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Michael, S., Achilleos, C., & Panayiotou, T. (2016). Inflammation Shapes Stem Cells and Stemness during Infection and Beyond. Frontiers in Cell and Developmental Biology, 4, 118. 
Added by: Dr. Enrique Feoli (31/05/2023, 18:53)   Last edited by: Dr. Enrique Feoli (31/05/2023, 18:55)
Resource type: Journal Article
DOI: 10.3389/fcell.2016.00118
ID no. (ISBN etc.): 2296-634X
BibTeX citation key: Michael2016
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Categories: BioAcyl Corp
Subcategories: Stemness
Creators: Achilleos, Michael, Panayiotou
Collection: Frontiers in Cell and Developmental Biology
Views: 1/135
Abstract
The outcome of an inflammatory incident can hang in the balance between restoring health and tissue integrity on the one hand, and promoting aberrant tissue homeostasis and adverse outcomes on the other. Both microbial-related and sterile inflammation is a complex response characterized by a range of innate immune cell types, which produce and respond to cytokine mediators and other inflammatory signals. In turn, cells native to the tissue in question can sense these mediators and respond by migrating, proliferating and regenerating the tissue. In this review we will discuss how the specific outcomes of inflammatory incidents are affected by the direct regulation of stem cells and cellular plasticity. While less well appreciated than the effects of inflammatory signals on immune cells and other differentiated cells, the effects are crucial in understanding inflammation and appropriately managing therapeutic interventions.
  
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Tissue damage can arise as a result of physical damage, chemical damage or pathogen infection. Once the damage is detected a homeostatic inflammatory response is activated to regenerate the tissue. This inflammation is characterized by the activation of immune cells, such as macrophages and monocytes and the release of inflammatory mediators, such as cytokines and interferons to the site of damage. These mediators in turn can affect native tissue cells to respond by migrating and proliferating resulting in tissue repair. Evidence suggest that the inflammatory response acts as a regulator of tissue stemness either by directly affecting tissue stem cells or by shifting differentiated cells toward a stem-like cell character. The balance in this inflammatory response and its mediated stemness is a critical driver of either maintaining tissue integrity or promoting aberrant homeostasis and disease.


  
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