Figure 1

An external file that holds a picture, illustration, etc.
Object name is WJG-20-16498-g001.jpg

Axes of host-microbial interaction that influence health. Short chain fatty acids (SCFAs) and microbe-associated molecular patterns (MAMPs) are the key microbial signals detected by the host. Outcomes of host-microbiome interactions are contingent on the microbial product involved, the type of host cells exposed to microbial signals and the location of contact. The primary intersection points occur at the intestinal epithelial interface. Sampling of luminal MAMPs and uptake of SCFAs have a direct impact on gut epithelium, lymphoid and neuroendocrine systems. The secondary intersection points occur externally to the intestinal tissues. Translocated or “escaped” microbial products can activate pattern recognition receptors (PRRs) and specific G protein coupled receptors (GPRs) on a wide range of host cells beyond the epithelium. A compromised gut barrier amplifies host-microbiome interactions in the secondary intersection points and the downstream effects of PRR and GPR signalling cascades. Host outcome is an emergent property of all axes of interactions.

2014 Nov 28;20(44):16498-16517.

Mechanistic links between gut microbial community dynamics, microbial functions and metabolic health.

Ha CW, Lam YY, Holmes AJ.

Author information

Abstract

Gut microbes comprise a high density, biologically active community that lies at the interface of an animal with its nutritional environment. Consequently their activity profoundly influences many aspects of the physiology and metabolism of the host animal. A range of microbial structural components and metabolites directly interact with host intestinal cells and tissues to influence nutrient uptake and epithelial health. Endocrine, neuronal and lymphoid cells in the gut also integrate signals from these microbial factors to influence systemic responses. Dysregulation of these host-microbe interactions is now recognised as a major risk factor in the development of metabolic dysfunction. This is a two-way process and understanding the factors that tip host-microbiome homeostasis over to dysbiosis requires greater appreciation of the host feedbacks that contribute to regulation of microbial community composition. To date, numerous studies have employed taxonomic profiling approaches to explore the links between microbial composition and host outcomes (especially obesity and its comorbidities), but inconsistent host-microbe associations have been reported. Available data indicates multiple factors have contributed to discrepancies between studies. These include the high level of functional redundancy in host-microbiome interactions combined with individual variation in microbiome composition; differences in study design, diet composition and host system between studies; and inherent limitations to the resolution of rRNA-based community profiling. Accounting for these factors allows for recognition of the common microbial and host factors driving community composition and development of dysbiosis on high fat diets. New therapeutic intervention options are now emerging.

KEYWORDS:

Bile; Dysbiosis; Enteroendocrine cells; High fat diet; Immunomodulation; Intestinal mucosa; Microbe-associated molecular patterns; Microbiome; Short chain fatty acids