Rosalino Vázquez-López

By Laila Gutiérrez-Kobeh, Jorge Rodríguez González, Rosalino Vázquez-López and Arturo Wilkins-Rodríguez

Apoptosis is a biological process carried out during maturation, remodeling, growth, and developmental processes in tissues, and also represents an important defense mechanism of cells against intracellular microorganisms. In counterpart, diverse intracellular pathogens have developed a wide array of strategies to evade apoptosis and persist inside cells. Apoptotic cell death can be triggered through different intracellular signaling pathways that lead to morphological changes and eventually cell death. Among these pathways, MAPK and PI3K play a central role. The precise control of the signaling pathways that lead to apoptosis is crucial for the maintenance of tissue homeostasis. Paradoxically, these same pathways are utilized during infection by distinct intracellular microorganisms in order to evade recognition by the immune system, inhibit apoptosis, and therefore survive, reproduce, and develop inside cells.

Part of the book: Current Understanding of Apoptosis

By Laila Gutiérrez-Kobeh, Jorge Rodríguez-González, Jesús Argueta- Donohué, Rosalino Vázquez-López and Arturo A. Wilkins- Rodríguez

Dendritic cells comprise a complex array of cell populations that play a leading role in immune defense. In an immature state, they have the capacity to sense and uptake different antigens. Upon capturing antigens, they become activated, mature, and migrate to lymph nodes where they present antigen-derived peptides to naïve T cells. Due to these excellent surveillance properties, dendritic cells play an important role against parasitic infections. Also, dendritic cells are an important source of IL-12, which is a fundamental proinflammatory cytokine in the control of intracellular parasites. The aim of this chapter is to review the most important characteristics and functions of dendritic cells and their role in the control of infection by parasites.

Part of the book: Dendritic Cells

By Sandra Georgina Solano-Gálvez, María Fernanda Valencia-Segrove, María José Ostos Prado, Ana Berenice López Boucieguez, Diego Abelardo Álvarez-Hernández and Rosalino Vázquez-López

Antimicrobial resistance is a worldwide problem. Various pathogenic bacteria can be resistant to one or several antibiotics, resulting in a serious public health problem. Isolation of pathogenic bacteria resistant to multiple last-generation antibiotics from hospital samples have been reported. In that sense, the isolation of pathogenic strains resistant to members of the quinolone family, from clinical samples, is an increasing phenomenon. Quinolones are a group of synthetic broad-spectrum antimicrobials, whose mechanism of action is the inhibition of DNA gyrase and topoisomerase IV, with the consequent DNA breakdown and cell death due to genotoxic damage. Three mechanisms have been determined by which bacteria can be resistant to quinolones: (1) Chromosomal mutations in coding genes (mutations that alter the objectives of the drug). (2) Mutations associated with the reduction of the intracytoplasmic concentration of quinolones. (3) Plasmid-mediated quinolone resistance genes (plasmids that protect cells from the lethal effects of quinolones). In this chapter, we analyze each of them and provide the most current connections and investigations of these processes.

Part of the book: Antimicrobial Resistance