2021
DOI: 10.3390/ijms22041933
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Dermal Drivers of Injury-Induced Inflammation: Contribution of Adipocytes and Fibroblasts

Abstract: Irregular inflammatory responses are a major contributor to tissue dysfunction and inefficient repair. Skin has proven to be a powerful model to study mechanisms that regulate inflammation. In particular, skin wound healing is dependent on a rapid, robust immune response and subsequent dampening of inflammatory signaling. While injury-induced inflammation has historically been attributed to keratinocytes and immune cells, a vast body of evidence supports the ability of non-immune cells to coordinate inflammati… Show more

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Cited by 29 publications
(19 citation statements)
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References 241 publications
(381 reference statements)
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“…Both bacteria and endotoxins elevate proinflammatory cytokines such as TNF- α and interleukin-1. Furthermore, inflammation increases protease enzyme in the tissue which degrades growth factors rapidly [ 26 , 27 ]. If this situation continues in the wound, it leads to failure in healing .…”
Section: Discussionmentioning
confidence: 99%
“…Both bacteria and endotoxins elevate proinflammatory cytokines such as TNF- α and interleukin-1. Furthermore, inflammation increases protease enzyme in the tissue which degrades growth factors rapidly [ 26 , 27 ]. If this situation continues in the wound, it leads to failure in healing .…”
Section: Discussionmentioning
confidence: 99%
“…Fibroblasts represent a very heterogeneous and plastic cell population regulating both the homeostasis of connective tissue and the inflammatory process and being involved in pathological conditions [ 80 , 105 , 197 , 198 ]. In particular, fibroblast populations are able to shift from an inactivated phenotype of quiescent fibroblasts to an activated phenotype of myofibroblasts or a constitutively activated phenotype of MAFs, depending on environmental modifications and cellular interactions [ 2 , 80 ].…”
Section: Discussionmentioning
confidence: 99%
“…Under the activation of IL-α released by keratinocytes and TLR ligands in the wound microenvironment, fibroblasts activate the NF-kB pathway for the induction and recruitment of inflammatory cells by proinflammatory cytokines (TNF α, INF γ, IL-6, IL-8), chemokines (CCL1, CCL2, CCL5, CXCL1, CXCL8, and CXCL10), and growth factors (granulocyte/macrophage colony stimulating factor (GM-CSF) and granulocyte colony stimulating factor (G-CSF) ( 4 , 9 , 90 , 91 ). CCL2 is closely associated with monocyte recruitment ( 92 ). Like keratinocytes, fibroblasts also synthesise AMPs and defensins (hBD-1 and hBD-2) to clean wounds ( 9 , 93 ).…”
Section: Role Of Non-inflammatory Cells In the Inflammatory Microenvi...mentioning
confidence: 99%
“…A large number of pro-inflammatory factors increased the release of MMPs and accelerated the degradation of the ECM, which further reduced the proliferation and collagen deposition of fibroblasts ( 4 , 166 ). In this pathological inflammatory microenvironment, inflammatory genes expressed by fibroblasts are up-regulated and keratinocytes release IL-1α and type I interferon, triggering an inflammatory chain reaction in adjacent stromal cells ( 92 , 162 ). This, in turn, promotes the flow of immune cells into the injured site.…”
Section: Cell-cell and Cell-ecm Interactionsmentioning
confidence: 99%