Abstract
Simple SummaryThe gastrointestinal tract is a complex organization of various types of epithelial cells forming a single layer of the mucosal barrier, the host mucosal immune system, and microorganisms termed as gut microbiota inhabiting this area. The mucosal barrier, including physical and chemical factors, spatially segregates gut microbiota and the host immune system preventing the development of immune response directed towards non-pathogenic commensals and dietary antigens. However, for the maintenance of the integrity of the mucosal surfaces, cross-talk between epithelial cells and microbiota is required. The microbiome and the intestinal epithelium developed a complex dependence necessary for sustaining intestinal homeostasis. In this review, we highlight the role of specific epithelial cell subtypes and their role in barrier arrangement, the mechanisms employed by them to control intestinal microbiota as well as the mechanisms utilized by the microbiome to regulate intestinal epithelial function. This review will provide information regarding the development of inflammatory disorders dependent on the loss of intestinal barrier function and composition of the intestinal microbiota.The gastrointestinal tract, which is constantly exposed to a multitude of stimuli, is considered responsible for maintaining the homeostasis of the host. It is inhabited by billions of microorganisms, the gut microbiota, which form a mutualistic relationship with the host. Although the microbiota is generally recognized as beneficial, at the same time, together with pathogens, they are a permanent threat to the host. Various populations of epithelial cells provide the first line of chemical and physical defense against external factors acting as the interface between luminal microorganisms and immunocompetent cells in lamina propria. In this review, we focus on some essential, innate mechanisms protecting mucosal integrity, thus responsible for maintaining intestine homeostasis. The characteristics of decisive cell populations involved in maintaining the barrier arrangement, based on mucus secretion, formation of intercellular junctions as well as production of antimicrobial peptides, responsible for shaping the gut microbiota, are presented. We emphasize the importance of cross-talk between gut microbiota and epithelial cells as a factor vital for the maintenance of the homeostasis of the GI tract. Finally, we discuss how the imbalance of these regulations leads to the compromised barrier integrity and dysbiosis considered to contribute to inflammatory disorders and metabolic diseases.
Highlights
The mucosal surfaces form one of the major barriers protecting the host against invasion and systemic dissemination of both pathogens and local microbiota
Studies performed on intestinal explants clearly presented that senGCs, featuring non-specific endocytosis, were able to respond to TLR2/1, TLR4, and TLR5 ligands, leading to NLRP6 inflammasome formation and production of reactive oxygen species, which in turn triggered the release of Ca2+ that passed through gap junctions
We focused on the role of specific epithelial cell populations engaged in the formation of the first line of defense against mucosa colonization with pathogens as well as their mutualistic relationship with the GI tract microbiota
Summary
The mucosal surfaces form one of the major barriers protecting the host against invasion and systemic dissemination of both pathogens and local microbiota. The gut microbiota is considered a biological barrier, protecting against colonization of the GI tract with pathogens This mutual GI tract-microbiota partnership does not lead to the stimulation of the immune response, at the same time, the physical barrier provides the sensing and defense mechanisms ready to protect against invading infectious agents. This recognition requires microbial sensing by host cells, which is carried out by pattern recognition receptors (PRRs), including Toll-like receptors (TLRs), nucleotide-binding oligomerization domain [NOD]like receptors (NLRs), C-type lectin receptors (CLR), retinoic acid-inducible gene I [RIG-I] receptors (RLRs), absence in melanoma 2 [AIM]-like receptors (ALRs), which recognize microbial-associated molecular patterns (MAMPs) that are molecular structures essential for microbial survival or damage-associated molecular patterns (DAMPs), released from host cells facing injury or molecular stress [2,3]. We will concentrate on the significance of this cross-talk in the prevention of intestinal inflammation
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