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11 Pág. Centro de Investigación en Sanidad Animal (CISA), Epidemiological studies associate biomass smoke with an increased risk for respiratory infections in children and adults in the developing world, with 500,000 premature deaths each year attributed to biomass smoke-related acute respiratory infections including infections caused by respiratory viruses. Animal dung is a biomass fuel of particular concern because it generates more toxic compounds per amount burned than wood, and is a fuel of last resort for the poorest households. Currently, there is little biological evidence on the effects of dung biomass smoke exposure on immune responses to respiratory viral infections. Here, we investigated the impact of dung biomass exposure on respiratory infection using a mouse model of dung biomass smoke and cultured primary human small airway epithelial cells (SAECs). Mice infected with influenza A virus (IAV) after dung biomass smoke exposure had increased mortality, lung inflammation and virus mRNA levels, and suppressed expression of innate anti-viral mediators compared to air exposed mice. Importantly, there was still significant tissue inflammation 14 days after infection in dung biomass smoke-exposed mice even after inflammation had resolved in air-exposed mice. Dung biomass smoke exposure also suppressed the production of anti-viral cytokines and interferons in cultured SAECs treated with poly(I:C) or IAV. This study shows that dung biomass smoke exposure impairs the immune response to respiratory viruses and contributes to biomass smoke-related susceptibility to respiratory viral infections, likely due to a failure to resolve the inflammatory effects of biomass smoke exposure., The authors thank Stephen J. Pollock for assistance with preparing figures. This work was funded in part by NIH grants R01HL120908,T32HL066988, T32ES007026, and P30ES001247 and the William Branch Porter Professorship (to PJS). This project described in this publication was supported in part by award number UL1TR002001 from the National Center for Advancing Translational Sciences of the National Institutes of Health to the University of Rochester. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. This work was not a product of the United States Government or the United States Environmental Protection Agency, and the authors did not do this work in any government capacity. The views expressed are those of the authors only and do not necessarily represent those of the United States or the US EPA.

As the climate warms, wildfire activity is increasing, posing a risk to human health. Studies have reported on particulate matter (PM) in wildfire smoke, yet the chemicals associated with PM have received considerably less attention. Here, we analyzed 13 years (2006–2018) of PM(2.5) chemical composition data from monitors in California on smoke-impacted days. Select chemicals (e.g., aluminum and sulfate) were statistically elevated on smoke-impacted days in over half of the years studied. Other chemicals, mostly trace metals harmful to human health (e.g., copper and lead), were elevated during particular fires only. For instance, in 2018, lead was more than 40 times higher on smoke days on average at the Point Reyes monitoring station due mostly to the Camp Fire, burning approximately 200 kilometers away. There was an association between these metals and the combustion of anthropogenic material (e.g., the burning of houses and vehicles). Although still currently rare, these infrastructure fires are likely becoming more common, and can mobilize trace metals in smoke far downwind, at levels generally unseen except in the most polluted areas of the country. We hope a better understanding of the chemicals in wildfire smoke will assist in the communication and reduction of public health risks.

Inhalation of tobacco smoke has been linked to increased risk of viral infection, such as influenza. Inhalation of electronic-cigarette (e-cigarette) aerosol has also recently been linked to immune suppression within the respiratory tract, specifically the nasal mucosa. We propose that changes in the nasal mucosal immune response modify antiviral host-defense responses in e-cigarette users. Nonsmokers, cigarette smokers, and e-cigarette users were inoculated with live-attenuated influenza virus (LAIV) to safely examine the innate immune response to influenza infection. Before and after LAIV inoculation, we collected nasal epithelial-lining fluid, nasal lavage fluid, nasal-scrape biopsy specimens, urine, and blood. Endpoints examined include cytokines and chemokines, influenza-specific IgA, immune-gene expression, and markers of viral load. Statistical analysis included primary comparisons of cigarette and e-cigarette groups with nonsmokers, as well as secondary analysis of demographic factors as potential modifiers. Markers of viral load did not differ among the three groups. Nasal-lavage-fluid anti-LAIV IgA levels increased in nonsmokers after LAIV inoculation but did not increase in e-cigarette users and cigarette smokers. LAIV-induced gene-expression changes in nasal biopsy specimens differed in cigarette smokers and e-cigarette users as compared with nonsmokers, with a greater number of genes changed in e-cigarette users, mostly resulting in decreased expression. The top downregulated genes in cigarette smokers were SMPD3, NOS2A, and KLRB1, and the top downregulated genes in e-cigarette users were MR1, NT5E, and HRAS. Similarly, LAIV-induced cytokine levels in nasal epithelial-lining fluid differed among the three groups, including decreased antiviral host-defense mediators (IFNγ, IL6, and IL12p40). We also detected that sex interacted with tobacco-product exposure to modify LAIV-induced immune-gene expression. Our results demonstrate that e-cigarette use altered nasal LAIV-induced immune responses, including gene expression, cytokine and chemokine release, and LAIV-specific IgA levels. Together, these data suggest that e-cigarette use induces changes in the nasal mucosa that are consistent with the potential for altered respiratory antiviral host-defense function. Clinical trial registered with www.clinicaltrials.gov (NCT 02019745).

The Enterobacteriales order is composed of Gram-negative bacteria that range from harmless symbionts to well-studied pathogens. We announce complete genome sequences of five related SO-1-like Enterobacteriales bacteriophages (also known as the Dhillonvirus genus) isolated from wastewater that infect Escherichia coli (Opt-212, Over9000, Pubbukkers, and Teewinot) or Shigella boydii (StarDew).

Research suggests that explicit pronunciation teaching improves second language speech production, but language teachers often lack the relevant knowledge to teach pronunciation. This study examined segmental error patterns in Finnish-accented English and the relationship between segmental errors and foreign accent ratings in two groups differing in amount of second language experience. Our study identified a number of common segmental error patterns in Finnish-accented English, which may guide formal pronunciation instruction. We further found that the sheer number of segmental errors in a sentence affected foreign accent ratings as did the number of vowel errors in a sentence. We speculate that the detrimental effect of vowel errors may be related to the finding that vowel errors resulted in non-English segments more often than consonant errors did. Finally, we found a facilitative effect of second language experience on foreign accent rating that cannot be reduced to number of segmental errors, despite the finding that number of consonant errors was reduced with increased second language experience.