TY - JOUR
T1 - Nanoparticles reduce monocytes within the lungs to improve outcomes after influenza virus infection in aged mice
AU - Kelley, William J.
AU - Wragg, Kathleen M.
AU - Chen, Judy
AU - Murthy, Tushar
AU - Xu, Qichen
AU - Boyne, Michael T.
AU - Podojil, Joseph R.
AU - Elhofy, Adam
AU - Goldstein, Daniel R.
N1 - Funding Information:
We are grateful for Min Zhang’s assessment of the biostatical approach and analysis of the data. This study was supported by COUR Pharma and, in part, by NIH award R01AG028082 and R35HL155169 to DRG. WJK was supported by NIH award T32HL007622. The graphical abstract was generated in Biorender via an Institutional License with an agreement no. BR241PD4JH.
Publisher Copyright:
© 2022, Kelley et al. This is an open access article published under the terms of the Creative Commons Attribution 4.0 International License.
PY - 2022/8/8
Y1 - 2022/8/8
N2 - Older people exhibit dysregulated innate immunity to respiratory viral infections, including influenza and SARS-CoV-2, and show an increase in morbidity and mortality. Nanoparticles are a potential practical therapeutic that could reduce exaggerated innate immune responses within the lungs during viral infection. However, such therapeutics have not been examined for effectiveness during respiratory viral infection, particular in aged hosts. Here, we employed a lethal model of influenza viral infection in vulnerable aged mice to examine the ability of biodegradable, cargo-free nanoparticles, designated ONP-302, to resolve innate immune dysfunction and improve outcomes during infection. We administered ONP-302 via i.v. injection to aged mice at day 3 after infection, when the hyperinflammatory innate immune response was already established. During infection, we found that ONP-302 treatment reduced the numbers of inflammatory monocytes within the lungs and increased their number in both the liver and spleen, without impacting viral clearance. Importantly, cargo-free nanoparticles reduced lung damage, reduced histological lung inflammation, and improved gas exchange and, ultimately, the clinical outcomes in influenza-infected aged mice. In conclusion, ONP-302 improves outcomes in influenza-infected aged mice. Thus, our study provides information concerning a practical therapeutic, which, if translated clinically, could improve disease outcomes for vulnerable older patients suffering from respiratory viral infections.
AB - Older people exhibit dysregulated innate immunity to respiratory viral infections, including influenza and SARS-CoV-2, and show an increase in morbidity and mortality. Nanoparticles are a potential practical therapeutic that could reduce exaggerated innate immune responses within the lungs during viral infection. However, such therapeutics have not been examined for effectiveness during respiratory viral infection, particular in aged hosts. Here, we employed a lethal model of influenza viral infection in vulnerable aged mice to examine the ability of biodegradable, cargo-free nanoparticles, designated ONP-302, to resolve innate immune dysfunction and improve outcomes during infection. We administered ONP-302 via i.v. injection to aged mice at day 3 after infection, when the hyperinflammatory innate immune response was already established. During infection, we found that ONP-302 treatment reduced the numbers of inflammatory monocytes within the lungs and increased their number in both the liver and spleen, without impacting viral clearance. Importantly, cargo-free nanoparticles reduced lung damage, reduced histological lung inflammation, and improved gas exchange and, ultimately, the clinical outcomes in influenza-infected aged mice. In conclusion, ONP-302 improves outcomes in influenza-infected aged mice. Thus, our study provides information concerning a practical therapeutic, which, if translated clinically, could improve disease outcomes for vulnerable older patients suffering from respiratory viral infections.
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U2 - 10.1172/jci.insight.156320
DO - 10.1172/jci.insight.156320
M3 - Article
C2 - 35737459
AN - SCOPUS:85135599741
SN - 2379-3708
VL - 7
JO - JCI Insight
JF - JCI Insight
IS - 15
M1 - e156320
ER -