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Macrophage polarisation in caesarean scar diverticulum
  1. Jinfa Huang1,
  2. Xiaochun Liu2,
  3. Yi Hou3,
  4. Yixuan Liu1,
  5. Kedan Liao1,
  6. Ning Xie1,
  7. Kaixian Deng1
  1. 1 Department of Gynecology, Shunde Hospital of Southern Medical University, Foshan, Guangdong, China
  2. 2 Department of Gynecology, Southern Medical University Affiliated Maternal & Child Health Hospital of Foshan, Foshan, Guangdong, China
  3. 3 Department of Bioinformatics, Guangzhou Regenerative Medicine and Health-Guangdong Laboratory, Guangzhou, Guangdong, China
  1. Correspondence to Dr Kaixian Deng, Department of Gynecology, Shunde Hospital of Southern Medical University, Foshan, Guangzhou, China; nsyfek{at}163.com

Abstract

Aims To determine immunohistochemical features and correlations between M1/M2 polarisation status with disease severity of post-caesarean scar diverticulum (CSD).

Methods Histological and immunohistological stainings were performed and inflammatory (CD16, CD163 and tumour necrosis factor-α (TNF-α)), fibrosis (α-smooth muscle actin (α-SMA)) and angiogenic (CD31) markers were examined in uterine tissues collected from patients with uterine scar diverticula (CSD) (n=37) and caesarean section (CS) (n=3).

Results CSD tissues have higher expression of α-SMA, TNF-α, CD16 and CD31 and lower expression of CD163 than CS tissue (p<0.05). Compared with adjacent tissues, thick-walled blood vessels, glands and fibrotic sites have higher expression of α-SMA, TNF-α and CD16. Statistical correlation was observed between the expression of CD16 and TNF-α (R=0.693, p<0.001), α-SMA (R=0.404, p<0.05) and CD31 (R=0.253, p<0.05) in CSD tissues, especially with the ratio of CD16/CD163 (R=0.590, p<0.01). A more significant difference was observed between the expression of CD16/CD163 and α-SMA (R=0.556, p<0.001), TNF-α (R=0.633, p<0.0001) and CD31 (R=0.336, p<0.05).

Conclusions In this study, TNF-α, α-SMA, CD16 and CD31 proteins were overexpressed in all CSD cases, and CD16/CD163 was positively correlated with tissue inflammation, fibrosis and neovascularisation. Abnormal mononuclear macrophage infiltration may be involved in the origin and progression of CSD.

  • inflammation
  • macrophages
  • uterus
  • fibrosis

Data availability statement

Data are available upon reasonable request. All data relevant to the study are included in the article or uploaded as supplementary information.

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Data availability statement

Data are available upon reasonable request. All data relevant to the study are included in the article or uploaded as supplementary information.

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Footnotes

  • Handling editor Mona El-Bahrawy.

  • Contributors KD conceptualised the study design and supervised the analysis. JH conducted the experiments, performed the statistical analysis and wrote the paper. XL prepared the samples. YH revised the manuscript. YL, NX and KL provided supervision of the analysis and prepared the article. All authors read and approved the final manuscript. JH is responsible for the overall content as the guarantor.

  • Funding This work was supported by the Foshan Science and Technology Bureau (2020001006077).

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.

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