Effect of Vitamin A Deficiency in Dysregulating Immune Responses to Influenza Virus and Increasing Mortality Rates After Bacterial Coinfections
| Autor: | Amber M. Smith, Amanda P. Smith, Jonathan A. McCullers, Peter Vogel, Rhiannon R. Penkert, Julia L. Hurwitz, Eike R. Hrincius |
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| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
Chemokine Orthomyxoviridae Pneumococcal Infections Virus Proinflammatory cytokine Major Articles and Brief Reports Mice 03 medical and health sciences 0302 clinical medicine Immune system Orthomyxoviridae Infections parasitic diseases medicine Animals Immunology and Allergy cardiovascular diseases Lung biology Coinfection Vitamin A Deficiency business.industry Immunity medicine.disease biology.organism_classification Mice Inbred C57BL Vitamin A deficiency Streptococcus pneumoniae 030104 developmental biology Infectious Diseases Immunology biology.protein Cytokines Respiratory virus biological phenomena cell phenomena and immunity business 030215 immunology |
| Zdroj: | J Infect Dis |
| ISSN: | 1537-6613 0022-1899 |
| Popis: | Background Secondary bacterial coinfections are ranked as a leading cause of hospitalization and morbid conditions associated with influenza. Because vitamin A deficiency (VAD) and insufficiency are frequent in both developed and developing countries, we asked how VAD influences coinfection severity. Methods VAD and control mice were infected with influenza virus for evaluation of inflammatory cytokines, cellular immune responses, and viral clearance. Influenza-infected mice were coinfected with Streptococcus pneumoniae to study weight loss and survival. Results Naive VAD mouse lungs exhibited dysregulated immune function. Neutrophils were enhanced in frequency and there was a significant reduction in RANTES (regulated on activation of normal T cells expressed and secreted), a chemokine instrumental in T-cell homing and recruitment. After influenza virus infection, VAD mice experienced failures in CD4+ T-cell recruitment and B-cell organization into lymphoid structures in the lung. VAD mice exhibited higher viral titers than controls and slow viral clearance. There were elevated levels of inflammatory cytokines and innate cell subsets in the lungs. However, arginase, a marker of alternatively activated M2 macrophages, was rare. When influenza-infected VAD animals were exposed to bacteria, they experienced a 100% mortality rate. Conclusion Data showed that VAD dysregulated the immune response. Consequently, secondary bacterial infections were 100% lethal in influenza-infected VAD mice. |
| Databáze: | OpenAIRE |
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