# Alcohol, bacterial dysbiosis, and inflammation during colitis

> **NIH NIH F30** · LOYOLA UNIVERSITY CHICAGO · 2020 · $50,520

## Abstract

Project Summary/Abstract
The goal of this project is to better understand how the intestinal epithelial cells and bacterial populations can
be altered by alcohol in the setting of intestinal inflammation. There are two main forms of inflammatory bowel
disease: Crohn's disease (CD) and ulcerative colitis (UC). UC is an inflammatory disease of the large intestine
with unknown etiology that affects more than three million individuals globally. These patients experience
periodic episodes of disease reactivation characterized by severe abdominal discomfort and bloody diarrhea,
often requiring hospitalization. Triggers of flares appear to be multifactorial but can be precipitated by certain
foods. Current guidelines recommend for physicians to caution UC patients against drinking alcohol, yet only a
few studies have examined the effects of alcohol in UC. One study found that patients with increased alcohol
consumption had increased rates of UC disease relapse, while another found that alcohol consumption
increased gastrointestinal symptoms associated with UC. Despite the implications of these studies, a
mechanism for alcohol-mediated relapse in UC or exacerbation of gastrointestinal symptoms is not defined.
Intestinal bacterial changes are common in UC patients and individuals with alcohol use. Altered intestinal
bacterial populations that are persistent can lead to intestinal tissue damage and perpetuate a cycle of
inflammation. In our lab, we developed a model to study UC and alcohol use. Mice are treated with dextran
sulfate sodium (DSS), which recapitulates aspects of the UC disease, followed by a binge ethanol treatment.
Mice that received the DSS and ethanol treatment had increases in intestinal tissue damage compared to mice
that received DSS only. This was accompanied by alterations in bacterial populations, i.e., increased
Enterobacteriaceae, that have been observed in UC. Furthermore, we identified increased expression of Nos2
which produces metabolites that can be used by Enterobacteriaceae. This led us to hypothesize that in the
setting of DSS-induced colitis, alcohol promotes expression of Nos2 in the intestine, which provides substrates
that allow for Enterobacteriaceae overgrowth. The increased Enterobacteriaceae exacerbates intestinal
damage. In Aim 1 we will determine if increased Nos2 expression leads to increased Enterobacteriaceae after
DSS and ethanol treatment. In Aim 2 we will determine if Nos2-mediated increase in Enterobacteriaceae
results in increased intestinal pathology. Overall, this study will aid in our understanding of the inflammatory
and bacterial changes that occur due to alcohol in UC.

## Key facts

- **NIH application ID:** 9854731
- **Project number:** 5F30AA027442-02
- **Recipient organization:** LOYOLA UNIVERSITY CHICAGO
- **Principal Investigator:** Paulius Kuprys
- **Activity code:** F30 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $50,520
- **Award type:** 5
- **Project period:** 2018-12-01 → 2021-11-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9854731

## Citation

> US National Institutes of Health, RePORTER application 9854731, Alcohol, bacterial dysbiosis, and inflammation during colitis (5F30AA027442-02). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/9854731. Licensed CC0.

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