About this Research Topic
The primary role of the gastrointestinal (GI) tract is breaking down ingested food and absorption of nutrients that fuel the entire body. Because of its importance, physiology and pathophysiology of GI tract has long been a focus of countless studies. Particularly the cells and tissues, whose physiological functions are related to the process of digestion, have been in the center of attention in the past centuries. Those cells include enterocytes, the main cell type in the intestinal epithelium primarily responsible for nutrient absorption; pancreatic acinar cells, that store, produce and release digestive enzymes; or hepatocytes, involved in the synthesis of bile salts aiding digestion of lipids.
Recently, increasing research efforts are directed towards less well known or less abundant cells in the GI tract. Such cells are not immediately associated with digestion and thus are often overlooked or simply taken for granted. Nevertheless, they perform accessory and supporting functions required for the homeostasis of the tissues building up the GI tract. For instance, these functions may be mediated by neuropeptides secreted by populations of certain cells scattered in the intestinal wall. Dysfunctions of these cells throw the homeostasis off balance, which may be manifested by harmful organ disorders, or even severe systemic eating disorders such as anorexia nervosa or bulimia.
Some other examples include pathophysiology of stellate cells, found in the liver and the pancreas. While the role of stellate cells in heath is still unclear, upon injury they undergo a transition from a quiescent to an activated phenotype and start producing the extracellular matrix components (EMC), which help maintain the tissue integrity. On the other hand, overproduction of EMC by stellate cells leads to excessive collagen deposition and may result in pancreatic fibrosis or liver cirrhosis.
What is more, the GI tract comes into contact with the external environment and is the ecological niche for microbes. Therefore, the resident GI cells had to develop mechanisms allowing them to maintain the balance between host-microbe interactions, particularly the defence against pathogens and tolerance towards symbionts and commensals. An interesting example are Paneth cells, that produce and secrete multiple peptides and proteins of antimicrobial activity, such as α-defensins able to disrupt bacterial cell membranes and thus playing an important role as part of the innate immunity response.
This Research Topic intends to put the “background actors” of the GI tract in the spotlight. The focus is placed on accessory, supporting or less common cell types, their physiological roles and the disorders related to their absence or dysfunctions, as well as state-of-the-art methods of their identification and isolation. This aims to increase our understanding of the complex homeostasis of the GI tract and encourage further research, also by providing the multidisciplinary platform to integrate the researchers from the fields of physiology, endocrinology, microbiology, and others.
We are specifically interested in original research, review and methods articles. While it is anticipated that in vitro and in vivo models, as well as clinical findings, will be the primary source of scientific information here, in silico models of physiological processes will also be considered.
Recently, increasing research efforts are directed towards less well known or less abundant cells in the GI tract. Such cells are not immediately associated with digestion and thus are often overlooked or simply taken for granted. Nevertheless, they perform accessory and supporting functions required for the homeostasis of the tissues building up the GI tract. For instance, these functions may be mediated by neuropeptides secreted by populations of certain cells scattered in the intestinal wall. Dysfunctions of these cells throw the homeostasis off balance, which may be manifested by harmful organ disorders, or even severe systemic eating disorders such as anorexia nervosa or bulimia.
Some other examples include pathophysiology of stellate cells, found in the liver and the pancreas. While the role of stellate cells in heath is still unclear, upon injury they undergo a transition from a quiescent to an activated phenotype and start producing the extracellular matrix components (EMC), which help maintain the tissue integrity. On the other hand, overproduction of EMC by stellate cells leads to excessive collagen deposition and may result in pancreatic fibrosis or liver cirrhosis.
What is more, the GI tract comes into contact with the external environment and is the ecological niche for microbes. Therefore, the resident GI cells had to develop mechanisms allowing them to maintain the balance between host-microbe interactions, particularly the defence against pathogens and tolerance towards symbionts and commensals. An interesting example are Paneth cells, that produce and secrete multiple peptides and proteins of antimicrobial activity, such as α-defensins able to disrupt bacterial cell membranes and thus playing an important role as part of the innate immunity response.
This Research Topic intends to put the “background actors” of the GI tract in the spotlight. The focus is placed on accessory, supporting or less common cell types, their physiological roles and the disorders related to their absence or dysfunctions, as well as state-of-the-art methods of their identification and isolation. This aims to increase our understanding of the complex homeostasis of the GI tract and encourage further research, also by providing the multidisciplinary platform to integrate the researchers from the fields of physiology, endocrinology, microbiology, and others.
We are specifically interested in original research, review and methods articles. While it is anticipated that in vitro and in vivo models, as well as clinical findings, will be the primary source of scientific information here, in silico models of physiological processes will also be considered.
Keywords: gastrointestinal tract, rare cell populations, pathophysiological signalling, innate immunity
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