Mucosal vaccination in mice provides protection from diverse respiratory threats
TL;DR
Imagine a special spray for your nose that teaches your body to fight off all kinds of germs that make you sick, like viruses and bacteria. It's like having a super shield against colds and flus.
Traditional vaccines target specific pathogens, limiting their scope against diverse respiratory threats. We describe an intranasal liposomal formulation combining toll-like receptor (TLR) 4 and 7/8 ligands with a model antigen, ovalbumin, that provided broad, durable protection in mice for at least 3 months against infection with SARS-CoV-2 and Staphylococcus aureus. In addition, the vaccine protected mice from other viruses (SARS-CoV-2, SARS, SCH014 coronavirus), bacteria (Acinetobacter baumannii), and allergens. Protection was mediated by persistent ovalbumin-specific CD4+ and CD8+ memory T cells that imprinted alveolar macrophages (AMs), enhancing antigen presentation and antiviral immunity. Following infection, vaccinated mice mounted rapid pathogen-specific T cell and antibody responses and formed ectopic lymphoid structures in the lung. These results reveal a class of "universal vaccines" against diverse respiratory threats.
- 1An intranasal liposomal vaccine combining TLR4 (GLA) and TLR7/8 (3M-052) agonists with ovalbumin (GLA-3M-052-LS + OVA) conferred broad, durable protection in mice for at least 3 months against SARS-CoV-2, SARS-CoV MA15, SCH014 coronavirus, Staphylococcus aureus, and Acinetobacter baumannii, as well as allergic asthma.
- 2Protection required both CD4+ and CD8+ antigen-specific tissue-resident memory T cells (TRMs), which epigenetically reprogrammed alveolar macrophages to enhance antigen presentation, phagocytosis, and antiviral immunity via RANKL-mediated signaling, independently of IFN-gamma.
- 3Vaccination induced persistent chromatin remodeling in alveolar macrophages, with sustained accessibility of antigen presentation genes (H2-Aa), interferon-stimulated genes (Ccl5, Ifnar2), and AP-1, STAT, IRF, and NF-kB transcription factor motifs for at least 3 months post-vaccination.
- 4Following pathogen challenge, vaccinated mice rapidly formed tertiary lymphoid structures (TLS) in the lung within 3 days of infection, enabling accelerated pathogen-specific T and B cell responses and reduced immunopathology including lower proinflammatory cytokine levels.
- 5The vaccine platform is antigen-agnostic in its protective mechanism: the antigen identity is irrelevant for breadth of protection, as TLR agonists combined with any antigen can engage memory T cells to reprogram resident alveolar macrophages and establish organ-level immunity against diverse respiratory threats.
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