# CAUSE Clinical Research Center New York (CAUSE-CRC)

> **NIH NIH U01** · COLUMBIA UNIVERSITY HEALTH SCIENCES · 2024 · $460,689

## Abstract

Project Summary/Abstract
Pediatric asthma disproportionately impacts children who live in urban communities partly due to environmental
exposure to allergens, stress and air pollution. This project establishes a Clinical Research Center to conduct
both network-wide and site-specific clinical studies and trials with the ultimate goal of developing effective asthma
treatment or prevention approaches applicable to children residing in low-income urban settings. For a significant
number of asthma patients, guideline-directed treatment does not achieve disease control, suggesting the need,
and potential benefit, for treatment(s) that are personalized to the phenotype of these patients. As evident by
cluster analyses in adults and children, there is a group of severe asthmatics that have fewer characteristics of
type 2 inflammation and in whom type 2 cytokine-targeting biologics may be less effective. Children living in
inner-cities are exposed and sensitized to allergens, particularly cockroach, triggering type 2 inflammatory
response and exposed to high levels of indoor and outdoor irritants and pollutants which can trigger TH1 and
TH17 neutrophilic inflammation. There is a need to have a better understanding of mechanisms of non-atopic
asthma. Systemic inflammation with IL-6 as a biomarker is a mechanism that is postulated to mediate asthma
severity. IL-6 is produced by cells of the immune system and secreted by airway epithelial cells and has been
proposed as a potential target for asthma therapy. While cytokine and soluble receptor levels, as well as genetic
studies of IL-6R have been examined in relation to asthma, the intrinsic capacity for the receptor to signal within
differing phenotypic populations has not. The objective of this study is to determine whether intrinsic signaling
responses to circulating IL6 and other cytokines differs between cockroach negative, lower atopic children and
cockroach allergic, higher atopic children with moderate to severe asthma. We hypothesize that and the
relationship of IL-6 receptor signaling to morbidity. We hypothesize that genetic polymorphisms will modify
intrinsic IL-6 signaling and that IL-6 signaling will be a determinant of morbidity. The protocol will test exploratory
hypotheses that pollution and stress lead to exacerbations in those with higher intrinsic signaling.
To test this hypothesis, we propose a study designed to identify differences in intrinsic IL-6 signaling in children
with asthma. The study will include children who: 1) are between the ages of 6 and 20 years; 2) have a history
of recurrent wheeze / persistent asthma of at least one year duration; and 3) live in low-income census tracts of
U.S. inner-city communities. Studies of intrinsic IL-6 signaling and SNP carrier status will be done on peripheral
blood mononuclear cells (PBMC) at baseline. These studies will be done on nasal epithelial cells on a subset
of participants. We propose a 12-month follow up at 3-month intervals to pros...

## Key facts

- **NIH application ID:** 10823243
- **Project number:** 5U01AI160075-04
- **Recipient organization:** COLUMBIA UNIVERSITY HEALTH SCIENCES
- **Principal Investigator:** Meyer Kattan
- **Activity code:** U01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $460,689
- **Award type:** 5
- **Project period:** 2021-04-22 → 2028-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10823243

## Citation

> US National Institutes of Health, RePORTER application 10823243, CAUSE Clinical Research Center New York (CAUSE-CRC) (5U01AI160075-04). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/10823243. Licensed CC0.

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