Increased production of B-cell-derived IL-10 and of neurotrophic factors are part of the parasite's regulation of host immunity and can alter the course of MS, potentially explaining environmental-related MS suppression observed in areas with low disease prevalence.

The concept of central nervous system (CNS) inflammation has evolved over the last decades. Neuroinflammation is the response of reactive CNS components to altered homeostasis, regardless of the cause to be endogenous or exogenous. Neurological diseases, whether traumatic, neoplastic, ischemic, metabolic, toxic, infectious, autoimmune, developmental, or degenerative, involve direct and indirect immune-related neuroinflammation. Brain infiltrates of the innate and adaptive immune system cells appear in response to an infective or otherwise noxious agent and produce inflammatory mediators. Mediators of inflammation include local and recruited cells and signals. Processes derived from extrinsic and intrinsic CNS diseases also elicit the CNS inflammatory response. A deeper understanding of immune-related inflammation in health and disease is necessary to find potential therapeutic targets for preventing or reducing CNS damage. This review is aimed at discussing the innate and adaptive immune system functions and their roles in regulating brain cell responses in disease and homeostasis maintenance.

No abstract

The economic and social burden associated with Chagas disease morbidity and mortality is regrettably large in Latin America causing more deaths than does any other parasitic disease. Inflammatory dilated cardiomyopathy is, by far, the most important clinical consequence of Trypanosoma cruzi infection. The insidious persistence of this parasite determines chronic myocarditis progression. The clinical outcome is multifactorial and depends on the particular parasite strain and virulence factors, the infective load and route of infection, the parasite ability to by-pass the protective immune response, the intensity and type of immune response during the acute infective phase, and the host genetic background. From the immunological viewpoint, host control of T. cruzi has been shown to depend on both humoral and cell-mediated adaptive responses and from the innate immune system. In this review, we discuss the most relevant literature conveying information on the relevance of identifying a subset of systemic inflammatory molecules as potential markers of cardiovascular risk morbidity and mortality in patients with Chagas disease. Concurrently, a direct role for the parasite in the perpetuation of myocardial inflammation is substantiated. Ultimately, host-parasite interactions determine the course of the ongoing systemic inflammation and the perpetuation of myocardial inflammation in genetically predisposed patients.

Introduction: Argentina has been a preferential target for Bolivian immigrants for decades. The relatively recent migratory flux includes Germany, France, the United States, Australia, Japan, and some Latin American countries. The aim of this cross-sectional study was to describe the prevalence of Chagas disease in pregnant women, analyzing the Bolivian-specific Chagas prevalence as the main contributor of migratory populations from Chagas disease-endemic areas to Buenos Aires city, Argentina, and to evaluate the impact of these migrant influxes on the process of the "urbanization" of the disease in reference hospital José Maria Ramos Mejia (JMRM). Methodology: Overall, 21,332 pregnant women (100%) between 15 and 49 years of age derived from the public maternity service of JMRMH were studied. Serology data was obtained from registered serological diagnosis data, consisting of three different serological tests performed at the Public Parasitology Unit. Results: Although general prevalence decreased during the analyzed period, the specific prevalence of pregnant women from Bolivian origin showed a sustained growth during 1983-2013. Solely 5% of the total pregnant women population from Bolivia contributed to one third of the total Chagas prevalence. Conclusions: This study showed that a cohort of pregnant women from Bolivia who attended JMRMH during the period 1983-2007 constituted a population at risk for congenital transmission. Increased migration from endemic areas of Bolivia might potentially increase the prevalence of Chagas disease among pregnant women. In addition, this study highlights the importance to analyze specific prevalence according to endemic areas to determine the profiles of potential hidden prevalence.