tetano
Editor, Senior Moderator
Clin Vaccine Immunol. 2012 Jul 11. [Epub ahead of print]
Memory CD8+ T cells are sufficient to alleviate impaired host resistance to influenza A virus infection caused by neonatal oxygen supplementation.
Giannandrea M, Yee M, O'Reilly MA, Lawrence BP.
Source
Departments of Environmental Medicine.
Abstract
Supplemental oxygen administered to preterm infants is an important clinical intervention, but it is associated with life-long changes in lung development and increased sensitivity to respiratory viral infections. The precise immunological changes caused by neonatal oxygen treatment remain poorly understood. We previously reported that adult mice exposed to supplemental oxygen as neonates display persistent pulmonary inflammation and enhanced mortality when given a sub-lethal influenza A virus infection. These changes suggest that neonatal hyperoxia may have impaired the cytotoxic CD8(+) T cell response required for clearing the virus. In this study, we show that although host resistance to several different strains of influenza A virus is reduced by neonatal hyperoxia, this treatment does not impair viral clearance, nor does it alter the magnitude of the virus-specific CD8(+) T cell response to primary infection. Moreover, memory T cells are sufficient to ameliorate the increased morbidity and mortality and alleviate excessive lung damage observed in mice exposed to hyperoxia as neonates, and attribute this principally to virus-specific memory CD8(+) T cells. Thus we show that neonatal hyperoxia reduces host resistance to influenza virus infection without diminishing the function of cytotoxic T lymphocytes or the generation of virus-specific memory T cells, and that CD8(+) memory T cells are sufficient to provide protection from negative consequences of this important life saving intervention. Our findings suggest vaccines that generate robust T cell memory may be efficacious at reducing the increased sensitivity to respiratory viral infections in people born prematurely.
PMID:
22787195
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/22787195
Memory CD8+ T cells are sufficient to alleviate impaired host resistance to influenza A virus infection caused by neonatal oxygen supplementation.
Giannandrea M, Yee M, O'Reilly MA, Lawrence BP.
Source
Departments of Environmental Medicine.
Abstract
Supplemental oxygen administered to preterm infants is an important clinical intervention, but it is associated with life-long changes in lung development and increased sensitivity to respiratory viral infections. The precise immunological changes caused by neonatal oxygen treatment remain poorly understood. We previously reported that adult mice exposed to supplemental oxygen as neonates display persistent pulmonary inflammation and enhanced mortality when given a sub-lethal influenza A virus infection. These changes suggest that neonatal hyperoxia may have impaired the cytotoxic CD8(+) T cell response required for clearing the virus. In this study, we show that although host resistance to several different strains of influenza A virus is reduced by neonatal hyperoxia, this treatment does not impair viral clearance, nor does it alter the magnitude of the virus-specific CD8(+) T cell response to primary infection. Moreover, memory T cells are sufficient to ameliorate the increased morbidity and mortality and alleviate excessive lung damage observed in mice exposed to hyperoxia as neonates, and attribute this principally to virus-specific memory CD8(+) T cells. Thus we show that neonatal hyperoxia reduces host resistance to influenza virus infection without diminishing the function of cytotoxic T lymphocytes or the generation of virus-specific memory T cells, and that CD8(+) memory T cells are sufficient to provide protection from negative consequences of this important life saving intervention. Our findings suggest vaccines that generate robust T cell memory may be efficacious at reducing the increased sensitivity to respiratory viral infections in people born prematurely.
PMID:
22787195
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/22787195