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May 16, 2026Frontiers in Cell and Developmental BiologyOpen Access

Monocytes and neutrophils promote cardiac fibroblast pro-fibrotic phenotypes through IL-6 and MIF

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Why the study?

The mechanisms linking early inflammation, immune cell recruitment, fibroblast activation, and the perpetuation of cardiac fibrosis remain unclear.

Population

Primary human cardiac fibroblasts, THP-1, HL-60, primary human monocytes, and neutrophils

Comparison

Direct co-culture or conditioned media vs controls, with recombinant cytokines or blocking antibodies

Design

In vitro controlled laboratory study

Key result

Monocytes and neutrophils, through the secretion of IL-6 and MIF, significantly promoted human cardiac fibroblast pro-fibrotic phenotypes including contractility, migration, and matrix deposition.

Authors

ZCZhongxiao CongAÍAleksandar ÍveticMPM Parsons

Discussion

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Overview

Elucidates inflammation-fibroblast links in fibrosis; leaves open whether targeting these mechanisms alters heart-failure progression.

Key Points

  • This research aims to uncover the mechanisms by which immune cells influence cardiac fibroblast activation and fibrosis.
  • Used cell-derived matrices and collagen gels to study primary human cardiac fibroblast responses.
  • Conducted co-culture experiments with primary human cardiac fibroblasts and immune cells THP-1 and HL-60.
  • Analyzed cytokine levels and function blocking effects using recombinant proteins and antibodies.
  • Co-culture of fibroblasts with THP-1 and HL-60 cells increased collagen gel contraction (p<0.05).
  • MIF and IL-6 levels were significantly upregulated in co-cultures (p<0.01).
  • IL-6 neutralizing antibody reduced THP-1 induced fibroblast migration (p<0.05).

Structured PICO

P
Population
Primary human cardiac fibroblasts (HCF), THP-1 cells, HL-60 cells, primary human monocytes, and neutrophils
I
Intervention
Co-culture with immune cells or conditioned media; treatment with recombinant MIF and IL-6 or neutralizing antibodies
C
Comparator
HCF cultured alone (control)
O
Outcome
HCF pro-fibrotic response (collagen gel contraction and cell migration)surrogate

Early exposure of human cardiac fibroblasts to monocytes and neutrophils promotes pro-fibrotic phenotypes via IL-6 and MIF, identifying potential therapeutic targets to prevent adverse cardiac remodeling.

Limitations

  • Short-term exposure to immune cells may not recapitulate in vivo settings where immune cells persist and dynamically shift in phenotype.
  • The model does not account for the contributions of other cell types present in cardiac tissue.
  • Did not assess IL-6 and MIF contributions to early disease features in vivo.
  • Immune cell types were introduced in equal numbers, which may not fully reflect their physiological ratios in vivo.

Cite This Study

Cong et al. (2026) studied Cardiac fibrosis. Monocytes, neutrophils, IL-6, and MIF vs. HCF alone was evaluated on Collagen gel contraction, migration, and extracellular matrix deposition. Monocytes and neutrophils, through the secretion of IL-6 and MIF, significantly promoted human cardiac fibroblast pro-fibrotic phenotypes including contractility, migration, and matrix deposition.

synapsesocial.com/papers/6a0808ffa487c87a6a40b086https://doi.org/10.3389/fcell.2026.1830777
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