Fibrosis Assay Services

Fibrosis is characterized by excessive deposition of extracellular matrix due to exaggerated repair in response to damage. Common features include the involvement of inflammation, appearance of myofibroblasts, and changes in epithelial cells and macrophages. The complex interactions between various cell types involved demand IPF disease-relevant in vitro fibrosis models and in vivo models to enable the discovery and development of new drugs for this fibrotic rare disease.

  • Epithelial-to-mesenchymal (EMT) assay: Primary human bronchial epithelial cells derived from IPF patients and healthy donors are stimulated with TGF-β1. The transdifferentiation of epithelial cells into motile mesenchymal cells is measured with biomarker fibronectin (FN1) via high-content imaging.
  • Fibroblasts-to-myofibroblasts (FMT) assay: Primary human bronchial fibroblasts derived from IPF patients and healthy donors are stimulated with TGF-β1. The transdifferentiation of fibroblasts-to-myofibroblasts is measured with biomarker alpha-smooth muscle actin (αSMA) via high-content imaging.
  • M1 polarization assay: M1 polarization of monocytes is measured by TNF-α secretion via the MSD platform in primary human blood cells derived from healthy donors.
  • M2 polarization assay: M2 polarization of monocytes is measured by CCL18 secretion via ELISA in IL-4/IL-10 induced primary human blood cells derived from healthy donors.
Scientific Poster

Scientific Poster entitled two in vitro assays relevant to lung fibrosis for evaluating the potency and efficacy of prospective anti-fibrotic drugs.
Two in vitro assays relevant to lung fibrosis for evaluating the potency and efficacy of prospective anti-fibrotic drugs.

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Additional fibrosis capabilities we offer include:

  • Fibroblast migration – scratch assay; wound closure
  • Epithelial migration – scratch assay; wound closure
  • Fibroblast gel contractility
  • Fibroblast impedance – contractility
  • Hepatic stellate cell to myofibroblast transition

 

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Fibrosis Assay FAQs

  • How do myofibroblasts impact IPF?

    Since myofibroblasts localize at sites undergoing active matrix deposition and display elevated collagen synthetic capacity, myofibroblasts are considered to play a major role in the pathology of IPF.

  • Why are TGF-β1, αSMA, and FN1 indicators of IPF?

    The well-established key fibrogenic mediator, transforming growth factor TGF-β1, induces FMT. In cells that have undergone FMT, increased expression of αSMA is observed and positively correlates with contraction of myofibroblast-populated collagen gels, indicating that αSMA is a strong marker of myofibroblast differentiation. Hence, a relevant readout for lung fibrosis. In cells that have undergone EMT, there is an increased synthesis of FN1, an important component of the extracellular matrix. Therefore, these substances are relevant readouts for lung fibrosis.

  • What is the role of monocytes and macrophages?

    Monocytes and macrophages are critical effectors and regulators of the innate immune response. Through their ability to clear pathogens and elicit an immune response, these cells play a key role in protecting the host but also contribute to the pathogenesis of inflammatory and degenerative diseases. Reprogramming of macrophages can be an interesting option for the treatment of diseases like cancer and autoimmune conditions.

  • What is the difference between M1 and M2 macrophages?

    Classically activated M1 macrophages are pro-inflammatory cells, which promote Th1 responses and tumoricidal activity. Alternatively, activated M2 macrophages have anti-inflammatory functions and elicit tissue repair responses, fibrosis, tumor growth, and progression.