598 resultados para Granuloma Anular


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São apresentados dados histológicos das glândulas com secreção urtificante da largata de Automeris incisa: 1. A célula glandular é a célula tricogênea da cerda inoculante. 2. O núcleo demonstra o polimorfismo típico para glândulas com células grandes em insetos; êle ramifica-se em forma de tubos chegando até as partes apicais da célula. 3. São apresentadas modificações citológicas durante as fases da secreção. 4. As estruturas da cutícula correspondem diretamente a função do órgão urtificante. 5. A cerda, que dá a picada é uma cerda verdadeira com inserção modificada. Não possui um lugar predestinado para quebrar durante a picada. 6. Uma zona de articulação na base dos ramos laterais froma, junto com uma placa anular perfurada e com uma massa esponjosa de fechamento formada pela endocutícula, uma válvula impedindo um refluxo do líquido do ramo. Por isso, durante a picada a peçonha pode sair da cerda. 7. Além de ramos laterais com cerdas encontram-se outros com pêlos finos. Provávelmente os últimos espalham a peçonha em cima da pele, enquanto que os primeiros inoculam-na no tecido do inimigo.

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O autor descreve a glândula odorífera, situada no abdômen do macho de Agylla argentea, do ponto de vista anatômico e histológico. A glândula encontra-se no fundo da cãmara genital de uma grande área glandular da hipoderme de um pincel irradiador. Cada célular possui uma comprida cerda odorífera. O aparêlho copulador é aberto por meio de um acréscimo da pressão no interior da cavidade abdominal. Atrás da parte ventral da câmara genital está situado um grande saco traqueal, que em virtude da pressão aumentada, se enche de ar e se dilata para trás, de modo que a região ventral da câmara genital é expulsa, formando um tubo que se projeta ao ar livre. Êste movimento é facilitado por uma grande dobra anular da parede membranosa da câmara genital. Pela mesma pressão um "corpo piriforme", situado na cavidade genital e possuindo uma cutícula elástica, é dilatado e deformado, dando, em seguida, ao tubo citado a sua forma. Encontramos na extremidade do tubo a glândula e o pincel irradiador, cujas cerdas estão divergindo. O retôrno para o estado de repouso verifica-se como processo automático que se inicia quando a pressão interna diminui e o corpo piriforme volta à sua forma original. É muito provável que a secreção da glândula da asa do macho, já descrita em outro trabalho, evite a reação de fuga da fêmea, enquanto a glândula abdominal estimula a fêmea para a própria cópula.

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While genetic polymorphisms play a paramount role in tuberculosis (TB), less is known about their contribution to the severity of diseases caused by other intracellular bacteria and fastidious microorganisms. We searched electronic databases for observational studies reporting on host factors and genetic predisposition to infections caused by intracellular fastidious bacteria published up to 30 May 2014. The contribution of genetic polymorphisms was documented for TB. This includes genetic defects in the mononuclear phagocyte/T helper cell type 1 (Th1) pathway contributing to disseminated TB disease in children and genome-wide linkage analysis (GWAS) in reactivated pulmonary TB in adults. Similarly, experimental studies supported the role of host genetic factors in the clinical presentation of illnesses resulting from other fastidious intracellular bacteria. These include IL-6 -174G/C or low mannose-binding (MBL) polymorphisms, which are incriminated in chronic pulmonary conditions triggered by C. pneumoniae, type 2-like cytokine secretion polymorphisms, which are correlated with various clinical patterns of M. pneumoniae infections, and genetic variation in the NOD2 gene, which is an indicator of tubal pathology resulting from Chamydia trachomatis infections. Monocyte/macrophage migration and T lymphocyte recruitment defects are corroborated to ineffective granuloma formation observed among patients with chronic Q fever. Similar genetic polymorphisms have also been suggested for infections caused by T. whipplei although not confirmed yet. In conclusion, this review supports the paramount role of genetic factors in clinical presentations and severity of infections caused by intracellular fastidious bacteria. Genetic predisposition should be further explored through such as exome sequencing.

