Simian human immunodeficiency virus-associated pneumonia correlates with increased expression of MCP-1, CXCL10, and viral RNA in the lungs of rhesus macaques

Yongjun Sui, Shanping Li, David Pinson, Istvan Adany, Zhuang Li, Francois Villinger, Opendra Narayan, Shilpa Buch

Research output: Contribution to journalArticle

19 Scopus citations

Abstract

Pulmonary disorders are the most frequent cause of death in HIV-1-infected individuals with AIDS and remain important even in the current era of potent antiretroviral therapy. Macaques infected with Simian/Human Immunodeficiency Virus (SHIV) develop pulmonary disease and concurrent opportunistic infections similar to those observed in HIV-infected individuals, thereby providing an excellent working model to elucidate the pathogenesis of the human lung disease. Since chemokines play a crucial role in the recruitment of inflammatory cells to tissues, we investigated the relationship between respiratory disease and the levels of chemokines, monocyte chemotactic protein-1 (MCP-1) and CXCL10, in the lungs of SHIV-infected rhesus macaques. We found that lung pathology in infected macaques was closely associated with overexpression of MCP-1 and CXCL10. In addition, these chemokines could, in part, be responsible for the recruitment of inflammatory cells infiltrating into the diseased lungs as demonstrated by chemotactic assays. Lung pathology and increased levels of MCP-1 and CXCL10 correlated with high viral loads in the lung parenchyma. Using confocal microscopy, we identified SHIV-infected macrophages as the major producers of MCP-1 and CXCL10 in the diseased lungs. These data suggest that chemokine overexpression plays an important role in the pathogenesis of SHIV-associated pulmonary disease in macaques.

Original languageEnglish (US)
Pages (from-to)355-365
Number of pages11
JournalAmerican Journal of Pathology
Volume166
Issue number2
DOIs
StatePublished - Feb 2005

ASJC Scopus subject areas

  • Pathology and Forensic Medicine

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