A localized defense response within the nasal cavity is crucial for warding off head colds, a study reveals.(Image credit: Getty)ShareShare by:
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Novel lab trials employed “noses-in-a-dish” to investigate why the average cold leads to a minor ailment for some individuals but necessitates hospitalization for others.
During the height of cold and influenza season, rhinoviruses — the most typical trigger of the common cold — render numerous individuals unwell, inducing signs and symptoms such as a congested nose, scratchy throat, and light coughing. However, in some individuals, rhinovirus infections constitute a much more severe affliction.
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Now, a fresh study, released on Jan. 19 in the journal Cell Press Blue, has exhibited that this variability hinges on the initiation of specific immune responses within the afflicted nasal tissue. The research team cultivated scaled-down representations of human nasal passages within petri dishes to scrutinize cellular reactions to infection.
The researchers suggest that these discoveries constitute a stride toward creating potent antiviral treatments for the common cold.
How to grow a nose in a dish
The epithelial cells coating the nasal cavity are the primary targets during typical cold infections. Upon detecting a viral presence, these cells transmit alerts to the innate immune apparatus — the body’s initial, nonspecific protective measure against pathogens. The release of molecules known as interferons are among the initial protective components this mechanism utilizes.
While the function of interferons in combatting viruses is well-recognized, scientists have experienced difficulties in comprehensively grasping their operational mechanisms at the cellular level.
The present research, steered by Dr. Ellen Foxman, an associate professor of laboratory medicine and immunobiology at Yale University, utilized a methodology termed single-cell RNA sequencing. This exposes the data transmitted from a cell’s core, where its DNA is found. This examination was carried out at the level of individual nasal epithelial cells.
Dr. Foxman’s group cultivated these cells within a dish environment designed to mirror the conditions within the human nose closely. Subsequently, these cells were exposed to a rhinovirus.
Clare Lloyd, a respiratory immunologist affiliated with Imperial College London, but uninvolved in the research, commented that this blend of methodologies furnished Dr. Foxman’s group with novel insights into the impact of rhinoviruses on nasal cells.
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Lloyd mentioned to Live Science that “I believe the combination of using a multicellular organoid [the nose-in-a-dish] along with deploying these significantly more responsive and precise methods permits us to observe the influence on ciliated cells and mucus-producing cells.” Ciliated cells — distinguished by minute, hairlike protrusions — and mucus-secreting cells are both situated within the nasal lining.
Foxman’s preliminary observation indicated that the nasal cells, even when detached from the remainder of the body, exhibited considerable proficiency in resisting rhinoviruses.
Foxman articulated in a statement that “During a peak reaction, viruses only infect roughly 1% of cells, and the infection begins to diminish within several days.” However, when the team administered a medication that hindered interferon signaling to the cells, their previously robust protections began to degrade.
Under these altered circumstances, cell infection rates surged beyond 30%, with a concomitant amplification of the immune response. Concentrations of pro-inflammatory molecules, notably cytokines, escalated sharply, accompanied by a substantial augmentation in mucus-protein synthesis.
In the absence of interferons, one protein stood out as the primary regulator of this amplified response: nuclear factor kappa B (NF-κB). This unchecked response mirrored the characteristic reaction that precipitates complications in severe rhinovirus cases among susceptible individuals.
Lloyd stated that a particularly severe rhinovirus infection might be indicative of compromised interferon production. She added that “Certain individuals possess genetic anomalies in interferon production, potentially impacting the magnitude of interferon response.”
Lab studies similar to these represent indispensable measures toward effectively managing prevalent viral maladies. However, Lloyd cautioned that antiviral treatments targeting the immune response must be meticulously balanced.
Lloyd emphasized the “delicate balance of the immune system.” “Completely suppressing NF-κB will suppress all kinds of cytokines and chemokines, thereby impeding the entire inflammatory response.” While inflammation can be detrimental when it spins out of control, a certain level is crucial for successfully combating infections.
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Foxman’s team tested certain antiviral agents on their cell models, which included an experimental drug termed rupintrivir. This drug displayed notable effectiveness in mitigating excessive immune activity, at least within the experimental models. Rupintrivir had earlier failed to demonstrate suppression of rhinovirus infections in human clinical trials. Yet, the study’s authors proposed that the drug may offer another avenue as a therapy aimed at moderating runaway viral immune responses in vulnerable cohorts, such as individuals with COPD (chronic obstructive pulmonary disease).
Mehul Suthar, a professor at Emory Vaccine Center with no direct involvement in the research, posited that medications that hone in on the virus directly would be more accurate than medications targeting a mediator of the immune response. For instance, rupintrivir targets viral proteins.
Rhinoviruses have persisted as a long-standing irritant for the human species on account of their capacity to swiftly undergo evolutionary alterations in response to treatments, thus acquiring resistance to them. Only through meticulous discernment regarding the etiologies of cold-induced illness might a conclusive solution be attained.
Suthar stated that “It’s undeniably very challenging.” “Otherwise, there would be treatments for every virus.”
Article Sources
Wang, B., Amat, J. A., Mihaylova, V. T., Kong, Y., Wang, G., & Foxman, E. F. (2026). Rhinovirus triggers distinct host responses through differential engagement of epithelial innate immune signaling. Cell Press Blue, 100001. https://doi.org/10.1016/j.cpblue.2025.100001
RJ MackenzieLive Science Contributor
RJ Mackenzie serves as a science and health journalist with award nominations. He earned degrees in neuroscience from both the University of Edinburgh and the University of Cambridge. His transition into writing stemmed from the realization that the most impactful contribution to science could be made through writing rather than laboratory work. His reporting scope encompasses a diverse array of topics, spanning from brain-interface technology to materials science characterized by shape-shifting properties, and from the expansion of predatory conferencing to the significance of newborn-screening programs. He is a former staff writer of Technology Networks.
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