1. Glucocorticoid administration accelerates mortality of pneumovirus-infected mice.
- Author
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Domachowske JB, Bonville CA, Ali-Ahmad D, Dyer KD, Easton AJ, and Rosenberg HF
- Subjects
- Animals, Chemokine CCL2 metabolism, Chemokine CCL4, Disease Models, Animal, Humans, Lung immunology, Lung virology, Macrophage Inflammatory Proteins metabolism, Mice, Mice, Inbred BALB C, Murine pneumonia virus isolation & purification, Pneumonia, Viral drug therapy, Pneumonia, Viral virology, Pneumovirus Infections drug therapy, Pneumovirus Infections mortality, Pneumovirus Infections virology, Treatment Outcome, Virus Replication drug effects, Anti-Inflammatory Agents administration & dosage, Hydrocortisone administration & dosage, Murine pneumonia virus physiology, Pneumonia, Viral immunology, Pneumovirus Infections immunology
- Abstract
The use of glucocorticoids for the treatment of symptoms associated with respiratory syncytial virus (RSV) infection has been questioned. To evaluate the sequelae of glucocorticoid administration in the setting of pneumovirus infection in vivo, hydrocortisone was administered to mice infected with pneumonia virus of mice (PVM), a pneumovirus and natural rodent pathogen that is closely related to RSV and replicates the signs and symptoms of severe human RSV infection. Results showed that hydrocortisone spared the pulmonary neutrophilia but resulted in ablation of the pulmonary eosinophilia, despite continued production of the relevant chemoattractant, macrophage inflammatory protein-1alpha. Hydrocortisone also led to diminished production of inducible nitric oxide synthase and accumulation of reactive nitrogen species in lung tissue and bronchoalveolar lavage fluid and diminished lymphocyte recruitment. PVM-infected mice responded to hydrocortisone with enhanced viral replication and accelerated mortality. These results suggest several mechanisms to explain why glucocorticoid therapy may be of limited benefit in the overall picture of pneumovirus infection.
- Published
- 2001
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