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An In vitro Model to Study Immune Responses of Human Peripheral Blood Mononuclear Cells to Human Respiratory Syncytial Virus Infection
Published on: December 10, 2013
Altered Treg and cytokine responses in RSV-infected infants
Allison F Christiaansen1, Muhammad A Syed2, Patrick P Ten Eyck3
1Department of Microbiology, University of Iowa, Iowa City, Iowa.
Insights
Severe RSV infection in infants is linked to fewer regulatory T cells (Tregs). Reduced Tregs impair immune control, leading to severe disease and inflammation. This finding offers new insights into RSV immunopathology.
Area of Science:
- Immunology
- Pediatrics
- Virology
Background:
- Respiratory syncytial virus (RSV) is a major cause of infant respiratory illness.
- The host immune response plays a critical role in RSV-induced disease severity.
- Insufficient regulation by regulatory T cells (Tregs) may lead to immunopathology in severe RSV infections.
Purpose of the Study:
- To investigate the role of regulatory T cells (Tregs) in severe RSV infection in infants.
- To explore the relationship between Treg frequencies, cytokine profiles, and clinical symptoms in RSV-infected infants.
Main Methods:
- Collected blood and nasal aspirates from RSV-infected and control infants.
- Quantified Treg frequencies using flow cytometry.
- Measured 24 cytokines in nasal aspirates using multiplex assays.
Main Results:
- Reduced frequency of activated Tregs observed in RSV-infected infants compared to controls.
- Th17-related cytokines (IL-1β, IL-17A, IL-23) correlated with decreased respiratory distress.
- Decreased levels of IL-33, important for Treg homeostasis, were found in RSV-infected children.
Conclusions:
- Decreased Treg numbers contribute to severe RSV infection by impairing immune response control.
- An inability to regulate the host inflammatory response is implicated in RSV pathogenesis.
- Findings suggest potential therapeutic targets for managing severe RSV disease.
Background:
Respiratory syncytial virus (RSV) is the leading cause of bronchiolitis and pneumonia in children under 1 y of age in the USA. The host immune response is believed to contribute to RSV-induced disease. We hypothesize that severe RSV infection in infants is mediated by insufficient regulation of the host immune response of regulatory T cells (Tregs) resulting in immunopathology.
Methods:
Blood and nasal aspirates from 23 RSV-infected and 17 control infants under 1 y of age were collected. Treg frequencies were determined by flow cytometry from peripheral blood mononuclear cells. Analysis of 24 cytokines was measured by multiplex assay on nasal aspirates.
Results:
We demonstrate that the frequency of activated Tregs is significantly reduced in the peripheral blood of RSV-infected infants compared with age-matched controls. Surprisingly, T helper (Th)17 related cytokines including interleukin (IL)-1β, IL-17A, and IL-23 were associated with a reduction in clinical symptoms of respiratory distress. In addition, the amount of IL-33 protein in nasal washes, a cytokine important in maintaining Treg homeostasis in mucosal tissues, was decreased in RSV-infected children.
Conclusion:
These results suggest that decreased Treg numbers and an inability to properly control the host inflammatory response results in severe RSV infection.
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