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The hepatic, intestinal and cardiopulmonary lesions produced by Schistosoma mansoni, S. haematobium and S. japonicum in man and experimental animals often bear striking similarities but usually have distinctive features as well. These are often related to parasitologic differences. Thus S. japonicum and S. haematobium lay their eggs in clusters which elicit the formation of large composite granulomas. The worms of these two species also tend to be sedentary, remaining in a single location for prolonged periods, thus producing large focal lesions in the intestines or urinary tract. Worm pairs of these two species also are gregarious and many worm pairs are often found in a single lesion. The size of circumoval granulomas, and the degree of fibrosis, are T cell dependent. The modulation of granuloma size is largely T cell dependent in mice infected with S. mansoni but is mostly regulated by serum factors in S. japonicum infected mice. In spite of these differences in egg laying and immunoregulation both S. mansoni and S. japonicum produce Symmers' fibrosis in the chimpanzee while S. haematobium does not, despite the presence of numerous eggs in the liver.

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Aquest estudi consisteix en l’augment de la resolució en la reconstrucció de la temperatura de l’aigua i l’aire del llac Baikal durant els últims 60.000 anys mitjançant l’ús de les proxies de reconstrucció de la temperatura TEX86 i MAAT, i la d’aportació de matèria orgànica d’origen terrestre, el BIT. L’objectiu general d’aquesta investigació és incrementar la resolució temporal en el mostreig del testimoni CON-01-603-02 per tal de millorar el registre de dades obtingudes i d’aquesta manera poder contrastar la hipòtesi de la interconnexió climàtica global, així com identificar esdeveniments climàtics sobtats, tals com els Heinrich events i els esdeveniments D-O. Un cop obtinguts els resultats s’ha realitzat l’anàlisi de la qualitat i fiabilitat de les dades a les resolucions de 5, 10 i 20 Kanys, i es conclou que existeixen diferències globals estadísticament significatives amb els resultats realitzats per Escala et al., (r.n.p [resultats no publicats]), la resolució dels quals es volia augmentar. S’han tractat d’anular aquestes diferències restant o bé sumant la diferència mitjana obtinguda entre les dues mostres en cada un dels intervals de 5 Kanys en què s’han donat aquestes. Els resultats integrats d’Escala et al.,(r.n.p) i els d’aquest estudi, aporten dades que recolzen l’hipòtesi de la interconnexió climàtica global, ja que al comparar-los amb els registres climàtics de Grenlàndia (GRIP2) i l’Antàrtica (Vostok) mostren respostes similars tant per les forces de Milankovitch com per les de subMilankovitch.

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A geogenic origin has been proposed in the aetiology of non-filarial elephantiasis of the feet and legs, recently renamed podoconiosis. Soil collected in an area of the Ethiopian Rift Valley, the borough of Ocholo, known for its high prevalence of podoconiosis (5.06%), has been submitted to mineral analysis. High values of sulphur (S), cerium (Ce), lanthanum (La) and neodymium (Nd), typical for basaltic bedrocks, were found. Of special interest were the values for zirconium (Zr) and beryllium (Be), 618 +/- 87 ppm and 4.6 +/- 0.5 ppm respectively, twice as high as those recorded for soils sampled in neighbouring areas where the prevalence of podoconiosis is low. To be noted also, a high content in vanadium, above 250 ppm, in half of the soil samples collected in this region. Year-long exposure of unprotected feet to Zr and Be, known for their ability to induce granuloma formation in the lymphoid tissue of man, and present in a clay rich in colloidal silica particle, highly abrasive to skin, is doubtlessly a factor involved in the development of lymph node sclerosis leading to elephantiasis.

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We report a case of superior vena cava syndrome developing progressively over twenty years in a 48-year-old Venezuelan woman. The investigations revealed a locoregional etiology for the vena cava obstruction, namely a granulomatous mediastinitis probably secondary to histoplasmosis. We discuss the etiology, the clinical features, the natural course, and the therapy of chronic mediastinitis.

