Molecular characterization of the Corynebacterium pseudotuberculosis hsp60-hsp10 operon, and evaluation of the immune response and protective efficacy induced by hsp60 DNA vaccination in mice

<p>Abstract</p> <p>Background</p> <p>Heat shock proteins (HSPs) are important candidates for the development of vaccines because they are usually able to promote both humoral and cellular immune responses in mammals. We identified and characterized the <it>hsp60-hsp10 </it>bicistronic operon of the animal pathogen <it>Corynebacterium pseudotuberculosis</it>, a Gram-positive bacterium of the class <it>Actinobacteria</it>, which causes caseous lymphadenitis (CLA) in small ruminants.</p> <p>Findings</p> <p>To construct the DNA vaccine, the <it>hsp60 </it>gene of <it>C. pseudotuberculosis </it>was cloned in a mammalian expression vector. BALB/c mice were immunized by intramuscular injection with the recombinant plasmid (pVAX1/<it>hsp60</it>).</p> <p>Conclusion</p> <p>This vaccination induced significant anti-hsp60 IgG, IgG1 and IgG2a isotype production. However, immunization with this DNA vaccine did not confer protective immunity.</p

IL-17 Produced during Trypanosoma cruzi Infection Plays a Central Role in Regulating Parasite-Induced Myocarditis

Chagas disease is caused by the intracellular parasite Trypanosoma cruzi. This infection has been considered one of the most neglected diseases and affects several million people in the Central and South America. Around 30% of the infected patients develop digestive and cardiac forms of the disease. Most patients are diagnosed during the chronic phase, when the treatment is not effective. Here, we showed by the first time that IL-17 is produced during experimental T. cruzi infection and that it plays a significant role in host defense, modulating parasite-induced myocarditis. Applying this analysis to humans could be of great value in unraveling the elements involved in the pathogenesis of chagasic cardiopathy and could be used in the development of alternative therapies to reduce morbidity during the chronic phase of the disease, as well as clinical markers of disease progression. The understanding of these aspects of disease may be helpful in reducing the disability-adjusted life years (DALYs) and costs to the public health service in developing countries

Conventional and molecular cytogenetics of human non-medullary thyroid carcinoma: characterization of eight cell line models and review of the literature on clinical samples

<p>Abstract</p> <p>Background</p> <p>Cell lines are often poorly characterized from a genetic point of view, reducing their usefulness as tumor models. Our purpose was to assess the genetic background of eight commonly used human thyroid carcinoma models and to compare the findings with those reported for primary tumors of the gland.</p> <p>Methods</p> <p>We used chromosome banding analysis and comparative genomic hybridization to profile eight non-medullary thyroid carcinoma cell lines of papillary (TPC-1, FB2, K1 and B-CPAP), follicular (XTC-1) or anaplastic origin (8505C, C643 and HTH74). To assess the representativeness of the findings, we additionally performed a thorough review of cytogenetic (n = 125) and DNA copy number information (n = 270) available in the literature on clinical samples of thyroid carcinoma.</p> <p>Results</p> <p>The detailed characterization of chromosomal markers specific for each cell line revealed two cases of mistaken identities: FB2 was shown to derive from TPC-1 cells, whereas K1 cells have their origin in cell line GLAG-66. All cellular models displayed genomic aberrations of varying complexity, and recurrent gains at 5p, 5q, 8q, and 20q (6/7 cell lines) and losses at 8p, 13q, 18q, and Xp (4/7 cell lines) were seen. Importantly, the genomic profiles were compatible with those of the respective primary tumors, as seen in the meta-analysis of the existing literature data.</p> <p>Conclusion</p> <p>We provide the genomic background of seven independent thyroid carcinoma models representative of the clinical tumors of the corresponding histotypes, and highlight regions of recurrent aberrations that may guide future studies aimed at identifying target genes. Our findings further support the importance of routinely performing cytogenetic studies on cell lines, to detect cross-contamination mishaps such as those identified here.</p

Network analysis of spreading of dengue, Zika and chikungunya in the state of Bahia based on notified, confirmed and discarded cases

Despite successful results of using complex networks to model and characterize the spread of dengue cases, works to date have mainly used data from primarily reported cases, without further consideration whether they were later confirmed or not. On the other hand, a study of the interdependence of confirmed and discarded cases of arboviruses have emphasized that the co-circulation of three arboviruses—dengue, Zika and chikungunya—may have led to false diagnoses due to several similarities in the early symptoms of the three diseases on acute phase. This implies that case notifications of one disease could be confirmed cases of others, and that discarded cases must be taken into account to avoid misinterpretations of the phenomenon. In this work we investigated the consequences of including information from discarded and confirmed cases in the analysis of arbovirus networks. This is done by firstly evaluating the possible changes in the networks after removing the discarded cases from the database of each arbovirus, and secondly by verifying the cross-relationship of the indices of the networks of confirmed and discarded cases of arboviruses. As will be detailed later on, our results reveal changes in the network indices when compared to when only confirmed cases are considered. The magnitudes of the changes are directly proportional to the amount of discarded cases. The results also reveal a strong correlation between the average degree of the networks of discarded cases of dengue and confirmed cases of Zika, but only a moderate correlation between that for networks of discarded cases of dengue and confirmed cases of chikungunya. This finding is compatible with the fact that dengue and Zika diseases are caused by closely related flaviviruses, what is not the case of the chikungunya caused by a togavirus