# The Role of Chronic Lung Disease in the Generation of Rheumatoid Arthritis Associated Antibodies

> **NIH NIH P20** · UNIVERSITY OF KANSAS MEDICAL CENTER · 2024 · $233,320

## Abstract

ABSTRACT
Idiopathic pulmonary fibrosis (IPF) is a progressive, scarring lung disease that, while rare, significantly impacts
survival for patients. The time to death from diagnosis for idiopathic pulmonary fibrosis patients is worse than
most solid cancers (except lung and pancreas). Despite the impact of this condition, treatments only slow
progression of the scarring in the lung and have yet to be able to impact survival or quality of life. The only “cure”
for IPF remains lung transplantation, which has a 50% survival at 5-years despite the significant medical
resources required. These patients need new therapies and deserve a better understanding of the disease to
inform clinical practice. Therefore, the overall objective of this proposal is to identify novel mechanisms and
markers of IPF lung injury. Our central hypothesis is that biologic and biochemical perturbations that occur in the
lung microenvironment of IPF patients will elucidate novel mechanisms of lung injury in IPF to advance precision
diagnostics and elucidate future targets to develop precise treatments. To begin to attain this overall objective,
we will pursue the following two Specific Aims. Our first aim is to identify differences in spatial gene expression
in areas of fibrosis and inflammation in lung tissue from IPF patients that correlate to survival. Our second aim
is to identify differential protein and metabolite levels in BALF from IPF patients that correlate to survival. We
propose to combine an established and well-characterized, large cohort of patients with a rare disease and
stored samples that are no longer collected in modern clinical or research eras (surgical lung biopsy tissue) with
cutting edge precision medicine tools like spatial transcriptomics and label-free quantitative proteomics and
metabolomics. Importantly, this cohort has paired lung fluid samples (bronchoalveolar lavage fluid) which allows
us to identify markers of these novel IPF phenotypes in the lung in a clinically accessible compartment via
bronchoalveolar lavage. This innovative proposal will define groups of IPF patients with unique molecular and/or
biologic pathways that can set the stage for prospective biomarker guided, therapeutic interventional trials.
Additionally, these findings will help us understand for the first time how IPF patients with poor survival are
different from those with better survival using precision medicine approaches at the individual molecular, protein
and metabolite level.

## Key facts

- **NIH application ID:** 10849364
- **Project number:** 2P20GM130423-06
- **Recipient organization:** UNIVERSITY OF KANSAS MEDICAL CENTER
- **Principal Investigator:** Scott Michael Matson
- **Activity code:** P20 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $233,320
- **Award type:** 2
- **Project period:** 2019-02-15 → 2029-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10849364

## Citation

> US National Institutes of Health, RePORTER application 10849364, The Role of Chronic Lung Disease in the Generation of Rheumatoid Arthritis Associated Antibodies (2P20GM130423-06). Retrieved via AI Analytics 2026-05-25 from https://api.ai-analytics.org/grant/nih/10849364. Licensed CC0.

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