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The blood-brain barrier (BBB) is a dynamic interface that regulates the exchange of molecules and cells between the brain parenchyma and the peripheral blood. The BBB is mainly composed of endothelial cells, astrocytes and pericytes. The integrity of this structure is essential for maintaining brain and spinal cord homeostasis and protection from injury or disease. However, in various neurological disorders, such as traumatic brain injury, Alzheimer's disease, and multiple sclerosis, the BBB can become compromised thus allowing passage of molecules and cells in and out of the central nervous system parenchyma. These agents, however, can serve as biomarkers of BBB permeability and neuronal damage, and provide valuable information for diagnosis, prognosis and treatment. Herein, we provide an overview of the BBB and changes due to aging, and summarize current knowledge on biomarkers of BBB disruption and neurodegeneration, including permeability, cellular, molecular and imaging biomarkers. We also discuss the challenges and opportunities for developing a biomarker toolkit that can reliably assess the BBB in physiologic and pathophysiologic states.

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INTRODUCTION: Tuberculosis is an infectious disease which is caused by bacilli from the M. tuberculosis complex. The Mycobacterium bovis Bacillus Calmette-Guérin vaccine is currently available as a prophylactic tool for preventing the disease; it has been shown to be efficient in preventing disseminated forms of tuberculosis during early ages; however, its efficiency is limited in areas where individuals have had prior exposure to environmental mycobacteria, and its efficacy decreases with a host's age. AREAS COVERED: Following a comprehensive search of the available literature, this review describes some of the most frequently used animal models, the most frequently used methods for evaluating efficacy in animal models and some in vitro strategies as alternatives for evaluating vaccines. EXPERT OPINION: Identifying the animal models used up to now for evaluating vaccines during their development stages, their characteristics and limitations, as well as knowledge regarding strategies for evaluating promising vaccine candidate efficacy, will ensure more efficient, reliable and reproducible pre-clinical trials. Although much of the knowledge accrued to date concerning vaccine effectiveness against tuberculosis has been based on animal models, it is clear that large questions still need to be resolved and that extrapolation of such efficacy to humans has yet to be achieved.

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El presente artículo revisa los mecanismos inhibitorios de la apoptosis usados por Chlamydia trachomatis frente a la familia de proteínas Bcl-2, para lograr su supervivencia intracelular. Chlamydia trachomatis es una bacteria intracelular obligada Gram negativa responsable de la infección de transmisión sexual más común en el mundo; éste microorganismo es capaz de inhibir la apoptosis de la célula huésped durante su ciclo de desarrollo, obteniendo un refugio seguro para su supervivencia. Frente a estímulos como la infección de la célula por un patógeno, la familia de proteínas Bcl-2 regula la apoptosis por medio de la liberación del citocromo c de la mitocondria para desencadenar la muerte celular programada (MCP). Ct usa diversos mecanismos de regulación antiapoptótica para sobrevivir dentro de la célula huésped; dentro de ellos se observa la secreción de proteínas tales como CPAF y CADD, la escisión de la proteína Bid, el secuestro de Bad y en general el bloqueo de proteínas pertenecientes a la familia Bcl-2 con dominio BH3, que afectan directamente la vía de mitocondrial ocasionando la persistencia, desarrollo y replicación de Ct en la célula huésped.

Chlamydia trachomatis (Ct) is a Gram-negative obligate intracellular bacteria responsible for the infection ofmost common sexually transmitted infection in the world; The organism is able to inhibit host cell apoptosis during development cycle, obtaining a safe survival. To stimuli such as infection of the cell by a pathogen, the Bcl-2 familyregulates cellapoptosisreleasing cytochrome c from mitochondria to trigger programmed cell death (PCD). Ct used various anti-apoptotic regulation mechanisms to survive within the host cell, such as:1. Proteins secretion of CPAF and CADD, 2. The cleavage of the protein Bid, 3.The Bad kidnapping and blockingproteins, belonging to the Bcl-2 family -(BH3 domain). All these mechanisms affect the cell mitochondrial pathway causingpersistence infection, development and Ct replicationwithin the host cell.The objective of this review is to show one of the anti-apoptotic mechanisms, which Ct can survive within the host cell, evading the immune systemresponse.

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