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Background <p>Air pollution, specifically fine particulate matter (PM<sub>2.5</sub>), in China is responsible for millions of excess deaths each decade. Examinations of Chinese municipalities have revealed correlations between ambient PM<sub>2.5</sub> levels and the prevalence and severity of respiratory viral infections. Seasonal sources of ambient PM<sub>2.5</sub> vary, with coal combustion for indoor heating significantly contributing during colder months. Due to this seasonality, we hypothesized that PM<sub>2.5</sub> collected in Xinxiang, China would differentially alter the response to subsequent influenza A/California/04/2009 (H1N1) viral infection in a primary human nasal epithelial cell (HNEC) culture model in a seasonality-specific manner. After the PM<sub>2.5</sub> samples were chemically analyzed, HNECs collected from males (<i>N</i> = 4) and females (<i>N</i> = 3) grown at air-liquid interface were exposed to 22&#xa0;µg/cm<sup>2</sup> of seasonal PM<sub>2.5</sub> followed by inoculation with influenza A H1N1 at MOI = 0.001. At 2 and 24&#xa0;h post infection (p.i.) we assessed transcriptional changes and basolateral release of immune and antiviral mediators.</p> Results <p>Summer and fall PM<sub>2.5</sub> samples contained a greater organic carbon mass fraction compared to winter and spring. Winter contained the largest mass fraction of anionic components and spring the largest inorganic element mass fraction. Exposure to the seasonal PM<sub>2.5</sub> samples without infection induced a moderate transcriptional response at 2&#xa0;h, with the winter PM<sub>2.5</sub> inducing the greatest response. The seasonal PM<sub>2.5</sub> exposures followed by viral infection resulted in a more robust transcriptional response at 2&#xa0;h p.i. with the winter, spring, and fall PM<sub>2.5</sub> samples (but not the summer PM<sub>2.5</sub>) upregulating many inflammatory pathways. At 24&#xa0;h p.i., only the spring PM<sub>2.5</sub> sample increased inflammatory and antiviral mediator proteins in the basolateral medium, while winter PM<sub>2.5</sub> increased these inflammatory markers in the mock infected cultures.</p> Conclusions <p>Seasonal variations in PM2.5 composition during winter, spring, and fall—coinciding with influenza season—likely enhance pro-inflammatory responses to viral infection, with early inflammation contributing to worsened pathogenesis.</p> Graphical abstract <p><InlineMediaObject> <ImageObject Color="Color" FileRef="MediaObjects/12989_2025_643_Figa_HTML.png" Format="PNG" Height="1154" Rendition="HTML" Resolution="300" Type="LinedrawHalftone" Width="2008" /> </InlineMediaObject></p>

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Seasonal PM2.5 exposures induce differential responses to influenza A virus infection in primary human airway epithelial cells

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年10月29日

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  • Stephanie A. Brocke,
  • Timothy Smyth,
  • Hong Dang,
  • Adam Speen,
  • Yong Ho Kim,
  • Cara Christianson,
  • Kasey Kovalcik,
  • Joseph Patrick Pancras,
  • Michael Hays,
  • Zhen An,
  • Weidong Wu,
  • Ilona Jaspers

摘要

Background

Air pollution, specifically fine particulate matter (PM2.5), in China is responsible for millions of excess deaths each decade. Examinations of Chinese municipalities have revealed correlations between ambient PM2.5 levels and the prevalence and severity of respiratory viral infections. Seasonal sources of ambient PM2.5 vary, with coal combustion for indoor heating significantly contributing during colder months. Due to this seasonality, we hypothesized that PM2.5 collected in Xinxiang, China would differentially alter the response to subsequent influenza A/California/04/2009 (H1N1) viral infection in a primary human nasal epithelial cell (HNEC) culture model in a seasonality-specific manner. After the PM2.5 samples were chemically analyzed, HNECs collected from males (N = 4) and females (N = 3) grown at air-liquid interface were exposed to 22 µg/cm2 of seasonal PM2.5 followed by inoculation with influenza A H1N1 at MOI = 0.001. At 2 and 24 h post infection (p.i.) we assessed transcriptional changes and basolateral release of immune and antiviral mediators.

Results

Summer and fall PM2.5 samples contained a greater organic carbon mass fraction compared to winter and spring. Winter contained the largest mass fraction of anionic components and spring the largest inorganic element mass fraction. Exposure to the seasonal PM2.5 samples without infection induced a moderate transcriptional response at 2 h, with the winter PM2.5 inducing the greatest response. The seasonal PM2.5 exposures followed by viral infection resulted in a more robust transcriptional response at 2 h p.i. with the winter, spring, and fall PM2.5 samples (but not the summer PM2.5) upregulating many inflammatory pathways. At 24 h p.i., only the spring PM2.5 sample increased inflammatory and antiviral mediator proteins in the basolateral medium, while winter PM2.5 increased these inflammatory markers in the mock infected cultures.

Conclusions

Seasonal variations in PM2.5 composition during winter, spring, and fall—coinciding with influenza season—likely enhance pro-inflammatory responses to viral infection, with early inflammation contributing to worsened pathogenesis.

Graphical abstract