2017
DOI: 10.1016/j.jdds.2016.09.001
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Critical role of tumor necrosis factor-α in the early process of wound healing in skin

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Cited by 140 publications
(91 citation statements)
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“…The result reported here was different from that obtained by Legler and co-workers who found more TNF-α elevation in case of infection which might play an important role in innate immunity and host defense against bacterial, fungal, and parasitic infections [16]. In the present study, TNF-α peak level was achieved at 72 hrs and it was 31.957 pg/ml for the infected wound and the same conclusion was reported by Ritsu and co-workers who showed that TNF-α was detected in wound with peak level of 82 pg/ml on the third day of wound injury [17]. Furthermore, Mori and co-workers concluded a rapid variation in TNF-α concentration and this might be due to its short half-life (14 -18 minutes) [18].…”
Section: Discussionsupporting
confidence: 89%
“…The result reported here was different from that obtained by Legler and co-workers who found more TNF-α elevation in case of infection which might play an important role in innate immunity and host defense against bacterial, fungal, and parasitic infections [16]. In the present study, TNF-α peak level was achieved at 72 hrs and it was 31.957 pg/ml for the infected wound and the same conclusion was reported by Ritsu and co-workers who showed that TNF-α was detected in wound with peak level of 82 pg/ml on the third day of wound injury [17]. Furthermore, Mori and co-workers concluded a rapid variation in TNF-α concentration and this might be due to its short half-life (14 -18 minutes) [18].…”
Section: Discussionsupporting
confidence: 89%
“…Tumor necrosis factor alpha (TNF-α) is a key pro-inflammatory cytokine involved in the early phase of most inflammatory events in the body. Employing mouse models, the expression of TNF-α at detectable levels was discovered to happen just after wound creation and sees an increase in the first several hours until it reaches a peak within 24 hours after which it returns to the basal level [17]. Vascular endothelial cells, keratinocytes, and fibroblasts are the major sources of TNF-α which cause an initiation of the inflammatory phase of the wound healing by promoting the recruitment of inflammatory leukocytes.…”
Section: Tumor Necrosis Factor-α (Tnf-α)mentioning
confidence: 99%
“…Vascular endothelial cells, keratinocytes, and fibroblasts are the major sources of TNF-α which cause an initiation of the inflammatory phase of the wound healing by promoting the recruitment of inflammatory leukocytes. TNF-α is also involved in the regulation of the activity of fibroblasts, keratinocytes, and vascular endothelial cells as well as in modulating synthesis of extracellular matrix proteins and matrix metalloproteinase [17,18]. Based on diabetic models, an increase in TNF-α level coupled with decrease in IL-10 that has anti-inflammatory properties results in sustained expression of chemokines CXCL2 and CCL2 and leads to continuous infiltration of leucocytes to the injury site.…”
Section: Tumor Necrosis Factor-α (Tnf-α)mentioning
confidence: 99%
“…In keeping with this finding, the biopsy and IHC analysis contained in this study were also performed within the same time frame. 16 The results of the study showed that the expression of TNF-α decreased with MASE-dose-dependent application. The MASE 50% showed the lowest expression of TNF-α.…”
Section: Discussionmentioning
confidence: 93%
“…Inflammation is a complex physiological process and the role of NF-κB in the inflammatory response cannot be extrapolated from in vitro studies. [15][16][17] In the onset of inflammation, NF-κB promotes pro-inflammatory gene induction and also anti-inflammatory genes. In the nucleus, NF-κB binds to specific DNA targets to form what are known as kβ sites.…”
Section: Discussionmentioning
confidence: 99%