By Joseph F. Albright
Well-known immunogerontologists evaluate the main positive factors and features of the immune process which are probably, or recognized, to be considerably altered by means of getting older, and supply insightful analyses of the results for these getting older topics who needs to deal with an infection. issues of distinctive curiosity contain the demographics and theories of immunosenescence, the sluggish breakdown of resistance to an infection within the elderly, and the results of getting older on chosen mechanisms of either innate and adaptive immunity to infections. The Albrights additionally clarify how advances might be made in figuring out the fundamental biology, the more moderen tools of therapy and prevention, and the review of such provocative principles as lifespan extension and dietary intervention to hold up immunosenescence.
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Additional resources for Aging, Immunity, and Infection (Infectious Disease)
To complete this brief discussion of antibiotic resistance, a word about transposons is in order. Those genetic elements, conveyed by resistance plasmids (R-plasmids), are responsible for much of the current microbial resistance to antibiotics. There are collections of bacteria, assembled in the preantibiotic era, that display recognizable plasmids; but most of those plasmids lack antibiotic-resistance elements. This must mean that current bacterial pathogens displaying antibiotic resistance harbor familiar plasmids that have become R-plasmids by acquiring resistance transposons.
Enterotoxigenic E. coli, Haemophilus influenzae, V. cholerae). Pathogens that penetrate epithelial barriers survive by invading and replicating in host cells. Tight junctions (zona occludens) that normally prevent penetration of epithelial cell layers also divide the epithelial cells into apical (lumenal) and basolateral surfaces. Some pathogenic bacteria such as Salmonella invade host cells from the apical surface whereas others (Yersinia, Shigella) interact with and invade through the basolateral surface.
Monocytogenes to obtain a T-cell response equal to that of the young, as found by Lovik and North, could be a reflection of inefficient antigen processing by dendritic cells of old mice, or a reflection of a requirement for more intense processed-anti- 28 Aging, Immunity, and Infection gen stimulation of senescence-altered T cells. The effects of aging on dendritic cells (DCs) and T cells are discussed in Chapter 4. At this point, it need only be mentioned that dendritic cells are the critical antigen-presenting cells that prepare microbial antigens for triggering immune responses.