# Interaction with Rip2 and IL-17 in Chronic Lung Infection

> **NIH NIH R01** · CEDARS-SINAI MEDICAL CENTER · 2020 · $321,840

## Abstract

Abstract
In this Administrative supplement (PA-18-591) to supplement an existing NIH RO1 to investigate Alzheimer’s
Disease, the original parent RO1 investigates the role of IL-17 signaling during Chlamydia Pneumonia (CP)
infection and chronic lung inflammation. In this administrative supplement, we will investigate the role of
Chlamydia pneumoniae infection in accelerating disease progression in Alzheimer's Disease (AD) utilizing the
AD mouse model ( APPSWE/PS1∆E9 mice). We also propose to determine the role and relevance of the Rip2/IL-
17 axis in Alzheimer's Disease as well as CP infection-mediated acceleration of Alzheimer's Disease using the
experimental model of AD, APPSWE/PS1∆E9 mice. Alzheimer's Disease (AD), a progressive irreversible senile
dementia, is the sixth leading cause of death in elderly, with an estimated 5.7 million Americans afflicted by this
debilitating disorder. These numbers are expected to double in the next 20 years presenting a significant
emotional and economic burden. Early hypotheses into the development of AD included infectious paradigms,
but these ideas were largely discarded. However, new data has led researchers to once again suggest that
infections may play a developmental and or accelerating role in AD progression. Among infectious organisms,
Chlamydia pneumoniae has been identified as the leading candidate for a pathogenic role in AD. CP, a
common cause of community acquired pneumonia, has been linked with many chronic inflammatory diseases,
including atherosclerosis, asthma, lung cancer, as well as AD. Studies also suggest that IL-17 inflammatory
cytokine may play a detrimental role in Neuroinflammatory diseases, including AD, but the specific role of IL-17
in AD pathogenesis is not known. Based on the large amount of data in the published literature presented above,
we hypothesize that Chlamydia pneumonia infection plays a role in progression and or development of
Alzheimer's Disease and that IL-17 induction and the IL-17 induced neuroinflammation may be responsible for
Chlamydia pneumonia infection-mediated acceleration of AD. Our expertise in CP infections and immune
responses such as IL-17 induced inflammation, in combination with our collaborator’s world-wide expertise in
AD and Ad mouse models, allows us a unique opportunity to investigate the relationship between Chlamydia
pneumoniae infection and Alzheimer’s Disease progression using a well-accepted and relevant experimental
murine model of AD. We hypothesize that CP infection plays a role in progression and or development of
Alzheimer's Disease and that IL-17 induction by this infection is the mechanism by which the CP infection
accelerates the brain pathology of AD. The two specific aims proposed are; Aim 1: To determine the role of
Chlamydia pneumoniae infection in accelerating disease progression in Alzheimer's Disease in a murine model
of AD ( APPSWE/PS1∆E9 mice). Aim 2: To determine the role and relevance of the Rip2/IL-17 axis in Alzheimer's...

## Key facts

- **NIH application ID:** 10144869
- **Project number:** 3R01AI117968-05S1
- **Recipient organization:** CEDARS-SINAI MEDICAL CENTER
- **Principal Investigator:** Moshe Arditi
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $321,840
- **Award type:** 3
- **Project period:** 2020-08-03 → 2021-01-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10144869

## Citation

> US National Institutes of Health, RePORTER application 10144869, Interaction with Rip2 and IL-17 in Chronic Lung Infection (3R01AI117968-05S1). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10144869. Licensed CC0.

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