Chapters authored
Immune System Links Psoriasis-Mediated Inflammation to Cardiovascular Diseases via Traditional and Non-Traditional Cardiovascular Risk Factors
Background. Cutaneous psoriasis and psoriatic arthritis increase the risk of cardiovascular diseases though the reasons are not clear. Here we discuss the role of the immune system in atherosclerosis and of the proinflammatory status in psoriasis and psoriatic arthritis diseases.
Part of the book: Psoriasis
Chagas Cardiomyopathy: Role of Sustained Host-Parasite Interaction in Systemic Inflammatory Burden
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.
Part of the book: Chagas Disease
Immune-Mediated Inflammation: Human T CD4 Helper Lymphocyte Diversity and Plasticity in Health and Disease
The CD4+ T helper (Th) cells have a critical role in organizing the adaptive immune response. The emerging cells of the differentiation after the immune synapse produce helper T cell subpopulations that activate, suppress, or regulate the immune response upon interaction with varying immune cells. There are two main Th cell functional categories: the “effector cells” and the “regulatory T cells.” Classic T helper lymphocytes can also be distinguished by their lineage according to the developmental microenvironment, the expression of cell adhesion-homing receptors, the profile of cytokines they are exposed to, and the involved transcription factors. Traditionally, the CD4+ and CD8+ phenotypes have been considered as helper and cytotoxic/suppressor T lymphocytes, respectively. Currently, the distinction is little rigorous. The immune response is exceedingly complex beyond the classic Th1 and Th2 effector cells’ involvement, and other populations of helper T lymphocytes like the Th17, Tfh, Th22, and Th9 lymphocytes have been phenotypically characterized. These lymphocytes also participate in the pathogenesis of several immune-mediated inflammatory disorders. Here, we revisit and discuss the essential aspects of the state of the art regarding phenotypic diversity and plasticity of TCD4 cells in the T lymphocyte repertoire frame and their potential implication in human inflammatory diseases.
Part of the book: Cells of the Immune System
Neuroprotective Properties of Cannabinoids in Cellular and Animal Models: Hypotheses and Facts
Progressive neuronal loss is a typical characteristic of neurodegenerative diseases. In Parkinson’s disease, the loss of dopaminergic neurons in the basal ganglia results in impaired mobility and flawed muscle control. The loss of cholinergic neurons largely in the basal forebrain contributes to memory and attention deficits and the overall cognitive impairment in Alzheimer’s disease. This being said, neuroprotective drugs should be expected to preserve and/or restore the functions affected by neuronal loss, and substantially prevent cell death. The endocannabinoid system, comprising lipid mediators able to bind to and activate cannabinoid receptors, has emerged as a therapeutic target of potential interest in a variety of central nervous system diseases. Palmitoylethanolamide (PEA) is one of the most important endocannabinoids, which has a key role in modulating oxidative stress and inflammatory response with neuroprotective potential in neurological disorders. Neurodegenerative diseases undergo varied, progressive stages. The current therapeutical approaches are beginning to fall short when it comes to meet the expected results, urging to either develop or identify or develop new effective treatments. This chapter discusses the neuroprotective potential of new drugs, aiming to shed some light on their proposed mechanism of action and their effect in cellular and animal models of neurodegeneration.
Part of the book: Neuroprotection