Abstract:The intestinal epithelium forms a vital barrier between luminal microbes and the underlying mucosal immune system. Epithelial barrier function is maintained by continuous renewal of the epithelium and is pivotal for gut homeostasis. Breaching of the barrier causes mobilization of immune cells to promote epithelial restitution. However, it is not known whether microbes at the luminal surface of a healthy epithelial barrier influence immune cell mobilization to modulate tissue homeostasis. Using a mouse colonic … Show more
“…Luminal bacteria promote mucus secretion and movement of monocytes closer to epithelial stem cells through an epithelial MyD88‐signalling pathway. Increased proximity of monocytes to epithelial stem cells results in increased crypt cell proliferation and intestinal stem cell numbers, which could be beneficial during intestinal injury response. Studies comparing GF mice to mice colonized with three strains of bacteria ( E. coli K‐12, Staphylococcus xylosus and Enterococcus faecalis ) reveal that GF mice have delayed microbial clearance, reduced inflammatory responses to intravenous E. coli K12 infection and a decreased myeloid cell pool size .…”
Section: Bacterial Components That Effect Innate and Adaptive Immunitymentioning
SummaryA complex relationship between the microbiota and the host emerges early at birth and continues throughout life. The microbiota includes the prokaryotes, viruses and eukaryotes living among us, all of which interact to different extents with various organs and tissues in the body, including the immune system. Although the microbiota is most dense in the lower intestine, its influence on host immunity extends beyond the gastrointestinal tract. These interactions with the immune system operate through the actions of various microbial structures and metabolites, with outcomes ranging from beneficial to deleterious for the host. These differential outcomes are dictated by host factors, environment, and the type of microbes or products present in a specific ecosystem. It is also becoming clear that the microbes are in turn affected and respond to the host immune system. Disruption of this complex dialogue between host and microbiota can lead to immune pathologies such as inflammatory bowel diseases, diabetes and obesity. This review will discuss recent advances regarding the ways in which the host immune system and microbiota interact and communicate with one another.
“…Luminal bacteria promote mucus secretion and movement of monocytes closer to epithelial stem cells through an epithelial MyD88‐signalling pathway. Increased proximity of monocytes to epithelial stem cells results in increased crypt cell proliferation and intestinal stem cell numbers, which could be beneficial during intestinal injury response. Studies comparing GF mice to mice colonized with three strains of bacteria ( E. coli K‐12, Staphylococcus xylosus and Enterococcus faecalis ) reveal that GF mice have delayed microbial clearance, reduced inflammatory responses to intravenous E. coli K12 infection and a decreased myeloid cell pool size .…”
Section: Bacterial Components That Effect Innate and Adaptive Immunitymentioning
SummaryA complex relationship between the microbiota and the host emerges early at birth and continues throughout life. The microbiota includes the prokaryotes, viruses and eukaryotes living among us, all of which interact to different extents with various organs and tissues in the body, including the immune system. Although the microbiota is most dense in the lower intestine, its influence on host immunity extends beyond the gastrointestinal tract. These interactions with the immune system operate through the actions of various microbial structures and metabolites, with outcomes ranging from beneficial to deleterious for the host. These differential outcomes are dictated by host factors, environment, and the type of microbes or products present in a specific ecosystem. It is also becoming clear that the microbes are in turn affected and respond to the host immune system. Disruption of this complex dialogue between host and microbiota can lead to immune pathologies such as inflammatory bowel diseases, diabetes and obesity. This review will discuss recent advances regarding the ways in which the host immune system and microbiota interact and communicate with one another.
“…Work in vertebrates has implicated immune cells in the induction of mitotic activity and regeneration in intestinal epithelia 23 , 24 , 25 . In Drosophila , macrophage-like hemocytes constitute a major population of blood cells 26 that mediate infection responses and tissue repair 27 , yet if and how these cells influence regeneration in the intestinal epithelium has not been addressed.…”
SUMMARYCoordination of stem cell activity with inflammatory responses is critical for regeneration and homeostasis of barrier epithelia. The temporal sequence of cell interactions during injury-induced regeneration is only beginning to be understood. Here we show that intestinal stem cells (ISCs) are regulated by macrophage-like hemocytes during the early phase of regenerative responses of the Drosophila intestinal epithelium. Upon tissue damage, hemocytes are recruited to the intestine and secrete the TGFβ/BMP homologue Dpp, inducing ISC proliferation by activating the Type I receptor Saxophone and the Smad homologue Smox. Activated ISCs then switch their response to Dpp by inducing expression of Thickveins, a second Type I receptor that has previously been shown to re-establish ISC quiescence by activating Mad. The interaction between hemocytes and ISCs promotes infection resistance, but also contributes to the development of intestinal dysplasia in aging flies. We propose that similar interactions influence pathologies like inflammatory bowel disease and colorectal cancer in humans.
“…Fast forward eons to organisms like humans that gain nutrition through a highly differentiated and multi-cellular digestive tract, and phagocytosis is a highly efficient process used only by specialized cells of the mononuclear phagocyte system (MPS). Microbes (in and on us) remain major targets as they not only out-number and out-proliferate our own cells but also invade through any and all compromised tissue barriers [2]. The principal cell types of the MPS are macrophages which reside in every tissue and monocytes that circulate out of the bone marrow to enter a tissue and differentiate to macrophages [3••,4].…”
Professional phagocytes of the mononuclear phagocyte system (MPS), especially ubiquitous macrophages, are commonly thought to engulf or not a target based strictly on ‘eat me’ molecules such as Antibodies. The target might be a viable ‘self’ cell or a drug-delivering nanoparticle, or it might be a cancer cell or a microbe. ‘Marker of Self’ CD47 signals into a macrophage to inhibit the acto-myosin cytoskeleton that makes engulfment efficient. In adhesion of any cell, the same machinery is generally activated by rigidity of target surfaces, and recent results confirm phagocytosis is likewise driven by the rigidity typical of microbes and many synthetics. Basic insights are already being applied in order to make macrophages eat cancer or to delay nanoparticle clearance for better drug delivery and imaging.
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