Evidence map›Paper›PMID 42135777›Full record

ArticleRespiratory research2026

The adult nasal mucosa is defined by distinct immune profiles that modulate in-vitro SARS-CoV-2 infection.

Sarah N Gowanlock, Victor H K Lam, Zeynep Güneş Tepe, Daniel E Park, Vera Tai, Juan E Salazar, Tony Pham, Yazan Khan, Sydney Nelson, Caitlin Horn and 8 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Respiratory research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

18 authors.

Sarah N Gowanlock *Department of Microbiology and Immunology, Western University, London, ON, Canada.
Victor H K Lam *Department of Microbiology and Immunology, Western University, London, ON, Canada.
Zeynep Güneş TepeDepartment of Microbiology and Immunology, Western University, London, ON, Canada.
Daniel E ParkDepartment of Environmental and Occupational Health, Milken Institute School of Public Health, George Washington University, Washington, DC, USA.
Vera TaiDepartment of Biology, Western University, London, ON, Canada.
Juan E SalazarDepartment of Environmental and Occupational Health, Milken Institute School of Public Health, George Washington University, Washington, DC, USA.
Tony PhamDepartment of Environmental and Occupational Health, Milken Institute School of Public Health, George Washington University, Washington, DC, USA.
Yazan KhanDepartment of Microbiology and Immunology, Western University, London, ON, Canada.
Sydney NelsonDepartment of Environmental and Occupational Health, Milken Institute School of Public Health, George Washington University, Washington, DC, USA.
Caitlin HornDepartment of Environmental and Occupational Health, Milken Institute School of Public Health, George Washington University, Washington, DC, USA.
David ZuanazziDepartment of Microbiology and Immunology, Western University, London, ON, Canada.
Diana YangDepartment of Immunology, University of Toronto, Toronto, ON, Canada.
Lance B PriceDepartment of Environmental and Occupational Health, Milken Institute School of Public Health, George Washington University, Washington, DC, USA.
Rupert KaulDepartment of Immunology, University of Toronto, Toronto, ON, Canada.
Leigh SowerbyDepartment of Otolaryngology-Head and Neck Surgery, Western University, London, ON, Canada.
Ryan M TroyerDepartment of Microbiology and Immunology, Western University, London, ON, Canada.
Cindy M Liu *Department of Environmental and Occupational Health, Milken Institute School of Public Health, George Washington University, Washington, DC, USA.
Jessica L Prodger *Department of Microbiology and Immunology, Western University, London, ON, Canada. jprodge@uwo.ca.

Funding

The dynamics of nasal bacterial ecology and S. aureus antagonismR01AI125562 · NIAID · GEORGE WASHINGTON UNIVERSITY · PI PRICE, LANCE BRADLEY · 2016 to 2020
$3.6M
Influence of the nasal microbiome on host susceptibility and response to respiratory virusesR01AI168182 · NIAID · GEORGE WASHINGTON UNIVERSITY · PI Cindy Liu · 2023 to 2026
$2.8M
Canada Foundation for Innovation CFI 42343Canada Institutes of Health Research, Canada Graduate Scholarship Doctoral Award 176586Canada Research Chairs Program CRC-2020-00175National Institute of Allergy and Infectious Diseases, National Institutes of Health R01AI125562-01National Institute of Allergy and Infectious Diseases, National Institutes of Health R01AI168182-01NIAID NIH HHS R01 AI125562NIAID NIH HHS R01 AI168182
6 · The paper itself

Abstract

backgroundThe nasal mucosa is the primary entry site for many respiratory viruses, and immune molecules present at the time of exposure may dictate if infection occurs. However, the baseline immune state in healthy adults - and how it influences susceptibility to viruses - remains poorly defined.

methodsLevels of 16 immune molecules were measured in nasal secretions from two independent cohorts of healthy adults (total n = 166, Luminex). Participants were clustered based on normalized concentrations of immune analytes to identify profiles. An in vitro organotypic model of the nasal epithelium was used to examine the effect of immune profiles on SARS-CoV-2 infection: primary human nasal epithelial cells (n = 9 donors) were grown at air-liquid interface to induce mucociliary differentiation (42 days), treated with recombinant human cytokines (72 h), and then challenged with wildtype SARS-CoV-2 Omicron BA.1 (24 h). SARS-CoV-2 entry factor expression (post-cytokines, pre-challenge) and viral infection (N gene) were measured by qRT-PCR.

resultsIn both cohorts, a unique cluster was observed, characterized by distinctly high levels of antiviral interferons - particularly IFN-λ3 - with comparatively low levels of inflammatory chemokines and cytokines. In contrast, individuals with high overall levels of inflammatory mediators had absent IFN-λ3. In vitro, pretreatment with IFN-λ3 and IFN-α2, but not with pro-inflammatory cytokines, significantly reduced SARS-CoV-2 replication in differentiated nasal epithelial cultures, despite upregulating ACE2 expression.

conclusionsHealthy adults exhibit distinct nasal immune profiles, with an exogenous IFN-λ3-dominant, low-inflammatory state conferring resistance to SARS-CoV-2 in an in vitro primary nasal epithelial model. The nasal immune milieu may influence susceptibility to respiratory viruses and the efficacy of mucosally administered vaccines.

Indexed as

COVID-19Nasal MucosaSARS-CoV-2AdultCells, CulturedCytokinesFemaleHumansMaleMiddle AgedCytokinesImmune profilingMucosal immunologyNasal inflammationNasal mucosaRespiratory virusesSARS-CoV-2Viral susceptibility

Identifiers

PMID42135777
PMCPMC13450510

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.