Aerosols, airflow, and more: examining the interaction of speech and the physical environment.

We describe ongoing efforts to better understand the interaction of spoken languages and their physical environments. We begin by briefly surveying research suggesting that languages evolve in ways that are influenced by the physical characteristics of their environments, however the primary focus is on the converse issue: how speech affects the physical environment. We discuss the speech-based production of airflow and aerosol particles that are buoyant in ambient air, based on some of the results in the literature. Most critically, we demonstrate a novel method used to capture aerosol, airflow, and acoustic data simultaneously. This method captures airflow data via a pneumotachograph and aerosol data via an electrical particle impactor. The data are collected underneath a laminar flow hood while participants breathe pure air, thereby eliminating background aerosol particles and isolating those produced during speech. Given the capabilities of the electrical particle impactor, which has not previously been used to analyze speech-based aerosols, the method allows for the detection of aerosol particles at temporal and physical resolutions exceeding those evident in the literature, even enabling the isolation of the role of individual sound types in the production of aerosols. The aerosols detected via this method range in size from 70 nanometers to 10 micrometers in diameter. Such aerosol particles are capable of hosting airborne pathogens. We discuss how this approach could ultimately yield data that are relevant to airborne disease transmission and offer preliminary results that illustrate such relevance. The method described can help uncover the actual articulatory gestures that generate aerosol emissions, as exemplified here through a discussion focused on plosive aspiration and vocal cord vibration. The results we describe illustrate in new ways the unseen and unheard ways in which spoken languages interact with their physical environments.

The Sea Spray Chemistry and Particle Evolution study (SeaSCAPE): overview and experimental methods.

Marine aerosols strongly influence climate through their interactions with solar radiation and clouds. However, significant questions remain regarding the influences of biological activity and seawater chemistry on the flux, chemical composition, and climate-relevant properties of marine aerosols and gases. Wave channels, a traditional tool of physical oceanography, have been adapted for large-scale ocean-atmosphere mesocosm experiments in the laboratory. These experiments enable the study of aerosols under controlled conditions which isolate the marine system from atmospheric anthropogenic and terrestrial influences. Here, we present an overview of the 2019 Sea Spray Chemistry and Particle Evolution (SeaSCAPE) study, which was conducted in an 11 800 L wave channel which was modified to facilitate atmospheric measurements. The SeaSCAPE campaign sought to determine the influence of biological activity in seawater on the production of primary sea spray aerosols, volatile organic compounds (VOCs), and secondary marine aerosols. Notably, the SeaSCAPE experiment also focused on understanding how photooxidative aging processes transform the composition of marine aerosols. In addition to a broad range of aerosol, gas, and seawater measurements, we present key results which highlight the experimental capabilities during the campaign, including the phytoplankton bloom dynamics, VOC production, and the effects of photochemical aging on aerosol production, morphology, and chemical composition. Additionally, we discuss the modifications made to the wave channel to improve aerosol production and reduce background contamination, as well as subsequent characterization experiments. The SeaSCAPE experiment provides unique insight into the connections between marine biology, atmospheric chemistry, and climate-relevant aerosol properties, and demonstrates how an ocean-atmosphere-interaction facility can be used to isolate and study reactions in the marine atmosphere in the laboratory under more controlled conditions.

SpxA1 and SpxA2 Act Coordinately To Fine-Tune Stress Responses and Virulence in Streptococcus pyogenes.

SpxA is a unique transcriptional regulator highly conserved among members of the phylum Firmicutes that binds RNA polymerase and can act as an antiactivator. Why some Firmicutes members have two highly similar SpxA paralogs is not understood. Here, we show that the SpxA paralogs of the pathogen Streptococcus pyogenes, SpxA1 and SpxA2, act coordinately to regulate virulence by fine-tuning toxin expression and stress resistance. Construction and analysis of mutants revealed that SpxA1- mutants were defective for growth under aerobic conditions, while SpxA2- mutants had severely attenuated responses to multiple stresses, including thermal and oxidative stresses. SpxA1- mutants had enhanced resistance to the cationic antimicrobial molecule polymyxin B, while SpxA2- mutants were more sensitive. In a murine model of soft tissue infection, a SpxA1- mutant was highly attenuated. In contrast, the highly stress-sensitive SpxA2- mutant was hypervirulent, exhibiting more extensive tissue damage and a greater bacterial burden than the wild-type strain. SpxA1- attenuation was associated with reduced expression of several toxins, including the SpeB cysteine protease. In contrast, SpxA2- hypervirulence correlated with toxin overexpression and could be suppressed to wild-type levels by deletion of speB These data show that SpxA1 and SpxA2 have opposing roles in virulence and stress resistance, suggesting that they act coordinately to fine-tune toxin expression in response to stress. SpxA2- hypervirulence also shows that stress resistance is not always essential for S. pyogenes pathogenesis in soft tissue.IMPORTANCE For many pathogens, it is generally assumed that stress resistance is essential for pathogenesis. For Streptococcus pyogenes, environmental stress is also used as a signal to alter toxin expression. The amount of stress likely informs the bacterium of the strength of the host's defense response, allowing it to adjust its toxin expression to produce the ideal amount of tissue damage, balancing between too little damage, which will result in its elimination, and too much damage, which will debilitate the host. Here we identify components of a genetic circuit involved in stress resistance and toxin expression that has a fine-tuning function in tissue damage. The circuit consists of two versions of the protein SpxA that regulate transcription and are highly similar but have opposing effects on the severity of soft tissue damage. These results will help us understand how virulence is fine-tuned in other pathogens that have two SpxA proteins.