Imunologia

Perinatal undernutrition may lead to important metabolic adaptations in adult life, short stature being the most visible. The present study aimed to evaluate the association between stature and total energy expenditure of low-income women. Women aged 19-45 years from low-income communities in Maceió-AL were recruited. A sample of 67 volunteers was selected and divided into either short stature (≤152.4 cm; n = 34) or non-short stature (≥158.7 cm; n = 33) group. Data on socioeconomic status, anthropometric variables, and hormonal profiles was collected. Total energy expenditure and body composition were assessed by the doubly labeled water technique with multiple points over 14 days. In addition, physical activity levels were measured with triaxial accelerometers and dietary intake data were collected using three 24-hour food records. The mean subject age was 30.94 years. Women of short stature had lower body weight and lean body mass compared to non-short women, but there were no dif...

The present study aimed to investigate the possible changes in anthropometric and biochemical parameters in low-income women living in the outskirts of Maceió (northeast Brazil), and to explore the possible role of dietary intake and physical activity in these changes. A prospective longitudinal study was conducted in a cohort of mothers of malnourished children who attended the Center for Nutritional Recovery and Education, an outreach programme of the Federal University of Alagoas. Socio-economic, anthropometric, biochemical and dietary intake data were assessed at baseline and after a follow-up period of 4 years. Energy expenditure (using doubly labelled water) and physical activity (using triaxial accelerometers) were assessed only in a subgroup of women after 4 years. A total of eighty-five women were assessed. Participants showed an altered biochemical profile, increased systolic blood pressure, decreased thyroid hormone levels, and body-weight gain. However, dietary intakes of the participants did not include large quantities of highly processed and high-glycaemic index foods. The energy intake of the participants did not differ from their total energy expenditure (7990·3 (7173·7 -8806·8) v. 8798·1 (8169·0-9432·4) kJ, respectively; P¼ 0·084). Multivariate analyses showed a significant effect of time spent watching television (b ¼ 0·639 (0·003 to 1·275); P¼ 0·048) and dietary diversity score (b ¼ 21·039 (2 2·010 to 2 0·067); P¼ 0·036) on weight gain. The present study indicates that poor women, who are mothers of malnourished children and have a reasonably balanced dietary intake, exhibit weight gain and are at risk of developing chronic diseases.

One-third of all Trypanosoma cruzi-infected patients eventually develop chronic Chagas' disease cardiomyopathy (CCC), a particularly lethal inflammatory dilated cardiomyopathy, where parasites are scarce and heart-infiltrating mononuclear cells seem to be the effectors of tissue damage. Since T. cruzi is a major inducer of interleukin-12 production, the role of inflammatory cytokines in the pathogenesis of CCC was investigated. We assayed cytokine production by peripheral blood mononuclear cells (PBMC) from CCC and asymptomatic T. cruzi-infected (ASY) individuals, as well as by T cell lines from endomyocardial biopsies from CCC patients. PBMC from CCC and ASY patients produced higher IFN-levels than normal (N) individuals in response to B13 protein and phytohaemagglutinin PHA; IFN-high responders (≥1 ng/ml) were 2-3 fold more frequent among CCC patients than ASY individuals. Conversely, IL-4 production in response to the same stimuli was suppressed among T. cruzi-infected patients. The frequency of PHA-induced IFNproducing cells on PBMC was significantly higher among CCC than ASY and N individuals. IFN-and TNF-were produced by ten out of ten PHAstimulated T cell lines from CCC patients; IL-2 and IL-10 were produced by four out of ten and one out of ten lines, respectively; IL-4, IL-1 , IL-1 , IL-6 and IL-12 were undetectable. Our results suggest that CCC and ASY patients may respond differentially to the IFN--inducing stimulus provided by T. cruzi infection. Given the T 1 -type cytokine profile of heart-infiltrating T cell lines from CCC patients, the ability to mount a vigorous IFN-response may play a role on the differential susceptibility to CCC development.

