New Study Reveals How Mucus Microdroplets Rapidly Carry Infections from the Upper Airways to the Lungs

A new single-author research paper by Saikat Basu, an associate professor of mechanical engineering at South Dakota State University, offers a detailed and highly technical explanation for how secondary lung infections—such as pneumonia—can develop so quickly after a simple upper respiratory tract infection like the common cold or a nasal infection. The study, published in PLOS One (2025), uses advanced fluid-dynamics modeling to show exactly how virus-laden mucus droplets formed inside the upper airway can be inhaled deeper into the lungs, potentially transporting high viral loads far faster than tissue-level pathogen spread alone would suggest.

This mechanism helps explain why some people—especially vulnerable groups like children, older adults, and those with compromised immunity—progress from mild symptoms to dangerous lower-respiratory infections in surprisingly short timeframes.

How the Study Explains Fast-Developing Lung Infections

The long-standing assumption in respiratory science has been that large droplets—generally greater than 10 micrometers (µm)—from outside air rarely make it past the nose or throat. These droplets normally get trapped by the body’s filtration zones, including the anterior nasal cavity. As a result, they cause infections mainly in the upper airway regions like the pharynx, but do not penetrate into the lungs.

The new research challenges that assumption by pointing out a different mechanism entirely: the lungs don’t need outside droplets to be exposed to pathogens, because infectious droplets can form inside the body itself.

According to the study:

• Pathogens settle in the upper airway during the initial infection.
• As we breathe, mucus fragments break off at these infected sites.
• These fragments form microdroplets that behave much like inhalable particles.
• Because of the straight geometry of the laryngeal–tracheal pathway, these droplets can move downward into the bronchial passages during normal inhalation.
• The droplets may reach sizes up to 15–20 µm, and still penetrate deep enough to deliver viral loads above typical infectious thresholds.

Importantly, the droplets forming from infected mucus may already contain a high concentration of viruses, making them highly efficient carriers for deeper infection spread within the same host.

This mechanism provides a physical and fluid-dynamical explanation for why deep lung infections can appear rapidly—often in a timeframe too short to be explained by gradual viral replication and tissue migration.

The Modeling Behind the Findings

To investigate this process, Basu used:

• Three-dimensional computer-generated airway models built from real CT scans
• Computational fluid dynamics (CFD) simulations of inhalation
• Large Eddy Simulation (LES) to capture realistic airflow structures
• Modeled inhalation rates of about 15 liters per minute, representing relaxed breathing
• Droplets sized 1–30 µm, made to behave like mucus-laden particles

The model followed droplet trajectories from the larynx downward through multiple generations of bronchi. Even larger droplets—traditionally believed to be too big to reach the lungs—were shown to travel deep into the bronchial tree.

To cross-verify, Basu used an additional reduced-order biomathematical model involving vortex dynamics. This helped confirm that the fluid-mechanical behaviors observed in the 3D simulation were consistent with expected airflow instabilities in human airways.

The combination of these approaches strengthens the argument that internal droplet formation and downward transport may be a significant contributor to rapid secondary infection onset.

Why This Finding Matters

This research helps answer a long-standing clinical mystery:
Why do some upper respiratory infections escalate into pneumonia so quickly?

Traditional explanations rely on:

• pathogen replication,
• spread via tissue,
• immune system failures,
• or separate external exposure.

But these pathways typically take longer to produce deep lung involvement.

The fluid-dynamics explanation offers a faster, physically reasonable, and biologically plausible route: internal transport via virus-laden mucus droplets.

This finding is particularly relevant for:

• Individuals with weakened mucociliary clearance
• People who produce thicker or more abundant mucus during infection
• Children with narrower airways
• Older adults with decreased respiratory resilience

It also provides insight into why respiratory infections like COVID-19, RSV, influenza, and adenoviruses can sometimes shift suddenly from mild throat or nasal symptoms to serious bronchial or pulmonary involvement.

Connecting the Study to Broader Respiratory Science

The findings fit into a growing scientific conversation about droplet vs. aerosol transmission, but instead of focusing on how pathogens travel between people, this research examines how they travel inside a single person. Traditionally:

• Droplets (≥10 µm) fall quickly and don’t travel deep.
• Aerosols (≤5 µm) can reach deeper lung regions.

This new mechanism adds a third category:
internally generated mucus microdroplets, which do not follow the same deposition rules as inhaled droplets from the outside environment.

Because these droplets originate from mucus in infected regions, they can bypass barriers that normally prevent large particles from reaching the lungs.

This insight may eventually influence:

• Clinical risk assessment for respiratory infections
• Monitoring strategies for high-risk patients
• Predictive models used by epidemiologists and immunologists
• Preventive guidance in hospitals and long-term care settings

It may also refine future drug delivery strategies, because understanding how internal droplets travel could inform new inhalation therapies.

Additional Scientific Context: How Mucus Behaves in the Airways

To help readers understand why this mechanism is plausible, here are some key facts about mucus physiology and droplet formation:

Mucus Microstructure

Mucus is not just a sticky fluid—it is a complex viscoelastic gel containing:

• water
• mucin proteins
• immune molecules
• salts
• cellular debris
• pathogens during infection

Its elasticity allows it to stretch and break into fragments under airflow stress.

Airflow-Induced Fragmentation

During inhalation:

• air accelerates in the laryngeal jet region, where airflow speeds up and becomes turbulent
• turbulence can shear off small droplets from mucus surfaces
• these droplets can become entrained in the airflow and travel downward

This same mechanism occurs in:

• coughing
• sneezing
• talking
• forceful breathing

But even quiet breathing can produce small droplets under certain conditions.

Droplet Transport Mechanisms

Droplets move not only by bulk airflow but also via:

• vortex structures in the trachea
• branching airflow patterns in the bronchi
• inertial effects that depend on droplet size and density

Larger droplets with higher inertia may actually continue deeper along straight airflow paths, especially in regions with less curvature—such as the larynx-to-trachea segment highlighted in the study.

What This Means for Future Research

Basu’s work opens the door to a new subfield that he refers to as bronchial biophysics, integrating:

• fluid mechanics
• virology
• bacteriology
• airway biomechanics
• immunology

Future studies may include:

• in vitro airway models
• experimental droplet imaging
• biological validation in animal or human tissues
• expansions into deeper bronchial generations
• modeling under different breathing conditions (sleep, exercise, coughing)

Understanding internal droplet transport may help clinicians predict not only who is at risk for severe secondary infections, but also when those infections are most likely to develop.

Research Paper Reference

On the mechanics of inhaled bronchial transmission of pathogenic microdroplets generated from the upper respiratory tract, with implications for downwind infection onset
https://doi.org/10.1371/journal.pone.0335962