# Social Disadvantage and Its Impact on Pathogen Burden and Immune Dysfunction Across the Life Course

> **NIH NIH R00** · UNIVERSITY OF MICHIGAN AT ANN ARBOR · 2022 · $249,000

## Abstract

Project Summary
 The process of aging often leads to increased disability, loss of physical functioning, cognitive decline,
and development of multiple chronic diseases. One critical driver of this process is senescence of the immune
system, or immunosenescence, which is known to be associated with chronic inflammation. However,
emerging evidence also points to immune dysfunction resulting from continual assault on the immune system
by multiple persistent infections. Together, these infections and resulting immune dysfunction set in motion a
cascade of events leading to accelerated immunosenescence. Accelerated immunosenescence may then be a
driver of health disparities later in life. New research suggests disparities in immune dysfunction across the life
course can be linked to social disadvantage extending back to childhood. A critical knowledge gap is how
early-life social disadvantage accelerates immunosenescence through immune dysfunction.
 The objective of the proposed research is to explore pathogen burden as a critical mediator in the
pathway from childhood social disadvantage to accelerated aging, as measured by inflammation and immune
dysfunction. To test this hypothesis, I will first define the association between childhood social disadvantage
and pathogen burden across the life course (Aim 1). Childhood social disadvantage is defined by both low
socioeconomic status and experiences of stressors, such as parental death or physical abuse, before 18 years
of age. I hypothesize that individuals experiencing higher levels of social disadvantage in childhood will have
increased levels of pathogen burden throughout the life course. I will then define the association between
pathogen burden and immune system dysfunction and inflammation (Aim 2). I will do this first by testing the
association between pathogen burden and inflammation in existing cohort studies. I hypothesize that higher
levels of pathogen burden will be associated with increased inflammation. I will then test the association
between pathogen burden and immune dysfunction longitudinally. I hypothesize that those experiencing higher
levels of childhood social disadvantage will experience increased immune dysfunction over the life course.
Lastly, I will examine the degree to which the association between childhood social disadvantage and
inflammation/immune dysfunction is mediated by pathogen burden (Aim 3). I hypothesize that pathogen
burden will partially mediate the relationship between childhood social disadvantage and immune dysfunction
and infllammation.
 At its conclusion, this project will yield an expansion of our knowledge of the aging process early in the
life course, specifically how childhood social disadvantage can induce accelerated aging through the
mechanism of pathogen burden and amplify disparities in aging. Ultimately, this will work will inform our
understanding of modifiable processes that cause disease, disability, and mortality across the life course.

## Key facts

- **NIH application ID:** 10405131
- **Project number:** 5R00AG062749-05
- **Recipient organization:** UNIVERSITY OF MICHIGAN AT ANN ARBOR
- **Principal Investigator:** Grace A Noppert
- **Activity code:** R00 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $249,000
- **Award type:** 5
- **Project period:** 2021-05-15 → 2024-02-28

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10405131

## Citation

> US National Institutes of Health, RePORTER application 10405131, Social Disadvantage and Its Impact on Pathogen Burden and Immune Dysfunction Across the Life Course (5R00AG062749-05). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/10405131. Licensed CC0.

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