| Autor: |
Seoudy, Wael M., Mohy El Dien, Sara M., Abdel Reheem, Talal A., Elfangary, Mona M., Erfan, Moatasem A. |
| Předmět: |
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| Zdroj: |
International Wound Journal; Jan2023, Vol. 20 Issue 1, p38-45, 8p |
| Abstrakt: |
The pathophysiology of keloid formation is unknown, however, macrophages are thought to play a role in keloid formation. Understanding the mechanism(s) of keloid development might be crucial in developing a new treatment regimen for keloids. The aim of this study was to understand possible status of M1 and M2 type macrophages in the pathogenesis of keloid. Thirty cases of Keloid tissues were selected according to our inclusion and exclusion criteria, as well as 30 normal scars, were enrolled in our study as a control group. An excisional biopsy was harvested and ELISA was done on keloid tissue and normal scar samples, with CD68, the surface marker for M1 and CD163 representing M2. The results revealed the low expression of M1 (CD68) in keloid tissue meanwhile high levels of M1 were detected in normal scars. We also detected that higher tissue expression of M2 (CD163) was significantly associated with keloid cases when compared to low M2 expression in the control group. An important finding that was discovered during our study is that the M1 and M2 are significant predictors of keloid. Every increase of 1 ng/mL in M1 decreases the risk of keloid by 0.99 while every increase of one unit in M2 increases the risk of keloid by 2.01. This study concluded that the keloid formation could be a result of an abnormal response to tissue injury where there is an excessive entry of inflammatory cells into the wound, including macrophages and that the keloid incidence might be related to a decrease in M1 and an increase in M2. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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