# Association between intestinal microbiota, inflammation and kidney disease in HIV

> **NIH NIH P01** · BAYLOR COLLEGE OF MEDICINE · 2020 · $107,294

## Abstract

PROJECT SUMMARY/ABSTRACT 
 It is increasingly clear that the intestinal microbiota plays a critical role in both normal host physiology as 
well as pathology during disease states. There is a growing body of data that changes in the microbiota are 
associated with many inflammatory diseases, however it is unclear if these changes initiate or support disease 
severity and progression. Data from animal models support both inflammatory conditions inducting dysbiosis 
as well as dysbiosis leading to disease, but the data supporting microbial dysbiosis causing disease in humans 
is less convincing. In HIV, a number of studies have identified intestinal dysbiosis which correlates with 
increased translocation of microbes and microbial products into the bloodstream and is thought to partially 
underlie the chronic inflammation observed in HIV patients. This increased systemic inflammation is thought to 
drive many of the co-morbidities associated with HIV including chronic kidney disease (CKD). We believe a 
positive feedback loop exists in HIV where disease pathology leads to dysbiosis and increased translocation of 
microbes and microbial products resulting in systemic inflammation and HIV associated comorbidities including 
CKD. In parallel, we believe HIV expression in kidney cells leads to reduced kidney function and induces 
intestinal dysbiosis and increased mucosal translocation through breakdowns in the intestinal barrier. We 
hypothesize that systemic inflammation and kidney disease drive each other through their combined effects on 
the microbiota. We believe manipulation of the microbiota will short circuit this loop and limit CKD in HIV+ 
patients. 
 We will use a combination of mouse models and primary patient analyses to test our hypotheses. We will 
take advantage of our established mouse model of HIV associated kidney disease, Tg26 mice. We observe 
differential disease progression correlated with differences in the microbiota. We will colonize germfree Tg26 
mice with different microbes to identify and characterize pathways impacted by differences in microbiota 
composition that impacts disease with the goal of identifying therapeutic interventions. Previous human studies 
have not addressed the combined effect of HIV and kidney disease on the intestinal microbiota. We will apply 
our expertise in microbiome compositional and functional analysis and in HIV-associated kidney disease, to 
understand the interrelationship between HIV, microbial dysbiosis, and kidney disease in an HIV+ patient 
population. Understanding the relationship between HIV, kidney disease and intestinal dysbiosis would open 
avenues for novel therapeutic strategies targeted toward prevention of CKD-related complications in HIV+ 
individuals. 
Aim 1: Determine if gastrointestinal microbiome shifts in Tg26 mice underlie kidney disease 
progression. 
Aim 2. Determine if the intestinal microbiota offers protection from kidney disease progression in an 
animal model of...

## Key facts

- **NIH application ID:** 9966965
- **Project number:** 5P01DK056492-20
- **Recipient organization:** BAYLOR COLLEGE OF MEDICINE
- **Principal Investigator:** PAUL Evan KLOTMAN
- **Activity code:** P01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $107,294
- **Award type:** 5
- **Project period:** — → —

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9966965

## Citation

> US National Institutes of Health, RePORTER application 9966965, Association between intestinal microbiota, inflammation and kidney disease in HIV (5P01DK056492-20). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/9966965. Licensed CC0.

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