Randomly amplified polymorphic DNA (RAPD) analysis of 35 Paracoccidioides brasiliensis isolates was carried out to evaluate the correlation of RAPD profiles with the virulence degree or the type of the clinical manifestations of human paracoccidioidomycosis. The dendrogram presented two main groups sharing 64% genetic similarity. Group A included two isolates from patients with chronic paracoccidioidomycosis ; group B comprised the following isolates showing 65% similarity: two non-virulent, six attenuated, five virulent, eight from patients with chronic paracoccidioidomycosis and two from patients with acute paracoccidioidomycosis. The virulent Pb18 isolate and six attenuated or non-virulent samples derived from it were genetically indistinguishable (100% of similarity). Thus, in our study, RAPD patterns could not discriminate among 35 P. brasiliensis isolates according to their differences either in the degree of virulence or in the type of the clinical manifestation of this fungal infection. ß

Host resistance to paracoccidiodomycosis, the main deep mycosis in Latin America, is mainly due to cellular immunity and gamma interferon (IFN-␥) production. To assess the role of interleukin-4 (IL-4), a Th2-inducing cytokine, pulmonary paracoccidioidomycosis was studied in IL-4-deficient (IL-4 ؊/؊ ) and wild-type (WT) C57BL/6 mice at the innate and acquired phases of immune response. Forty-eight hours after infection, equivalent numbers of viable Paracoccidioides brasiliensis yeast cells were recovered from the lungs of IL-4 ؊/؊ and WT mice intratracheally infected with one million fungal cells. Alveolar macrophages from infected IL-4 ؊/؊ mice controlled in vitro fungal growth more efficiently than macrophages from WT mice and secreted higher levels of nitric oxide. Compared with WT mice, IL-4 ؊/؊ animals presented increased levels of pulmonary IFN-␥ and augmented polymorphonuclear leukocyte influx to the lungs. Decreased pulmonary fungal loads were characterized in deficient mice at week 2 postinfection, concomitant with diminished presence of IL-10. At week 8, lower numbers of yeasts were recovered from lungs and liver of IL-4 ؊/؊ mice associated with increased production of IFN-␥ but impaired synthesis of IL-5 and IL-10. However, a clear shift to a Th1 pattern was not characterized, since IL-4 ؊/؊ mice did not alter delayed-type hypersensitivity anergy or IL-2 levels. In addition, IL-4 deficiency resulted in significantly reduced levels of pulmonary IL-12, granulocyte-macrophage colony-stimulating factor, IL-3, monocyte chemotactic protein 1, and specific antibody isotypes. In IL-4 ؊/؊ mice, well-organized granulomas restraining fungal cells replaced the more extensive lesions containing high numbers of fungi and inflammatory leukocytes developed by IL-4-sufficient mice. These results clearly showed that genetically determined deficiency of IL-4 can exert a protective role in pulmonary paracoccidioidomycosis.

To compare the sequential evolution of lesions developed by resistant (A/Sn) and susceptible (B10.A) mice to Paracoccidioides brasiliensis infection we inoculated a virulent isolate of the fungus and collected the pancreas/peripancreatic omentum monthly (from 1 to 6 months) post infection. After ®xation, tissue sections were stained by conventional methods for light microscopy to investigate the cellular composition, the extracellular matrix (ECM) patterns and the morphology of the yeasts in the lesions. In both strains, the fungal lesions were localized mostly in the omentum; a few lesions in the pancreatic parenchyma were observed, mostly in B10.A mice. In both strains, macrophages and plasmocytes were the predominant cells in all lesions, followed by neutrophils (PMN) and macrophages transformed into giant and epithelioid cells. Remarkable dierences were observed between resistant and susceptible mice, specially related to the ECM structure of the granulomatous lesions. In A/Sn mice, from the 1st month on, the coexistence of two types of lesions was observed: one type showed a well-de®ned encapsulated nodule, constituted mainly of type I collagen. Neutrophils were abundant in areas of massive fungal destruction and few viable yeasts were observed. The other type showed residual characteristics, with sparse collagen deposits and presence of xantomatous-like macrophages, containing degenerated fungi. Such residual lesions predominated after the 2nd month and were the only type observed from the 4th month on, indicating the control of the infection. In B10.A mice, on the contrary, only one type of lesion was observed, showing less tendency to encapsulation and the formation of multiple small granulomatous foci, individualized by reticular type III collagen ®bers. There were many plasmocytes in the periphery and large numbers of budding yeasts, with no evidence of fungal destruction. In the course of the infection the lesions progressively increased in number and size. Altogether, the comparative histopathological analysis demonstrates the in¯uence of the genetic pattern of the host on the lesions developed by resistant and susceptible mice to P. brasiliensis infection.