Aeromonas salmonicida induced immune gene expression in Aloe vera fed steelhead trout, Oncorhynchus mykiss (Walbaum)

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Interferon-gamma production by human neutrophils upon stimulation by IL-12, IL-15 and IL-18 and challenge with Paracoccidioides brasiliensis

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Mannose-binding lectin gene polymorphism and risk factors for cardiovascular disease in postmenopausal women

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Mycetoma caused by Nocardia brasiliensis in an immunocompetent patient

Dendritic cells play a central role in the regulation of immunological reactivity. The existence of functionally specialized populations of dendritic cells in the skin is a consequence of qualitatively different attacks on our organism. slanDCs are human inflammatory dendritic cells that are characterized by the specific expression of the carbohydrate 6-sulfo LacNAc (slan). After phenotypic maturation, slanDCs are capable of producing very high amounts of proinflammatory mediators such as IL-12, TNF-, IL-1 and IL-23. Recent data describe a potential role of slanDCs in a number of different diseases like psoriasis, lupus erythematosus, and tumors, thus opening up new areas of research on their respective pathogenesis. Furthermore, a slanDC-specific targeting system has been developed as a basis for direct therapeutic manipulation. Future challenges of slanDC research include deepening our understanding of the significance of slanDCs in the regulation of adaptive and innate immune responses, as well as translating this knowledge into therapeutic options.

Compartmentalized gene expression of toll-like receptors 2, 4 and 9 in the brain and peripheral lymphoid organs during canine visceral leishmaniasis

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Expression of Protease Activated Receptor-1 in Chronic Periodontitis

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Cord blood cytokine levels in focal early-onset neonatal infection after preterm premature rupture of membranes

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Um Modelo Espacial para a Resposta Imunológica Adaptativa da Hepatite B

This paper proposed a two-dimensional spatial model to describe the adaptive immune response for viral hepatitis B. This model considered six populations: healthy hepatocytes T, infected hepatocytes Y , hepatitis B virus V , innate immune system I, active immune system X and memory cells, X. First, a compartmental model was constructed and its equilibrium solutions and also the threshold values related to the stability of each solution were obtained. Using this model, we was able to reproduce the different trends observed for the disease, which are: individuals that eliminate the infection without forming immune response, patients with acute and chronic carriers. By including dispersion of defense cells of the immune system and virus (spatial model), we analyze two situations: homogeneous model, in which the model parameters are the same at all points of the network, and heterogeneous model, which characterizes cells more permeable and less permeable to virus invasion. For the two spatial models (homogeneous and heterogeneous) the times relatead to the viral erradication and/or virus invasion and persistence becoming smaller in relation to the compartmental model. The results also showed that for the set of values used in the simulations and if the two diffusion rates are different from zero, the model is sensitive to variations in the rate of viral spread and not dependent on the dispersion of memory cells. Finally, the heterogeneous model when compared to the homogeneous model shows that the infection can be spatially limited depending on the type of the cell involved in the infection process

Novos peptídeos sintéticos e estudo da interação com membranas modelo: efeito de modificações no N-terminal na atividade lítica e antimicrobiana

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Imunidade inata, patogênese e diagnóstico de salmonelose, brucelose e leishmaniose

This work provides a systematic and critical review of part of the scientific production of its author. It includes three research topics, namely salmonellosis, brucellosis, and leishmaniasis. Each one of these topics is discussed in individual chapters. Most of the data discussed here refers to pathology, pathogenesis, hostpathogen interactions, innate immunity, and diagnosis of these diseases. Instead of being organized as a traditional literature reviews, the chapters actually emphasize the scientific contribution of the author’s publications in each of these fields.

Resposta imune inata em sistema nervoso central de camundongos experimentalmente infectados com amostras de vírus rábico isoladas de diferentes espécies

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

RANKL expression is differentially modulated by TLR2 and TLR4 signaling in fibroblasts and osteoblasts

Resident, non-immune cells express various pattern-recognition receptors and produce inflammatory cytokines in response to microbial antigens, during the innate immune response. Alveolar bone resorption is the hallmark of destructive periodontitis and it is caused by the host response to bacteria and their mediators present on the biofilm. The balance between the expression levels of receptor activator of nuclear factorkappa B ligand (RANKL) and osteoprotegerin (OPG) is pivotal for osteoclast differentiation and activity and has been implicated in the progression of bone loss in periodontitis. To assess the contribution of resident cells to the bone resorption mediated by innate immune signaling, we stimulated fibroblasts and osteoblastic cells with LPS from. Escherichia coli (TLR4 agonist), Porphyromonas gingivalis (TLR2 and -4 agonist), and interleukin-1 beta (as a control for cytokine signaling through Toll/IL-1receptor domain) in time-response experiments. Expression of RANKL and OPG mRNA was studied by RT-PCR, whereas the production of RANKL protein and the activation of p38 MAPK and NF-kB signaling pathways were analyzed by western blot. We used biochemical inhibitors to assess the relative contribution of p38 MAPK and NF-kB signaling to the expression of RANKL and OPG induced by TLR2, -4 and IL1β in these cells. Both p38 MAPK and NFkB pathways were activated by these stimuli in fibroblasts and osteoblasts, but the kinetics of this activation varied in each cell type and with the nature of the stimulation. E. coli LPS was a stronger inducer of RANKL mRNA in fibroblasts, whereas LPS from P. gingivalis downregulated RANKL mRNA in periodontal ligament cells but increased its expression in osteoblasts. IL-1β induced RANKL in both cell types and without a marked effect on OPG expression. p38 MAPK was more relevant than NF-kB for the expression of RANKL and OPG in these cell types.