Tumor-associated macrophage expression in colorectal adenomas and carcinomas: relationship to Helicobacter pylori

Wenming Wang1,2, Yueyong Zhu1, Yunchao Zhu2

  • 1Liver Disease Diagnosis and Treatment Center, The First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian, China.

Frontiers in Oncology
|December 15, 2025
PubMed
Abstract

Insights

Helicobacter pylori infection is linked to increased CD163+ and CD86+ tumor-associated macrophages in colorectal lesions. These macrophages are associated with lesion progression and CRC development, influenced by H. pylori.

Area of Science:

  • Oncology
  • Immunology
  • Gastroenterology

Background:

  • Tumor-associated macrophages (TAMs) play a crucial role in colorectal cancer (CRC) progression.
  • CD163+ and CD86+ TAMs are key subsets involved in tumor microenvironment modulation.
  • Helicobacter pylori (H. pylori) infection is a known risk factor for gastric cancer and may influence colorectal neoplasia.

Purpose of the Study:

  • To investigate the association between H. pylori infection and the expression of CD163+ and CD86+ TAMs in colorectal adenoma (CRA) and CRC.
  • To analyze how H. pylori infection and other factors influence TAM expression during colorectal lesion progression.

Main Methods:

  • Immunohistochemistry (IHC) and multiplex immunofluorescence (mIF) were used to quantify CD163+ and CD86+ TAMs in colorectal tissues.
  • The 14C-urea breath test (UBT) was employed to detect H. pylori infection.
  • Statistical analyses, including multiple linear regression, were performed to assess correlations.

Main Results:

  • Colorectal lesion progression was significantly associated with increased CD163+ and CD86+ TAMs, and H. pylori infection (P < 0.05).
  • H. pylori-infected patients showed significantly higher TAM expression compared to non-infected individuals (P < 0.05).
  • TAM expression correlated positively with lesion severity, adenoma size (≥ 1 cm), and CRC in obese patients.

Conclusions:

  • CD163+ and CD86+ TAM expression dynamically changes with colorectal lesion progression.
  • H. pylori infection, adenoma size, tumor differentiation, and patient metabolic status significantly influence TAM expression in colorectal neoplasia.