pulmonary fibrosis

Respiratory Assays

Pulmonary Fibrosis

Q: What models are used to study pulmonary fibrosis?

Cellomatics employs a range of advanced in vitro and ex vivo models, including primary human lung fibroblast activation assays and epithelial–mesenchymal transition (EMT) systems. These models are supported by the use of primary human cells and disease-relevant culture conditions to better replicate fibrotic pathology and improve translational relevance.

Q: How do these services support early-phase research?

Screening cascades include assays for myofibroblast differentiation, collagen deposition, and pro-fibrotic cytokine production, enabling identification of promising anti-fibrotic candidates. These workflows are integrated at Cellomatics with high-content analysis and molecular readouts to deliver robust, mechanism-focused data that supports early decision-making.

Q: Can biomarker analysis be performed?

Yes. Multiplex assays and high-content imaging are used to quantify fibrosis-related biomarkers and assess compound efficacy.

Q: What makes these services unique?

Cellomatics combines advanced assay platforms with human-relevant models, including primary cells, to generate data that better reflects clinical biology.

Q: Is bespoke assay development available?

Yes. Custom assays can be developed to target specific fibrotic pathways, ensuring alignment with the mechanism of action of therapeutic candidates. This is supported at Cellomatics through close collaboration with clients, combining primary human cell models, pathway-specific readouts, and tailored assay design to generate precise, mechanism-driven data for fibrosis research.

Idiopathic pulmonary fibrosis (IPF) is the commonest interstitial lung disease (ILD) and is characterised by progressive scarring of the lungs. An impaired pulmonary wound healing response following lung injury coupled with excessive production of collagens leads to a pathogenic lung fibrosis. Our Fibrosis Drug Development Services support researchers investigating the underlying mechanisms of pulmonary fibrosis and evaluating novel therapeutic strategies.

These Fibrosis Drug Development Services provide robust in vitro data that can help accelerate the identification and optimisation of anti-fibrotic drug candidates.

Inflammatory mediators – TGFβ stimulation

Pirfenidone modulates TGFβ-induced cytokine release in primary human lung fibroblasts.

Primary human lung fibroblasts were pre-treated with pirfenidone, then stimulated with TGFβ; supernatants analysed by Luminex multiplex for a panel of cytokines (n=3) (Stats: one-way ANOVA; n as stated; mean ± SEM; *p<0.05, **p<0.01, ***p<0.001)

Extracellular Matrix Deposition

TGFβ-induced gene expression is modulated by Pirfenidone.

Primary Human Lung Fibroblasts pre-treated with Pirfenidone for 1 hour then stimulated with TGFβ for 24 hours followed by QuantiGene multiplex gene expression; n=3. (Stats: one-way ANOVA; n as stated; mean ± SEM; *p<0.05, **p<0.01, ***p<0.001)

Inflammatory mediators – TGFβ stimulation

Pirfenidone modulates TGFβ-induced cytokine release in IPF lung fibroblasts.

Primary human lung fibroblasts (IPF donor) were pre-treated with pirfenidone (1 hour) then stimulated with TGFβ (48 hours); supernatants analysed by Luminex Assay for a panel of inflammatory and extracellular matrix markers; n=3 (Stats: one-way ANOVA; n as stated; mean ± SEM; *p<0.05, **p<0.01, ***p<0.001)

Collagen Biomarkers and ROS production with H2O2

Pirfenidone attenuates H2O2-induced collagen gene expression and reduces intracellular ROS in primary human lung fibroblasts.

Primary human lung fibroblasts pre-treated with Pirfenidone then stimulated with H2O2. [A] Collagen gene expression measured by QuantiGene multiplex and [B] intracellular ROS measured using a fluorescence detection kit; n=3 (Stats: one-way ANOVA; n as stated; mean ± SEM; *p<0.05, **p<0.01, ***p<0.001)

EMT: Epithelial to mesenchymal transition following TGFβ stimulation

TGF-β induces α-SMA mRNA expression in A549 cells and SB525334 inhibits this effect in A549 cells (IC50 12 nM).

