By Joseph F. Albright
Renowned immunogerontologists evaluation the main beneficial properties and features of the immune process which are probably, or recognized, to be considerably altered by means of getting older, and provide insightful analyses of the results for these getting older matters who needs to do something about an infection. themes of specific curiosity comprise the demographics and theories of immunosenescence, the slow 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 will be made in figuring out the fundamental biology, the more recent tools of therapy and prevention, and the assessment of such provocative rules as lifespan extension and dietary intervention to hold up immunosenescence.
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Additional resources for Aging, Immunity, and Infection (Infectious Disease)
33). Although not a pathogen of elderly humans, what has been learned about adherence of B. pertussis to human cells is broadly instructive. Ciliated cells and macrophages are the host cells to which B. pertussis binds. Mutant strains of B. pertussis have been prepared that lack either FHA or PT or both (34). When tested in normal rabbits, wildtype strains localized to cilia in the respiratory tract and produced lesions. 30 Aging, Immunity, and Infection Mutants lacking both FHA and PT were cleared without inducing pathology.
The formation of biofilms by P. aeruginosa has received considerable attention because it is a critical event in the devastating disease, cystic fibrosis (59,61). This same bacterium is found in most healthy individuals in whom it causes no disease. It is an opportunistic organism that only becomes pathogenic in compromised individuals. A brief account of biofilm formation by P. aeruginosa on the epithelial linings of the lungs of cystic fibrosis patients provides a concept of the process. Attachment factors are present on hairlike appendages of the bacteria called type IV pili (62).
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. That is a consequence of the excessive use of antibiotics, which has given selective advantage to bacteria possessing R-plasmids.
Aging, Immunity, and Infection (Infectious Disease) by Joseph F. Albright