Topical Exposure to Triclosan Inhibits Th1 Immune Responses and Reduces T Cells Responding to Influenza Infection in Mice

Details

• Personal Author:
  Anderson, Stacey E. ; Baur R ; Blachere F ; Lukomska E ; Marshall NB ; Noti JD ; Othumpangat S ; Shane HL ; Weatherly LM
• Description:
  Healthcare workers concurrently may be at a higher risk of developing respiratory infections and allergic disease, such as asthma, than the general public. Increased incidence of allergic diseases is thought to be caused, in part, due to occupational exposure to chemicals that induce or augment Th2 immune responses. However, whether exposure to these chemical antimicrobials can influence immune responses to respiratory pathogens is unknown. Here, we use a BALB/c murine model to test if the Th2-promoting antimicrobial chemical triclosan influences immune responses to influenza A virus. Mice were dermally exposed to 2% triclosan for 7 days prior to infection with a sub-lethal dose of mouse adapted PR8 A(H1N1) virus (50 pfu); triclosan exposure continued until 10 days post infection (dpi). Infected mice exposed to triclosan did not show an increase in morbidity or mortality, and viral titers were unchanged. Assessment of T cell responses at 10 dpi showed a decrease in the number of total and activated (CD44hi) CD4+ and CD8+ T cells at the site of infection (BAL and lung) in triclosan exposed mice compared to controls. Influenza-specific CD4+ and CD8+ T cells were assessed using MHCI and MHCII tetramers, with reduced populations, although not reaching statistical significance at these sites following triclosan exposure. Reductions in the Th1 transcription factor T-bet were seen in both activated and tetramer+ CD4+ and CD8+ T cells in the lungs of triclosan exposed infected mice, indicating reduced Th1 polarization and providing a potential mechanism for numerical reduction in T cells. Overall, these results indicate that the immune environment induced by triclosan exposure has the potential to influence the developing immune response to a respiratory viral infection and may have implications for healthcare workers who may be at an increased risk for developing infectious diseases. [Description provided by NIOSH]
• Subjects:
  Animals Asthma Asthma, Occupational Environmental Exposure Health Personnel Hypersensitivity Laboratories Lung Lung Diseases Occupational Health Respiratory System Respiratory Tract Diseases Risk Assessment Risk Factors Safety Viral Diseases

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• Keywords:
  Allergic Disorders Bronchial Asthma Chemicals Diseases Exposure Levels Health Care Health Care Workers Laboratory Animals Lung Disorders Pulmonary System Disorders Respiratory Infections Reticuloendothelial System Disorders Risk Factors Viral Infections

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• ISSN:
  1932-6203
• Document Type:
  Text
• Genre:
  Journal Article
• Place as Subject:
  OSHA Region 3 ; West Virginia
• CIO:
  National Institute for Occupational Safety and Health (NIOSH)
• Division:
  HELD - Health Effects Laboratory Division
• Topic:
  Workplace Safety & Health
• Location:
  North America
• Volume:
  15
• Issue:
  12
• NIOSHTIC Number:
  nn:20061862
• Citation:
  PLoS One 2020 Dec; 15(12):e0244436
• Contact Point Address:
  Hillary L.Shane, Allergy and Clinical Immunology Branch, Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Centers for Disease Control and Prevention, Morgantown, WV
• Email:
  hshane@cdc.gov
• CAS Registry Number:
  Triclosan (CAS RN 3380-34-5)
• Federal Fiscal Year:
  2021
• NORA Priority Area:
  Healthcare and Social Assistance
• Peer Reviewed:
  True
• Source Full Name:
  PLoS One
• Collection(s):
  National Institute for Occupational Safety and Health
• Main Document Checksum:
  urn:sha-512:0a643282c2ca04e5fa9189181759c05174fee4dc6ee9e862edf51b658054f947803c0e67abcc4a5925fc3ff6337cdc7d270a2c8e5feebe7406fbd78e546989f3
• Download URL:
  https://stacks.cdc.gov/view/cdc/225220/cdc_225220_DS1.pdf
• File Type:
  [PDF - 2.58 MB ]