This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Simian Immunodeficiency Virus (SIV) infection of macaques is an important animal model for the acquired immunodeficiency syndrome (AIDS) that recapitulates most features of HIV infection, including CNS disease. Alcohol has been shown to exacerbate other disease states, notably pneumonia. Activation of NFKB is known to be an initial step in the development of disease. To determine if SIV infection of macaques exacerbates the activation of NFKB and its subsequent translocation from the cytoplasm to the perinuclear area we obtained bronchoalveolar lavage (BAL) fluids from rhesus macaques before and after infection with pneumococcus. We also examined lung tissues obtained from the same macaques at necropsy. In situ hybridization and immunohistochemistry was performed on these tissues to determine if there is colocaliztion of the virus and NFKB within nucleus of cells. In addition to increased expression in type II pneumocytes, NFKB was activated in SIV-infected macrophages and also in adjacent macrophages that have recently migrated into lungs in response to pneumococcus challenge. These experiments can be only performed in the rhesus macaque model due to obtaining samples before infection with SIV and at timed intervals thereafter. Immunohistochemistry and in situ hybridization indicate that inoculation of an SIV-infected macaque with pneumococcus leads to an increase in NFKB activation and increased numbers of SIV-infected cells within the lungs when compared with cells derived from the same lung in the same animal previously.

Agency
National Institute of Health (NIH)
Institute
National Center for Research Resources (NCRR)
Type
Primate Research Center Grants (P51)
Project #
5P51RR000164-45
Application #
7349002
Study Section
Special Emphasis Panel (ZRR1-CM-9 (01))
Project Start
2006-05-01
Project End
2007-04-30
Budget Start
2006-05-01
Budget End
2007-04-30
Support Year
45
Fiscal Year
2006
Total Cost
$65,435
Indirect Cost
Name
Tulane University
Department
Pathology
Type
Schools of Medicine
DUNS #
053785812
City
New Orleans
State
LA
Country
United States
Zip Code
70118
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Kumar, Vinay; Mansfield, Joshua; Fan, Rong et al. (2018) miR-130a and miR-212 Disrupt the Intestinal Epithelial Barrier through Modulation of PPAR? and Occludin Expression in Chronic Simian Immunodeficiency Virus-Infected Rhesus Macaques. J Immunol 200:2677-2689
Parthasarathy, Geetha; Philipp, Mario T (2018) Intracellular TLR7 is activated in human oligodendrocytes in response to Borrelia burgdorferi exposure. Neurosci Lett 671:38-42
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Yi, Fei; Guo, Jia; Dabbagh, Deemah et al. (2017) Discovery of Novel Small-Molecule Inhibitors of LIM Domain Kinase for Inhibiting HIV-1. J Virol 91:
Jorgensen, Matthew J; Lambert, Kelsey R; Breaux, Sarah D et al. (2017) Pair housing of Vervets/African Green Monkeys for biomedical research. Am J Primatol 79:1-10
Ramesh, Geeta; Martinez, Alejandra N; Martin, Dale S et al. (2017) Effects of dexamethasone and meloxicam on Borrelia burgdorferi-induced inflammation in glial and neuronal cells of the central nervous system. J Neuroinflammation 14:28
Parthasarathy, Geetha; Philipp, Mario T (2017) Receptor tyrosine kinases play a significant role in human oligodendrocyte inflammation and cell death associated with the Lyme disease bacterium Borrelia burgdorferi. J Neuroinflammation 14:110

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