Galectin-3, Galectin-9, and Interleukin-18 Are Associated with Monocyte/Macrophage Activation and Turnover More so than Simian Immunodeficiency Virus-Associated Cardiac Pathology or Encephalitis.

Autor: Ding AK; Department of Biology, Boston College, Chestnut Hill, Massachusetts, USA., Wallis ZK; Department of Biology, Boston College, Chestnut Hill, Massachusetts, USA., White KS; Department of Biology, Boston College, Chestnut Hill, Massachusetts, USA., Sumer CE; Department of Biology, Boston College, Chestnut Hill, Massachusetts, USA., Kim WK; Division of Microbiology, Tulane National Primate Research Center, Tulane University, Covington, Louisiana, USA.; Department of Microbiology & Immunology, Tulane University School of Medicine, New Orleans, Louisiana, USA., Ardeshir A; Division of Microbiology, Tulane National Primate Research Center, Tulane University, Covington, Louisiana, USA.; Department of Microbiology & Immunology, Tulane University School of Medicine, New Orleans, Louisiana, USA., Williams KC; Department of Biology, Boston College, Chestnut Hill, Massachusetts, USA.
Jazyk: angličtina
Zdroj: AIDS research and human retroviruses [AIDS Res Hum Retroviruses] 2024 Sep; Vol. 40 (9), pp. 531-542. Date of Electronic Publication: 2024 Jun 12.
DOI: 10.1089/AID.2024.0008
Abstrakt: Despite antiretroviral therapy (ART), people living with HIV (PLWH) are at increased risk of developing cardiovascular disease (CVD) and HIV-associated neurocognitive disorder (HAND), among other comorbidities. Studies from ART-treated individuals identified galectin-3 (gal-3) and interleukin (IL)-18 as CVD biomarkers, galectin-9 (gal-9) as a HAND biomarker, and sCD163, a marker of monocyte/macrophage activation, as a biomarker of both. We asked if plasma gal-3, gal-9, and IL-18 are associated with an individual comorbidity or increase in both with animals that develop AIDS with both pathologies versus (CVD-path) alone or simian immunodeficiency virus encephalitis (SIVE) alone. We found that no biomarkers were selective between individual pathologies, and all biomarkers increased with co-development of CVD-path and SIVE (gal-3, p = 0.11; gal-9, p = 0.001; IL-18, p = 0.007; sCD163, p < 0.001; %BrdU p = 0.02). Although gal-3, gal-9, and IL-18 did not distinguish between pathologies, they correlated strongly with one another, with sCD163, a marker of monocyte/macrophage activation, and the %BrdU monocytes, a marker of monocyte turnover. Compared to animals with CVD-path or SIVE alone, animals that co-developed both pathologies had consistently elevated IL-18 throughout infection ( p = 0.02) and increased sCD163 in late infection ( p = 0.01). These data indicate that gal-3, gal-9, and IL-18 are associated with monocyte/macrophage activation by sCD163 and monocyte turnover by the %BrdU+ monocytes more so than CVD-path or SIVE.
Databáze: MEDLINE