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The Evolutionary Adaptation of Gut Symbiotic Microorganisms
The research of gut microbes' symbiotic mechanism is a typical case of evolutionary pathological ecology.
Most animals form intimate, life-long associations with microbial communities; for example, the commensal microbiota resident in the human gastrointestinal tract. Animal-associated microbial communities are established at stereotyped times in development, often prior to the maturation of their host organs, but they are often overlooked by developmental biologists as critical developmental determinants.* It is therefore possible that indigenous gut bacteria profoundly influence the development of the intestinal adaptive immune system.* These contributions are most obvious in the gut.
The mammalian intestine is inhabited by more than four hundred species of bacteria. Almost all analyses to date indicate that profound changes occur in the intestinal ecosystem when young mammals are weaned from their mother's milk onto solid food. For example, the intestines of neonatal humans contain large numbers of facultative anaerobes, including Escherichia coli and streptococci. These decline in number during weaning as obligate anaerobes establish a foothold in the ecosystem. Over time, the gut ecosystem evolves into a stable climax community consisting predominantly of obligate anaerobes, including bacteroides and clostridium species.*
The mammalian microflora is a metabolically active entity that plays a crucial role in nutrition by degrading dietary substances that are otherwise indigestible by the host. This arrangement makes sense from an evolutionary perspective. By recruiting a society of resident microbes with diverse metabolic capabilities that allow the breakdown of numerous dietary compounds, mammals have been relieved of the need to evolve such functions. The host also achieves a degree of metabolic adaptability that can help it deal with abrupt changes in diet and nutrient availability. In return, gut bacteria are given a protected nutrient-rich habitat in which to multiply.*
The changing microbial ecology during weaning is coincident with a marked functional and morphological maturation of the gut. Dramatic shifts in the metabolic capacity of the small intestine facilitate the transition from a high-fat milk-based diet to a diet rich in carbohydrates. Important changes in immune function take place at the same time, including a withdrawal of the passive immunity conferred by maternal immunoglobulins that are present in milk. For example, increased numbers of B and T cells are found in the villus lamina propria and in the intraepithelial spaces following weaning. In addition, the polymeric immunoglobulin A receptor, which transports antibodies from the basolateral to the apical surfaces of gut epithelial cells, is markedly induced during this developmental transition.*
Studies in germ-free mice have revealed that bacteria play an essential role in driving key aspects of postnatal gut maturation.*
The indigenous microbiota of both fish and mammals serve similar functions in the digestive tract: they ferment polysaccharides to short chain fatty acids and confer protection against infection by pathogens.*
In this review, we argue that the microbial diversity of the human gut is the result of coevolution between microbial communities and their hosts. We suggest that the peculiar structure of microbial diversity in the human gut resulted from natural selection operating at two levels. Host level, top-down selection on the community favors stable societies with a high degree of functional redundancy. An opposing bottom-up selection pressures driving microbial cells to become functionally specialized. In addition to the selection pressures shaping microbes in the gut, we discuss factors that constrain diversity. Finally, we present an ecologic view of pathogenic relationships: the challenges potential pathogens face when encountering a microbiota where there is functional redundancy with virtually all niches and habitats filled, and the idea that microbial community structure should be considered as a factor that can influence predisposition to specific diseases in certain host contexts.*
The gut epithelium is a vital barrier between the internal milieu of mammals and the vast microbial societies in the lumen. In addition to acting as a physical barrier, gut epithelia also actively secrete antimicrobial proteins. Paneth cells are key effectors of this type of innate mucosal defense in the small intestine. These specialized epithelial cells harbor secretory granules that contain high concentrations of several microbicidal proteins and react to the presence of bacteria by discharging their granule contents into the gut lumen.*
Angiogenin-4 (Ang4) exhibits potent bactericidal activity that establishes its role in epithelial host defense. In conventional mice, Ang4 expression increases dramatically during weaning and quickly reaches adult levels. By contrast, germ-free mice never achieve high Ang4 expression levels, suggesting that induction of Ang4 expression during weaning requires a gut microbiota.
The intestinal immune system is separated from the vast luminal microflora by as little as a single epithelial layer. Furthermore, gut lymphocytes go through crucial developmental transitions after encountering intestinal antigen in local lymphoid structures, such as Peyer's patches. It is therefore possible that indigenous gut bacteria profoundly influence the development of the intestinal adaptive immune system.*
The epidemiology of inflammatory bowel diseases (IBDs) provides a circumstantial but compelling argument in favor of microbes as a driving force in mucosal immune system development. This group of diseases, which includes ulcerative colitis and Crohn's disease, is frequently characterized by a breakdown in immune tolerance toward resident gut bacteria. The mechanisms underlying this dysregulation are poorly understood. However, the incidence of IBDs has increased dramatically in the United States during the past fifty years, and has been linked to the presence of overly hygienic conditions in early childhood. These observations evoke the hygiene hypothesis: the idea that early childhood exposure to microbes can direct the maturing immune system to develop a tolerance to innocuous environmental antigens. The hygiene hypothesis is invoked most frequently to explain the rise in allergy incidence in industrialized countries, where there is increasing antibiotic usage and an emphasis on overly hygienic environments. However, IBDs and allergies are similar in that both are characterized by inappropriate immune responses to otherwise innocuous environmental antigens. Therefore, the hygiene hypothesis might also offer insight into the underlying causes of some IBDs.*
The gastrointestinal tract and the microbes colonizing it form a complex ecosystem that has various effects on the wellbeing of the host. In addition to acute infections, the composition of the gastrointestinal microbiota has been suspected to influence the etiopathogenesis of many chronic diseases, such as rheumatoid arthritis and inflammatory bowel diseases.
* For further details, please refer to Deep Structure Studies 7: Experimental Reviews and References I.
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