Omentin-1 inhibits the development of benign prostatic hyperplasia by attenuating local inflammation

Mol Med. 2024 Mar 22;30(1):41. doi: 10.1186/s10020-024-00805-y.

Abstract

Background: Benign prostatic hyperplasia (BPH) is a prevalent disease affecting elderly men, with chronic inflammation being a critical factor in its development. Omentin-1, also known as intelectin-1 (ITLN-1), is an anti-inflammatory protein primarily found in the epithelial cells of the small intestine. This study aimed to investigate the potential of ITLN-1 in mitigating BPH by modulating local inflammation in the prostate gland.

Methods: Our investigation involved two in vivo experimental models. Firstly, ITLN-1 knockout mice (Itln-1-/-) were used to study the absence of ITLN-1 in BPH development. Secondly, a testosterone propionate (TP)-induced BPH mouse model was treated with an ITLN-1 overexpressing adenovirus. We assessed BPH severity using prostate weight index and histological analysis, including H&E staining, immunohistochemistry, and enzyme-linked immunosorbent assay. In vitro, the impact of ITLN-1 on BPH-1 cell proliferation and inflammatory response was evaluated using cell proliferation assays and enzyme-linked immunosorbent assay.

Results: In vivo, Itln-1-/- mice exhibited elevated prostate weight index, enlarged lumen area, and higher TNF-α levels compared to wild-type littermates. In contrast, ITLN-1 overexpression in TP-induced BPH mice resulted in reduced prostate weight index, lumen area, and TNF-α levels. In vitro studies indicated that ITLN-1 suppressed the proliferation of prostate epithelial cells and reduced TNF-α production in macrophages, suggesting a mechanism involving the inhibition of macrophage-mediated inflammation.

Conclusion: The study demonstrates that ITLN-1 plays a significant role in inhibiting the development of BPH by reducing local inflammation in the prostate gland. These findings highlight the potential of ITLN-1 as a therapeutic target in the management of BPH.

Keywords: Benign prostatic hyperplasia; Inflammation; Intelectin-1; Macrophages; Omentin-1; Prostate epithelial cells.

MeSH terms

  • Animals
  • Cytokines / genetics
  • Cytokines / metabolism
  • GPI-Linked Proteins* / genetics
  • GPI-Linked Proteins* / metabolism
  • Inflammation / pathology
  • Lectins* / genetics
  • Lectins* / metabolism
  • Male
  • Mice
  • Plant Extracts / pharmacology
  • Prostate / metabolism
  • Prostate / pathology
  • Prostatic Hyperplasia* / drug therapy
  • Prostatic Hyperplasia* / genetics
  • Prostatic Hyperplasia* / metabolism
  • Tumor Necrosis Factor-alpha

Substances

  • Cytokines
  • GPI-Linked Proteins
  • Lectins
  • Plant Extracts
  • Tumor Necrosis Factor-alpha
  • Itln1 protein, mouse