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In vitro, Toll-like receptors (TLR)2, 4 and 9 as well as NOD-like receptor 2 critically determine macrophage responses to Mycobacterium tuberculosis (Mtb) infection. However, in low-dose experimental murine tuberculosis, single or multiple deficiencies in TLRs 2, 4, 9 or NOD2 have little, if any, impact on early mycobacterial growth containment, granuloma formation and survival. Here, we analyzed the relevance of NALP3, one component of the danger-signaling inflammasome, for (i) Mtb-induced cytokine secretion in vitro and in vivo, (ii) restriction of Mtb replication in infected organs and (iii) granuloma formation. In the absence of functional NALP3, there was no IL-1beta and IL-18 production in Mtb-infected dendritic cells and macrophages in vitro, whereas secretion of IL-1alpha, IL-12p40 and TNF remained unaffected. After three weeks of infection, NALP3-deficient as well as IL-18-deficient mice were as capable as wildtype mice of restricting Mtb loads at a plateau level within well-differentiated granulomas. In conclusion, despite its involvement in cytokine processing, NALP3 is not essential for induction of protective immunity to Mtb.

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A histological, morphometric and immunocytochemical study of schistosomal periovular granulomas in the liver and intestines of mice revealed that intestinal granulomas are smaller and contain less collagen than those in the liver. After curative treatment intestinal granulomas undergo a relatively more rapid resorption, although the general pattern of collagen degradation apparently does not differ from that observed in the liver. Tendency to form scattered, usually isolated granulomas that are only mildly fibrogenic, coupled with a well-balanced process of resorption appear as the explanation why intestinal fibrosis is not an outstanding feature of schistosomiasis as it is in the liver.

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BACKGROUND/AIMS: After treatment with heat-killed Propionibacterium acnes mice show dense hepatic granuloma formation. Such mice develop liver injury in an interleukin (IL)-18-dependent manner after challenge with a sublethal dose LPS. As previously shown, LPS-stimulated Kupffer cells secrete IL-18 depending on caspase-1 and Toll-like receptor (TLR)-4 but independently of its signal adaptor myeloid differentiation factor 88 (MyD88), suggesting importance of another signal adaptor TIR domain-containing adapter inducing IFN-beta (TRIF). Nalp3 inflammasome reportedly controls caspase-1 activation. Here we investigated the roles of MyD88 and TRIF in P. acnes-induced hepatic granuloma formation and LPS-induced caspase-1 activation for IL-18 release. METHODS: Mice were sequentially treated with P. acnes and LPS, and their serum IL-18 levels and liver injuries were determined by ELISA and ALT/AST measurement, respectively. Active caspase-1 in LPS-stimulated Kupffer cells was determined by Western blotting. RESULTS: Macrophage-ablated mice lacked P. acnes-induced hepatic granuloma formation and LPS-induced serum IL-18 elevation and liver injury. Myd88(-/-) Kupffer cells, but not Trif(-/-) cells, exhibited normal caspase-1 activation upon TLR4 engagement in vitro. Myd88(-/-) mice failed to develop hepatic granulomas after P. acnes treatment and liver injury induced by LPS challenge. In contrast, Trif(-/-) mice normally formed the hepatic granulomas, but could not release IL-18 or develop the liver injury. Nalp3(-/-) mice showed the same phenotypes of Trif(-/-) mice. CONCLUSIONS: Propionibacterium acnes treatment MyD88-dependently induced hepatic granuloma formation. Subsequent LPS TRIF-dependently activated caspase-1 via Nalp3 inflammasome and induced IL-18 release, eventually leading to the liver injury.

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Cytokines are important in the cell-mediated response to Schistosoma mansoni eggs. We have found that Th2 cytokine responses (e.G. IL-4 and IL-5) are argumented after egg laying begins while the response (IL-2 and IFN-*) are down regulated in S. mansoni infected mice. Treatment of mice with anti-IL-5 monoclonal antibodies (Mab) suppressed the eosinophil response almost completley but did not affect granuloma size and slightly increased hepatic fibrosis. Anti-IL-4 treatment abolished IgE responses in infected mice and decreased hepatic fibrosis slightly. Anti-IFN-* treatment had no effect on hepatic pathology. Anti-IL-2 treatment decreased granuloma size significantly and decreased hepatic fibrosis markedly. Anti-IL-2 treatment dramatically decreased IL-5 secretion by splenic cells in vitro and decreased peripheral blood and tissue eosinophilia. In contrast IL-4 secretion was unaffected and serum IgE was normal or increased. IL-2 and IFN-* secretion by splenic cells of treated mice were slightly but not significantly increased suggesting that anti-IL-2 treatment affecting Th2 rather than Th1 responses.

