Interferon-beta, but not tumor necrosis factor-alpha, production in response to poly I:C is maintained despite exhaustive exercise in mice

[1]  Wilbert A. Derbigny,et al.  The Chlamydia muridarum-Induced IFN-β Response Is TLR3-Dependent in Murine Oviduct Epithelial Cells , 2010, The Journal of Immunology.

[2]  H. Yano,et al.  Exhaustive exercise reduces TNF-α and IFN-α production in response to R-848 via toll-like receptor 7 in mice , 2010, European Journal of Applied Physiology.

[3]  H. Yano,et al.  Exhaustive Exercise Reduces Tumor Necrosis Factor-α Production in Response to Lipopolysaccharide in Mice , 2010, Neuroimmunomodulation.

[4]  J. Davis,et al.  Exercise stress increases susceptibility to influenza infection , 2008, Brain, Behavior, and Immunity.

[5]  Michael Gale,et al.  Toll-Like Receptor 3 Has a Protective Role against West Nile Virus Infection , 2008, Journal of Virology.

[6]  H. Yano,et al.  The reduction of voluntary physical activity after poly I:C injection is independent of the effect of poly I:C-induced interferon-beta in mice , 2008, Physiology & Behavior.

[7]  F. Mooren,et al.  Exercise-induced redistribution of T lymphocytes is regulated by adrenergic mechanisms , 2008, Brain, Behavior, and Immunity.

[8]  J. Woods,et al.  Beta-Adrenergic Receptor Blockade Attenuates the Exercise-Induced Suppression of TNF-Alpha in Response to Lipopolysaccharide in Rats , 2007, Neuroimmunomodulation.

[9]  S. Cole,et al.  Adrenergic inhibition of innate anti-viral response: PKA blockade of Type I interferon gene transcription mediates catecholamine support for HIV-1 replication , 2006, Brain, Behavior, and Immunity.

[10]  T. Muta,et al.  A missense mutation of the Toll-like receptor 3 gene in a patient with influenza-associated encephalopathy. , 2006, Clinical immunology.

[11]  S. Akira,et al.  Pathogen Recognition and Innate Immunity , 2006, Cell.

[12]  A. Leon,et al.  Dopamine inhibits responses of astroglia-enriched cultures to lipopolysaccharide via a β-adrenoreceptor-mediated mechanism , 2004, Journal of Neuroimmunology.

[13]  C. Szabó,et al.  Dopamine suppresses IL-12 p40 production by lipopolysaccharide-stimulated macrophages via a β-adrenoceptor-mediated mechanism , 2002, Journal of Neuroimmunology.

[14]  R. Flavell,et al.  Recognition of double-stranded RNA and activation of NF-κB by Toll-like receptor 3 , 2001, Nature.

[15]  M. Kohut,et al.  Prolonged exercise suppresses antigen-specific cytokine response to upper respiratory infection. , 2001, Journal of applied physiology.

[16]  J. Woods Exercise and Neuroendocrine Modulation of Macrophage Function , 2000, International journal of sports medicine.

[17]  N. Kadowaki,et al.  The nature of the principal type 1 interferon-producing cells in human blood. , 1999, Science.

[18]  J. Davis,et al.  Exercise effects on IFN-β expression and viral replication in lung macrophages after HSV-1 infection. , 1998, American journal of physiology. Lung cellular and molecular physiology.

[19]  C. E. Andrade-Mena Catecholamines inhibit α/β interferon production induced by lipopolysaccharide , 1996, Regulatory Peptides.

[20]  R. Spengler,et al.  Temporal regulation by adrenergic receptor stimulation of macrophage ( MΦ)-derived tumor necrosis factor (TNF) production post-LPS challenge , 1996, Journal of Neuroimmunology.

[21]  G. Bagby,et al.  Prior exercise suppresses the plasma tumor necrosis factor response to bacterial lipopolysaccharide. , 1994, Journal of applied physiology.

[22]  H. Ullum,et al.  NK cell response to physical activity: possible mechanisms of action. , 1994, Medicine and science in sports and exercise.

[23]  J. Woods,et al.  Moderate exercise early after influenza virus infection reduces the Th1 inflammatory response in lungs of mice. , 2006, Exercise immunology review.

[24]  C. E. Andrade-Mena Catecholamines inhibit alpha/beta interferon production induced by lipopolysaccharide. , 1996, Regulatory peptides.