Host–pathogen dynamics: it's complicated!
نویسنده
چکیده
T his set of three review articles on hostÁpathogen interactions begins with a discussion of emerging concepts on homeostasis of a specific microbiome, that of the gut, and how disruption of the microbial status quo can result in several syndromes (1). The following papers highlight research on hostÁpathogen interactions with two oral bacteria: the dynamics between Treponema denticola virulence factors and host proteins (2); and Porphyromonas gingivalis infection of a novel animal model that will ultimately shed light on pathogen-esis and innate immune responses to the organism (3). Research on the pathogenic infection of animal hosts began with whole animal studies (see (4) for a review of the work by Pasteur and Koch, and Riedel (5) for the work of Jenner on small pox vaccination), an approach that yielded many milestones in our understanding of infection and tremendous medical benefits for generations of humans. With the advent of bacterial genetics, and later molecular biology, the reductionist approach has held sway for the past 40 years with obvious triumphs such as the development of the field of cellular microbiology and whole genome sequencing of pathogenic (and non-pathogenic) microorganisms. More recently, the ability to isolate and amplify nucleic acids from small biological/ clinical samples together with technological advances in high throughput deep sequencing enables us to look beyond which organisms are present in a specific ecological niche (i.e. the microbiome of the oral cavity, skin, gut, etc.) and ask 'what are they doing?' This is the key to understanding how a specific microbiome communicates with the host in both health and disease. Because we and our microbiome have evolved together, we rationalize that the equilibrium between us results in health, and disruption of the homeostasis leads to disease. The constituent microbes in a microbiome do not act alone and alliances have evolved with each other, and with host proteins and cells. Recently, Brown & Whitely examined the metabolic relationship between the oral bacteria Aggregatibacter actinomycetemcomitans (Aa) and streptococci. Because they inhabit the same environmental niche, the gingival pocket, it was reasoned that Aa must derive benefits from this coexistence. Streptococci efficiently produce lactic acid from 6-carbon sugars and dietary sucrose, and it was established that Aa preferentially utilizes lactic acid as a carbon source over glucose, fructose, mannose, even at the cost of a lowered growth rate (6). Furthermore, Aa consumed the lactate produced from sucrose catabolized by S. gordonii. Microarray-based comparative …
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عنوان ژورنال:
دوره 4 شماره
صفحات -
تاریخ انتشار 2012