G
Gerwyn
Guest
Increased proinflammatory cytokine and chemokine responses and microglial infection following inoculation with neural stem cells infected with polytropic murine retroviruses(XMRV type Viruses)
Purchase the full-text article
References and further reading may be available for this article. To view references and further reading you must purchase this article.
Karin E. Petersona, Corresponding Author Contact Information, E-mail The Corresponding Author, Leonard H. Evansb, Kathy Wehrlyb and Bruce Chesebrob
aDepartment of Pathobiological Sciences, School of Veterinary Medicine, Louisiana State University, Skip Bertman Dr., Baton Rouge, LA 70803, USA
bLaboratory of Persistent Viral Diseases, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, 903 South 4th Street, Hamilton, MT 59840, USA
Received 13 April 2006;
revised 22 May 2006;
accepted 12 June 2006.
Available online 27 July 2006.
Abstract
Proinflammatory cytokines and chemokines are often detected in brain tissue of patients with neurological diseases such as multiple sclerosis (MS), HIV-associated dementia (HAD) and Alzheimer's disease (AD). We have utilized a mouse model of retrovirus-induced neurological disease to examine how these proinflammatory responses contribute to neuropathogenesis. In previous studies with this model, a correlation was found between neurovirulence and cytokine and chemokine expression. However, it was unclear whether the induction of these cytokines and chemokines was in response to specific virus envelope determinants or was regulated by the level of virus infection in the brain. In the current study, we demonstrated that multiple polytropic retroviruses induced cytokine and chemokine mRNA expression following increased virus levels in the brain. Increased virus levels of polytropic viruses also correlated with increased neuropathogenesis. In contrast, the ecotropic retrovirus, FB29, did not induce cytokine or chemokine mRNA expression or neurological disease, despite virus levels either similar to or higher than the polytropic retroviruses. As polytropic and ecotropic viruses utilize different receptors for entry, these receptors may play a critical role in the induction of these innate immune responses in the brain.
Keywords: Chemokines; Cytokines; Brain; Neuropathogenesis; Microglia; Retrovirus; Mouse
Purchase the full-text article
References and further reading may be available for this article. To view references and further reading you must purchase this article.
Karin E. Petersona, Corresponding Author Contact Information, E-mail The Corresponding Author, Leonard H. Evansb, Kathy Wehrlyb and Bruce Chesebrob
aDepartment of Pathobiological Sciences, School of Veterinary Medicine, Louisiana State University, Skip Bertman Dr., Baton Rouge, LA 70803, USA
bLaboratory of Persistent Viral Diseases, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, 903 South 4th Street, Hamilton, MT 59840, USA
Received 13 April 2006;
revised 22 May 2006;
accepted 12 June 2006.
Available online 27 July 2006.
Abstract
Proinflammatory cytokines and chemokines are often detected in brain tissue of patients with neurological diseases such as multiple sclerosis (MS), HIV-associated dementia (HAD) and Alzheimer's disease (AD). We have utilized a mouse model of retrovirus-induced neurological disease to examine how these proinflammatory responses contribute to neuropathogenesis. In previous studies with this model, a correlation was found between neurovirulence and cytokine and chemokine expression. However, it was unclear whether the induction of these cytokines and chemokines was in response to specific virus envelope determinants or was regulated by the level of virus infection in the brain. In the current study, we demonstrated that multiple polytropic retroviruses induced cytokine and chemokine mRNA expression following increased virus levels in the brain. Increased virus levels of polytropic viruses also correlated with increased neuropathogenesis. In contrast, the ecotropic retrovirus, FB29, did not induce cytokine or chemokine mRNA expression or neurological disease, despite virus levels either similar to or higher than the polytropic retroviruses. As polytropic and ecotropic viruses utilize different receptors for entry, these receptors may play a critical role in the induction of these innate immune responses in the brain.
Keywords: Chemokines; Cytokines; Brain; Neuropathogenesis; Microglia; Retrovirus; Mouse