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Peer-reviewedCC BY-NCJournal of immunology (Baltimore, Md. : 1950)

Vaccine immunity can drive eosinophil recruitment in influenza breakthrough infection with mouse strain–specific outcomes

  • Lauren A Chang1,2,3
  • Eleanor Burgess1,2,3
  • Moataz Noureddine1,2,3
  • Anthony J Wells4
  • Johanna Vandekerckhove1,3
  • Juan García-Bernalt Diego1,3
  • Brett T Webb5
  • Leonie J Grüneberg1,3
  • Seok-Chan Park1,3
  • Gabriel Laghlali1,3
  • Vivian Yan1,2,3
  • Farah El-Ayache1,3
4 more authors
  • Bart N Lambrecht6,7,8
  • Pamela T Wong9,10,11
  • Amali E Samarasinghe4,12
  • Michael Schotsaert1,3,13,14,15
15 affiliations
  1. 1Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY, United States.
  2. 2Graduate School of Biomedical Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, United States.
  3. 3Global Health and Emerging Pathogens Institute, Icahn School of Medicine at Mount Sinai, New York, NY, United States.
  4. 4Department of Pediatrics, University of Tennessee Health Science Center, Memphis, TN, United States.
  5. 5Veterinary Diagnostic Laboratory, North Dakota State University, Fargo, ND, United States.
  6. 6Laboratory of Immunoregulation and Mucosal Immunology, VIB-UGent Center for Inflammation Research, Ghent, Belgium.
  7. 7Department of Internal Medicine and Pediatrics, Ghent University, Ghent, Belgium.
  8. 8Department of Pulmonary Medicine, Erasmus University Medical Center Rotterdam, Rotterdam, the Netherlands.
  9. 9Michigan Nanotechnology Institute for Medicine and Biological Sciences, University of Michigan Medical School, Ann Arbor, MI, United States.
  10. 10Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI, United States.
  11. 11Department of Biomedical Engineering, University of Michigan, Ann Arbor, MI, United States.
  12. 12Department of Medicine, University of Wisconsin, Madison, WI, United States.
  13. 13Marc and Jennifer Lipschultz Precision Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY, United States.
  14. 14Icahn Genomics Institute, Icahn School of Medicine at Mount Sinai, New York, NY, United States.
  15. 15Department of Immunology and Immunotherapy, Icahn School of Medicine at Mount Sinai, New York, NY, United States.
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Abstract

Eosinophils are pleiotropic cells and can respond to a wide array of inflammatory stimuli, including respiratory viral infection. Although they are historically associated with adverse outcomes in vaccinated hosts after breakthrough infection, such as during vaccine-associated enhanced respiratory disease (VAERD) for respiratory syncytial virus (RSV), eosinophils can also help mediate antiviral immunity. We previously observed mild, nonpathological lung eosinophilia in vaccinated mice experiencing influenza breakthrough infection, distinct from VAERD. Here, we investigated the factors driving this eosinophil recruitment and their contribution to host outcomes during influenza breakthrough infection. Vaccine-elicited Abs partially mediate eosinophil recruitment to the lungs during infection but do not confer full protection against viral replication or disease. Live viral replication was needed for robust eosinophil recruitment. Furthermore, both CD4 and CD8 T cells were required for optimal eosinophil accumulation in the lungs. Intramuscular vaccination resulted in the induction of a balanced type 1/2 response in the spleen and mainly a type 2 response in the lung upon infection, whereas a type 1 immune response dominated in the lungs of unvaccinated mice upon infection. Eosinophil depletion studies revealed strain-dependent effects: in BALB/c mice, eosinophil depletion did not significantly affect morbidity, viral load, lung inflammation, or lung lesion severity. However, in C57BL/6 mice, eosinophil depletion improved viral control and reduced pro-inflammatory cytokine expression. Our findings highlight the complex interplay among vaccine-induced immunity, eosinophil recruitment, and host genetic background in shaping outcomes during influenza breakthrough infection, with implications for vaccine strategies and immunopathology mitigation in diverse populations.

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Cite

BibTeXRIS
BibTeX
@article{chang2026vaccine,
  title = {{Vaccine immunity can drive eosinophil recruitment in influenza breakthrough infection with mouse strain–specific outcomes}},
  author = {Lauren A Chang and Eleanor Burgess and Moataz Noureddine and Anthony J Wells and Johanna Vandekerckhove and Juan García-Bernalt Diego and Brett T Webb and Leonie J Grüneberg and Seok-Chan Park and Gabriel Laghlali and Vivian Yan and Farah El-Ayache and Bart N Lambrecht and Pamela T Wong and Amali E Samarasinghe and Michael Schotsaert},
  journal = {Journal of immunology (Baltimore, Md. : 1950)},
  year = {2026},
  month = oct,
  doi = {10.1093/jimmun/vkag279},
  url = {https://europepmc.org/article/PMC/PMC13718889},
  note = {CC BY-NC},
}
RIS
TY  - JOUR
TI  - Vaccine immunity can drive eosinophil recruitment in influenza breakthrough infection with mouse strain–specific outcomes
AU  - Lauren A Chang
AU  - Eleanor Burgess
AU  - Moataz Noureddine
AU  - Anthony J Wells
AU  - Johanna Vandekerckhove
AU  - Juan García-Bernalt Diego
AU  - Brett T Webb
AU  - Leonie J Grüneberg
AU  - Seok-Chan Park
AU  - Gabriel Laghlali
AU  - Vivian Yan
AU  - Farah El-Ayache
AU  - Bart N Lambrecht
AU  - Pamela T Wong
AU  - Amali E Samarasinghe
AU  - Michael Schotsaert
PY  - 2026
DA  - 2026/10/01
JO  - Journal of immunology (Baltimore, Md. : 1950)
DO  - 10.1093/jimmun/vkag279
UR  - https://europepmc.org/article/PMC/PMC13718889
AB  - Eosinophils are pleiotropic cells and can respond to a wide array of inflammatory stimuli, including respiratory viral infection. Although they are historically associated with adverse outcomes in vaccinated hosts after breakthrough infection, such as during vaccine-associated enhanced respiratory disease (VAERD) for respiratory syncytial virus (RSV), eosinophils can also help mediate antiviral immunity. We previously observed mild, nonpathological lung eosinophilia in vaccinated mice experiencing influenza breakthrough infection, distinct from VAERD. Here, we investigated the factors driving this eosinophil recruitment and their contribution to host outcomes during influenza breakthrough infection. Vaccine-elicited Abs partially mediate eosinophil recruitment to the lungs during infection but do not confer full protection against viral replication or disease. Live viral replication was needed for robust eosinophil recruitment. Furthermore, both CD4 and CD8 T cells were required for optimal eosinophil accumulation in the lungs. Intramuscular vaccination resulted in the induction of a balanced type 1/2 response in the spleen and mainly a type 2 response in the lung upon infection, whereas a type 1 immune response dominated in the lungs of unvaccinated mice upon infection. Eosinophil depletion studies revealed strain-dependent effects: in BALB/c mice, eosinophil depletion did not significantly affect morbidity, viral load, lung inflammation, or lung lesion severity. However, in C57BL/6 mice, eosinophil depletion improved viral control and reduced pro-inflammatory cytokine expression. Our findings highlight the complex interplay among vaccine-induced immunity, eosinophil recruitment, and host genetic background in shaping outcomes during influenza breakthrough infection, with implications for vaccine strategies and immunopathology mitigation in diverse populations.
SN  - 0022-1767
SN  - 1550-6606
ER  -