including cytochrome c, Smac/Diablo, and apoptosisinducing factor (AIF) into the cytosol (Scott 2010). In addition, mitochondrial apoptotic signaling and mitochondrial-outermembrane permeabilization (MOMP) are controlled by the B-cell lymphoma 2 (BCL-2) family of proteins (Castanier and Arnoult 2011). The anti-apoptotic BCL-2 family proteins, such as BCL-2, BCL-w, BCL-xl, and myeloid cell leukemia 1 (MCL1), are generally aggregated into the outer mitochondrial membrane. Under death stimuli, Bax, another member of the BCL-2 family, displays a pro-apoptotic effect (Schwartzman and Cidlowski 1993; Moore and Ting 2008; Castanier and Arnoult 2011). Mammalian DNA and RNA viruses are among the stimuli that have been associated with cell apoptosis. Viruses possess various biochemical and genetic mechanisms to evade and/or induce apoptosis modulation through virus-encoded proteins (Ohata and Nishiyama 2011; Tiede et al 2011; West et al 2011).Caspases are a family of cysteine proteases that mediate apoptosis induced by various stimuli (Tiede et al 2011). Based on their structures and order in cell death pathways, caspases can be divided into initiators (such as caspase-2, -8, -9, -10, and -12) and effectors (such as caspase-3, -6, and -7). The intrinsic and extrinsic death pathways of caspase-dependent apoptosis have been identified in most cases (Best 2008). From the host's point of view, the death of the pathogen-infected cells may be required to kill the intracellular pathogens and reduce or eliminate the production of viable pathogenic organisms (Best 2008).The role of host cell apoptosis and the underlying molecular processes differ among pathogens, reflecting the diversity of the pathogenic mechanisms involved in a given type of infection (Paroli et al 2000). Inhibitors of apoptosis proteins (IAPs) are a family of proteins that interfere with the activation of caspases by various mechanisms (Altieri 2006). Increased expression of various IAPs has been reported in several types of cancer. It is thought to contribute to the phenomenon of resistance to Abstract Canine distemper virus (CDV) has been described to induce apoptosis in lymphoid tissues, lymphoid cells, and the cerebellum of naturally infected dogs. The immunosuppression stage established from CDV infection is not always associated with virus detection in damaged cells. Examining the host response at the early stages of immunosuppression, especially the expression of activators and/or inhibitors of apoptosis processes, can provide an important understanding of how the immune responses to CDV are orchestrated. For this purpose, canine peripheral blood mononuclear cells (PBMC) collected from healthy dogs were cultured and infected by the CDV vaccine strain (Onderstepoor...

Canine mammary carcinomas represent an important pathology in small animal clinic, and benign mixed type carcinomas (MC-BMT) are one of the most diagnosed worldwide. The use of chemotherapeutic carboplatin has been one of the new protocols for the treatment of BMT. In this respect, three-dimensional cell culture (3D) represents an alternative in the evaluation of drugs by simulating what occurs in vivo. The present study aimed to verify the effect of carboplatin on 3D culture of cells derived from TMB, in addition to possible changes in cell viability, ballpoint size, apoptosis and Bcl-2/Bax ratio. For this, tumours samples were collected during mastectomy surgery procedure in private veterinary clinics, which were submitted to in vitro culture and part to histopathological analysis. After 28 days of 3D culture, spheroids were documented in both groups (treated and control) and sizes and morphology were compared. The carboplatin interfered in the cell viability by affecting their division and promoting apoptotic events. In the treated group, a higher transcription of Bax and caspase 3 was observed, in addition to low levels of caspases 2, 8 and 9, which was not observed in the control group. We thus suggest that mitochondrial dysfunction plays a critical role in cancer progression and that targeting mitochondrial alterations and mitochondrial retrograde signalling might be a promising strategy for the development of selective anticancer therapy. Thus, it was possible to demonstrate that the results achieved may contribute to the establishment of a new chemotherapy therapy in female dogs with MC-BMT.

Emerging coronavirus infections are a major threat to global public health. In this respect, a novel recombination of canine coronavirus (CCoV) and feline coronavirus (FCoV) was described among human biological samples, giving rise to a potential zoonosis. Despite all efforts, the host‒virus immune response related to CCoV is missing. In this study, pantropic CCoV infection of canine macrophages derived from peripheral blood monocytes was performed. After infection, macrophages were first polarized to the M1 and/or M2 phenotype. Moreover, infection kinetics, cell viability, apoptosis, mitochondrial dysfunction associated with reactive oxygen species and oxide nitric production were measured. Our results demonstrated that virus infection mainly polarized host macrophages to the classically activated (M1) phenotype, as demonstrated by amoeboid morphology with numerous fibrillary cytoplasmic processes followed by classical phenotypes. Viral infection released new particles at 18 h post-infection associated with a decrease in viable cells. Furthermore, upon CCoV infection, M1 cells exhibited reduced phagocytosis properties, as evidenced by a neutral red uptake assay. This in vitro method open an avenue for further studies on host-virus interaction.

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