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Impact of Obesity on Pulmonary Innate Immune Cells in the Setting of Viral Infection

Identification

Public canonical key

radar:r-b0d0595faadc75f5f47ffcfec90adbae

Authors

Laura A. Barnes · A.J. Kumar · J.A. Masso Silva · Alexia N. Perryman · Laura E. Crotty Alexander · Mark Hepokoski

Reported year

2025

Reported language

en

Source type

conference-abstract

First detected

2026-11-14T02:29:19.786756+00:00

Last metadata observation

2026-11-14T02:29:19.786756+00:00

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Not checked

Institutions reported by the source

University of California San Diego

Reported affiliation countries

US

Documentary abstract — original language

Abstract RATIONALE: Respiratory infections due to influenza remain a major public health concern, affecting 32 million people per year in the US. Concurrently, the prevalence of obesity continues to rise and many studies have shown that obese patients have increased mortality due to influenza. However, this data is still controversial, given that some studies show that obese patients do better, the so-called obesity paradox. Furthermore, the stimulator of interferon genes (STING), a key innate immune defense against viruses, is increased in pulmonary macrophages in obese patients, and has been implicated in obesity-mediated lung inflammation. Here we sought to characterize effects of obesity on pulmonary innate immune cells in the setting of influenza infection. We hypothesize that obese mice have increased STING expression in interstitial macrophages, which predisposes to increased lung inflammation and worse outcomes in influenza. METHODS: Four-week-old male C57BL/6 mice were divided into two groups and fed either a high fat diet (research diets D12492) or standard chow. At 10-weeks, mice were intranasally infected with 35ul of influenza (A/PR/8/1934). One week later, mice were sacrificed and whole lung tissue with and without bronchoalveolar lavage (BAL) underwent detailed immunoprofiling via flow cytometry. RESULTS: There was a trend towards, but no significant difference, in weight loss between obese and lean mice (15.65% obese and 8.75% lean, p=0.1045). In whole lung without BAL, obese mice had decreased monocyte-derived alveolar macrophages compared to lean mice (2.52x105 obese vs. 8.51x104 lean, p=0.022), but obese mice had increased interstitial macrophages (4.16x106 obese vs. 1.97x106 lean, p=0.038). STING expression was unchanged between obese and lean groups in both monocyte-derived alveolar macrophages (6.16x104 obese and 5.65x104 lean, p=0.230) and interstitial macrophages (2.42x104 obese vs. 2.25x104 lean, p=0.273). There was no difference in eosinophils, T cells, leukocytes or inflammatory monocytes between groups. CONCLUSIONS: Understanding the impact of obesity on pulmonary immune cells is vital to elucidate mechanisms underlying clinical differences in responses to lung insults, such as viral infections. In our study, obese mice had a 2-fold increase in interstitial macrophages, which are considered by some to be the gate-keepers of homeostasis, demonstrating obesity induced immunomodulation. We are planning further studies to determine if overall increase in STING signaling (due to increased interstitial macrophages) leads to amplification of factors downstream of STING, resulting in inflammation. More studies are needed to further investigate the role of macrophages in different compartments in viral injury and obesity to identify novel therapeutic strategies.

Identifiers

OPENALEX

https://openalex.org/W4410273090

DOI

10.1164/ajrccm.2025.211.abstracts.a4713

Documentary context

Documentary family

unknown

Source-reported types

conference-abstract

Publishers

American Thoracic Society

Entity mentions are not evidence of legal recognition. Jurisdiction studied is separate from author affiliation country.

Sources

OpenAlex · Record 1

• Document · https://doi.org/10.1164/ajrccm.2025.211.abstracts.a4713

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