A paracoccidioidomicose (PCM), infecção sistêmica causada pelo fungo Paracoccidioides brasiliensis, é considerada a mais importante micose profunda da América Latina 48 . Pode ser considerada, ainda, um problema de saúde pública em função de seus elevados custos sociais e econômicos decorrentes não apenas Paracoccidioidomicose com comprometimento do sistema nervoso central: revisão sistemática da literatura ABSTRAcTThis study is the first systematic review of cases of neuroparacoccidioidomycosis available in the literature. Through searches in the MEDLINE and LILACS databases, 257 cases were found in 81 published studies, mainly after the 1970s-1980s. Approximately 93% of the patients were men, especially farm laborers, with a mean age of 43 years. The characteristic symptoms were motor deficits or intracranial hypertension. The chronic pseudotumoral form predominated. The mean period of evolution was 4.9 months. The lesions were mainly supratentorial (66.8%), located in the frontal and parietal lobes. The diagnosis was determined by biopsy in 57.2% of the cases and neuroimaging methods were used in 64.6% of them. A large proportion of the cases were associated with the pulmonary form of the disease (59.1%). The mortality rate was 44.1%, and 50.1% of the survivors developed sequelae, especially motor impairment. Thus, neuroparacoccidioidomycosis should be considered in the differential diagnosis for expansive and meningoencephalitic processes in the central nervous system, in order to establish early treatment and to avoid disabling sequelae. Key-words:Paracoccidioidomycosis. Fungal infection. Neuroparacoccidioidomycosis. Central nervous system. Systematic review.da doença em atividade, mas também das freqüentes seqüelas, motivo comum de incapacitação para o trabalho 15 49 . Afeta indivíduos em todas as faixas etárias a partir dos dois anos de idade, mas há marcante predomínio entre os 30 e os 50 anos de vida, período que compreende o auge da capacidade produtiva dos pacientes. A incidência é a mesma para ambos os sexos até a puberdade, entretanto, na vida adulta, torna-se mais freqüente entre os indivíduos do sexo masculino, em proporção de 11:1 22 .A doença pode manifestar-se de inúmeras maneiras e o fungo pode causar lesões em virtualmente qualquer órgão. De modo geral, os pulmões são os órgãos mais frequentemente acometidos, mas lesões cutâneas, de mucosas, linfonodais e adrenais também são comuns. Nas últimas décadas, com o surgimento de novos métodos diagnósticos, especialmente os de imagem, constatou-se que o envolvimento do sistema nervoso central (SNC) é bem mais frequente do que se admitia, ocorrendo em torno de 12,5% dos casos de PCM e chegando, em alguns estudos, até 36% dos casos 62 .

Cerebral malaria (CM) is a severe complication resulting from Plasmodium falciparum infection. The underlying mechanisms of CM pathogenesis remain incompletely understood. The imbalance between the release of proinflammatory and anti-inflammatory cytokines has been associated with central nervous system dysfunction found in human and experimental CM. The current study investigated anxiety-like behavior, histopathological changes and release of brain cytokines in C57BL/6 mice infected with Plasmodium berghei strain ANKA (PbA). Anxiety-like behavior was assessed in control and PbA-infected mice using the elevated plus maze test. Histopathological changes in brain tissue were assessed by haematoxylin and eosin staining. Brain concentration of the cytokines IL-1β, IL-4, IL-10, TNF-α and IFN-γ was determined by ELISA. We found that PbA-infected mice on day 5 post-infection presented anxiety symptoms, histopathological alterations in the brainstem, cerebrum and hippocampus and increased cerebral levels of proinflammatory cytokines IL-1β and TNF-α. These findings suggest an involvement of central nervous system inflammatory mediators in anxiety symptoms found in CM.

Phosphatidylinositol-3-kinase gamma (PI3Kgamma) plays an important role in the motility of leukocytes in several models of inflammation. In this work, the role of PI3Kgamma in experimental autoimmune encephalomyelitis (EAE) was investigated. EAE was induced in wild-type and PI3Kgamma deficient mice (PI3Kgamma(-)(/)(-)). WT animals had a peak of clinical symptoms around day 14 post-induction (p.i.). PI3Kgamma(-)(/)(-) animals developed milder EAE signs and peak of disease was noticed only on day 21 p.i. Better clinical outcome correlated with the absence of perivascular cuffs on day 14 p.i. and with decreased levels of CCL2 and CCL5 in brain of PI3Kgamma(-)(/)(-) mice. There was increased leukocyte rolling and adhesion in pial vessels, as assessed by intravital microscopy, at day 14 after EAE induction in WT mice. The latter parameters were unaltered in PI3Kgamma(-)(/)(-) mice subjected to EAE. Moreover, the PI3Kgamma inhibitor AS-605240 given just before the intravital microscopy failed to affect leukocyte rolling or adhesion. Finally, there was a significant increase in the number of apoptotic cells in the CNS of EAE-induced PI3Kgamma(-/-) mice. Our results suggest that PI3Kgamma is involved in EAE and plays a more important role in mediating leukocyte survival than leukocyte adhesion in this experimental model of multiple sclerosis.

Objective: Neuroinflammatory processes seem to contribute to the degeneration of dopaminergic neurons in Parkinson’s disease (PD). Chemokines play a role in the pathogenesis of inflammatory diseases, acting mainly as mediators of leukocyte recruitment to inflammatory sites. The aim of the present study was to compare the serum levels of chemokines between healthy subjects and PD patients and to correlate these levels with the severity of PD. Methods: We used ELISA to measure the levels of CCL3, CCL11, CCL24, CXCL8 and CXCL10 chemokines in the serum of PD patients (n = 47) and age- and gender-matched controls (n = 23). Patients were also clinically evaluated with the Unified Parkinson’s Disease Rating Scale, the Modified Hoehn and Yahr Staging Scale and the Modified Schwab and England Activities of Daily Living Scale. Results: There was no significant difference in serum levels of chemokines between controls and PD patients. There was no correlation between the serum levels of chemokines and the clinical measures of disease severity. Conclusions: These findings suggest that serum levels of chemokines may not be considered as potential biomarkers of PD.

No abstract