A.A549 cells treated with TGF-β (2.5–10 ng/mL) for 6 or 24 h; α-SMA mRNA quantified by qPCR; n=3 (Stats: one-way ANOVA; n as stated; mean ± SEM)

B.A549 cells treated with TGF-β (1.25–10 ng/mL) for 72 hours; α-SMA protein quantified by Western Blotting.

C.A549 cells treated with TGF-β ± SB525334 (dose response); α-SMA mRNA measured by qPCR; CRC illustrating SB525334 potency, IC50: 12 nM. n=6 (Stats: one-way ANOVA; n as stated; mean ± SEM; *p<0.05, **p<0.01, ***p<0.001.)

Proliferation with PDGF stimulation

Nintedanib modulates PDGF-driven proliferation in IPF lung fibroblasts.

IPF human pulmonary fibroblasts were pre-treated with nintedanib prior to PDGF stimulation for 72 hours; Cell Titer-Glo quantification (n=3) (Stats: one-way ANOVA; n as stated; mean ± SEM; *p<0.05, **p<0.01, ***p<0.001.)

Inflammation – Cytokine Release

Nintedanib modulates cytokine release in IPF fibroblasts.

Human lung fibroblasts from idiopathic pulmonary fibrosis (IPF) donors were treated with nintedanib ± TGF-β for 24–72 hours; cytokines in culture supernatants were measured by ELISA; n=3 technical replicates.

Inflammation – Cytokine Release (cont.)

Nintedanib alters cytokine release by IPF lung fibroblasts.

Human IPF lung fibroblasts (3 donors) treated with nintedanib ± TGF-β for 24–72 h; panel of cytokines quantified in supernatants (n=3) and expressed in pg/mL.

Inflammation – Gene expression

Nintedanib modulates gene expression in IPF lung fibroblasts.

IPF human lung fibroblasts (3 donors) were treated with nintedanib ± TGF-β for 24–72 h; gene expression fold change vs TGF-β–stimulated condition was measured (n=3 technical replicates).

These Fibrosis Drug Development Services provide robust in vitro data that can help accelerate the identification and optimisation of anti-fibrotic drug candidates.

FAQ's

What models are used to study pulmonary fibrosis?

Cellomatics employs a range of advanced in vitro and ex vivo models, including primary human lung fibroblast activation assays and epithelial–mesenchymal transition (EMT) systems. These models are supported by the use of primary human cells and disease-relevant culture conditions to better replicate fibrotic pathology and improve translational relevance.

How do these services support early-phase research?

Screening cascades include assays for myofibroblast differentiation, collagen deposition, and pro-fibrotic cytokine production, enabling identification of promising anti-fibrotic candidates. These workflows are integrated at Cellomatics with high-content analysis and molecular readouts to deliver robust, mechanism-focused data that supports early decision-making.

Can biomarker analysis be performed?

Yes. Multiplex assays and high-content imaging are used to quantify fibrosis-related biomarkers and assess compound efficacy.

What makes these services unique?

Cellomatics combines advanced assay platforms with human-relevant models, including primary cells, to generate data that better reflects clinical biology.

Is bespoke assay development available?

Yes. Custom assays can be developed to target specific fibrotic pathways, ensuring alignment with the mechanism of action of therapeutic candidates. This is supported at Cellomatics through close collaboration with clients, combining primary human cell models, pathway-specific readouts, and tailored assay design to generate precise, mechanism-driven data for fibrosis research.

Request a consultation with Cellomatics Biosciences today

Our experienced team of in vitro laboratory scientists will work with you to understand your project and provide a bespoke project plan with a professional, flexible service and a fast turnaround time. Cellomatics offers customised Fibrosis Drug Development Services to assist biotechnology and pharmaceutical companies in advancing fibrosis-focused research programmes.

To request a consultation where we can discuss your exact requirements, please contact Cellomatics Biosciences.