Perinatal exposure to Environmental Tobacco Smoke (ETS) enhances susceptibility to viral and secondary bacterial infections

Jocelyn A. Claude, Amy Grimm, Hannah P. Savage, Kent E Pinkerton

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

Studies suggest childhood exposure to environmental tobacco smoke (ETS) leads to increased incidence of infections of the lower respiratory tract. The objective of this study was to determine whether perinatal exposure to ETS increases the incidence, morbidity and severity of respiratory influenza infection and whether a secondary bacterial challenge at the peak of a pre-existing viral infection creates an enhanced host-pathogen susceptibility to an opportunistic infection. Timed-pregnant female Balb/c mice were exposed to either ETS for 6 h/day, 7 d/week beginning on gestation day 14 and continuing with the neonates to 6 weeks of age. Control animals were exposed to filtered air (FA). At the end of exposure, mice were intranasally inoculated with a murine-adapted influenza A. One week later, an intranasal inoculation of S. aureus bacteria was administered. The respective treatment groups were: bacteria only, virus only or virus+bacteria for both FA and ETS-exposed animals for a total of six treatment groups. Animal behavior and body weights were documented daily following infection. Mice were necropsied 1-day post-bacterial infection. Bronchoalveolar lavage fluid (BALF) cell analysis demonstrated perinatal exposure to ETS, compared to FA, leads to delayed but enhanced clinical symptoms and enhanced total cell influx into the lungs associated with viral infection followed by bacterial challenge. Viral infection significantly increases the number of neutrophils entering the lungs following bacterial challenge with either FA or ETS exposure, while the influx of lymphocytes and monocytes is significantly enhanced only by perinatal ETS exposure. There is a significant increase in peribronchiolar inflammation following viral infection in pups exposed to ETS compared with pups exposed to FA, but no change is noted in the degree of lung injury between FA and ETS-exposed animals following bacterial challenge. The data suggests perinatal exposure to ETS alters the response of neonates to the timing and severity of infection as well as ETS alters the pattern of inflammation and cellular influx into the lungs due to viral and bacterial infection.

Original languageEnglish (US)
Pages (from-to)3954-3964
Number of pages11
JournalInternational Journal of Environmental Research and Public Health
Volume9
Issue number11
DOIs
StatePublished - Nov 2012

Fingerprint

Environmental Exposure
Coinfection
Bacterial Infections
Smoke
Tobacco
Virus Diseases
Air
Bacteria
Respiratory Tract Infections
Lung
Human Influenza
Viruses
Inflammation
Animal Behavior
Incidence
Opportunistic Infections
Bronchoalveolar Lavage Fluid
Lung Injury
Infection
Monocytes

Keywords

  • Environmental tobacco smoke (ETS)
  • Influenza A
  • Perinatal
  • S. aureus

ASJC Scopus subject areas

  • Public Health, Environmental and Occupational Health
  • Health, Toxicology and Mutagenesis

Cite this

Perinatal exposure to Environmental Tobacco Smoke (ETS) enhances susceptibility to viral and secondary bacterial infections. / Claude, Jocelyn A.; Grimm, Amy; Savage, Hannah P.; Pinkerton, Kent E.

In: International Journal of Environmental Research and Public Health, Vol. 9, No. 11, 11.2012, p. 3954-3964.

Research output: Contribution to journalArticle

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abstract = "Studies suggest childhood exposure to environmental tobacco smoke (ETS) leads to increased incidence of infections of the lower respiratory tract. The objective of this study was to determine whether perinatal exposure to ETS increases the incidence, morbidity and severity of respiratory influenza infection and whether a secondary bacterial challenge at the peak of a pre-existing viral infection creates an enhanced host-pathogen susceptibility to an opportunistic infection. Timed-pregnant female Balb/c mice were exposed to either ETS for 6 h/day, 7 d/week beginning on gestation day 14 and continuing with the neonates to 6 weeks of age. Control animals were exposed to filtered air (FA). At the end of exposure, mice were intranasally inoculated with a murine-adapted influenza A. One week later, an intranasal inoculation of S. aureus bacteria was administered. The respective treatment groups were: bacteria only, virus only or virus+bacteria for both FA and ETS-exposed animals for a total of six treatment groups. Animal behavior and body weights were documented daily following infection. Mice were necropsied 1-day post-bacterial infection. Bronchoalveolar lavage fluid (BALF) cell analysis demonstrated perinatal exposure to ETS, compared to FA, leads to delayed but enhanced clinical symptoms and enhanced total cell influx into the lungs associated with viral infection followed by bacterial challenge. Viral infection significantly increases the number of neutrophils entering the lungs following bacterial challenge with either FA or ETS exposure, while the influx of lymphocytes and monocytes is significantly enhanced only by perinatal ETS exposure. There is a significant increase in peribronchiolar inflammation following viral infection in pups exposed to ETS compared with pups exposed to FA, but no change is noted in the degree of lung injury between FA and ETS-exposed animals following bacterial challenge. The data suggests perinatal exposure to ETS alters the response of neonates to the timing and severity of infection as well as ETS alters the pattern of inflammation and cellular influx into the lungs due to viral and bacterial infection.",
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