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Morbidity in schistosomiasis mansoni occurs primaryly as a result of the complications of hepatic fibrosis. Yet, the pathogenesis of schistosomal hepatic fibrosis is poorly understood. The fact that hepatic egg granuloma is the hallmark of this infection suggests a potential role for granulomatous inflamation in hepatic fibrogenesis. Our studies in a murine schistosomiasis model indicate that hepatic granuloma cells secrete a variety of fibrogenic cytokines that may initiate the scarring process. Among these cytokines, we identified a novel protein that we designated fibroplast stimulating factor-1 (FsF-1). FsF-1 is a lymphokine that can stimulate fibroplast growth and matrix synthesis. A notable feature of hepatic fibrosis in this model is that production of FsF-1 and other granuloma-derived fibrogenic cytokines is down-regulated in chronic infection, an event that may be under immunological control. The spontaneous reduction of FsF-1 secretion presumably accounts for reduced scar formation late in infection of mice. In the context of relevant clinical studies, our findings engender the hypothesis that Symmer's fibrosis may develop in a small suppopulation of individuals as a result of immunogenetically-determined dysregulation of fibrogenic cytokine production.

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The dual function of eosinophils is clearly illustred in schistosomiasis. Well equipped in membrane receptors for immunoglobulins and complement, and due to the presence of granule basic proteins, eosinophils can become cytotoxic for parasite larvae and thus participate to protective immunity. However mediators can also exert their cytolytic effect on normal cells or tissues, inducing therefore pathology. Through ADCC mechanisms against schistosome larvae in vitro involving different antibody isotypes (IgG, IgE and IgA) and also in experiments performed in vivo, eosinophils have been clearly involved in protective immunity. Although no direct evidence of the protective role of eosinophils were brought in humans, the striking association of eosinophil-dependent cytotoxic antibody isotypes with resistance to reinfection (for instance IgE and IgA antibodies), whereas in vitro blocking antibody isotypes (IgG4, IgM) were detected in susceptible subjects, strongly, suggested the participation of eosinophils in antibody-dependent protective immune response. However eosinophils could also participate to granuloma formation around S. mansoni eggs and consequently to the pathological reactions induced by schistosomiasis.

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The functional duality of eosinophils, involved in a protective response or in pathogenesis is illustrated in various parasitic infections. In schistosomiasis, eosinophils have been shown to mediate schistosomula killing, in the presence of antibodies. The association of eosinophil-dependent cytotoxic antibody isotypes with resistance of reinfection (IgE and IgA antibodies), whereas in vitro blocking antibody isotypes (IgG4, IgM) were detected in susceptible subjects, suggested a participation of eosinophils in antibody-dependent protective response. However eosinophils could participate to granuloma formation and consequently to the pathological reactions during schistosomiasis. Activation of eosinophils by antibodies, leading to release of granule proteins have been studied in patients with filariasis. Eosinophil peroxidase, EPO was released safter IgE-dependent activation whereas Eosinophil Cationic Protein, ECP, was released after IgG- and IgA-dependent activation of eosinophils, results suggesting a process of differential release mediators. Interactions between eosinophils and interleukins, and specially IL-5 are discussed. Whereas a receptor for IL-5 has been characterized on human eosinophils, recent studies have shown that eosinophils, expressed the messenger RNA encoding IL-5. These results associated to data showing the synthesis of other cytokines indicate that eosinophils are not only the source of cytotoxic mediators involved in the effector phase of immunity but also of growth and regualtory factors, participating to immunoregulation.

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The hypothesis that granuloma modulation and disease abatement in chronic infection with Schistosoma japonicum could be ascribed to antibody-mediated effects on egg maturation and egg viability, arose from studies performed with mice in the Philippines. This novel hypothesis has not yet been integrated into the schistosomiasis literature despite being formulated more than a decade ago. One reason for this is that the phenomenon might be confined to S. japonicum, even S. japonicum (Philippines).