TLR4 Polymorphisms Mediate Impaired Responses to Respiratory Syncytial Virus and Lipopolysaccharide
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Severe bronchiolitis following respiratory syncytial virus (RSV) infection occurs in only a small subset of infected infants and the basis for variations in disease severity is not understood. Innate immune responses to RSV are mediated by TLR-4, and the 299Gly and 399Ile alleles of the TLR4 gene have been linked epidemiologically with increased severity of RSV disease in children. We hypothesized that cellular immune responses to RSV mediated by these variant forms of the receptor are defective relative to responses mediated via the common form of the receptor. Human bronchial epithelial cells were transfected with TLR4 constructs encoding the common TLR4 gene sequence (299Asp/399Thr), or the 299Gly or 399Ile alleles, and cytokine responses to in vitro RSV challenge were analyzed in the different transfected cells. Follow-up studies compared RSV-induced responses in PBMC from children expressing these same TLR4 genotypes. Human bronchial epithelial expressing 299Gly or 399Ile displayed normal levels of intracellular TLR4 but failed to efficiently translocate the receptor to the cell surface. This was associated with reduced NF-κB signaling post-TLR4 engagement, reduced production of IFNs, IL-8, IL-10, IL-12p35, IL-18, and CCL8, and the absence of acute-phase TNF-α. These findings were mirrored by blunted PBMC responses to RSV in children expressing the same TLR4 variants. Compromised first-line defense against RSV at the airway-epithelial surface of children expressing these TLR4 variants may thus confer increased susceptibility to severe infections with this virus.
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TLR4 variants may attenuate innate immune responses by disrupting RSV triggering of TLR4 surface expression.
“and TLR4 variants may attenuate innate immune responses by disrupting RSV triggering of TLR4 surface expression (142).”
From Into the Eye of the Cytokine Storm (2012) · cites this paper as [142]
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- Authors
- Tulic, M. K., Hurrelbrink, R. J., Prêle, C. M., Laing, I. A., Upham, J. W., Le Souef, P., Sly, P. D., & Holt, P. G.
- Affiliations
- Division of Cell Biology, University of Western Australia , Perth ,
- The University of Western Australia (AU)
- Division of Molecular Biotechnology, University of Western Australia , Perth ,
- School of Paediatrics and Child Health, University of Western Australia , Perth ,
- The Kids Research Institute Australia (AU)
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2007-07-01
- Volume
- 179
- Issue
- 1
- Pages
- 132-140
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W1591790122
- Cited by
- 140
- References
- 31
- Citations by year
- 2026: 2 · 2025: 5 · 2024: 2 · 2023: 5 · 2022: 7 · 2021: 4 · 2020: 6 · 2019: 5 · 2018: 2 · 2017: 10 · 2016: 4 · 2015: 8 · 2014: 7 · 2013: 11 · 2012: 6
- FWCI
- 5.91
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- The Journal of Immunology (publishedVersion, cc-by)
- PubMed (publishedVersion)
- UWA Profiles and Research Repository (UWA) (submittedVersion)
- Murdoch University Research Portal (submittedVersion)
- Figshare (submittedVersion, cc-by)
- Funders
- Yale University
- Australian Respiratory Council
- Medical Research Council
- National Health and Medical Research Council
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Health Sciences › Medicine › Epidemiology › Respiratory viral infections research
- Life Sciences › Immunology and Microbiology › Immunology › Immune responses and vaccinations
- Keywords
- TLR4 polymorphisms, respiratory syncytial virus, bronchiolitis, innate immunity, NF-κB signaling, cytokine response, bronchial epithelial cells, peripheral blood mononuclear cells, disease susceptibility, lipopolysaccharide
- MeSH terms
- Bronchi, Cell Line, Cell Membrane, Cells, Cultured, Child, Glycine, Humans, Intracellular Fluid, Isoleucine, Lipopolysaccharides, Monocytes, Polymorphism, Genetic, Respiratory Syncytial Viruses, Transfection, Ultraviolet Rays, Gene Expression Regulation, Viral, Mutagenesis, Site-Directed, Respiratory Mucosa, Protein Transport, Toll-Like Receptor 4
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