Abstract：
:The presence of metabolic syndrome (MS) per se or its separated components in HIV-infected patients contributes to an accelerated aging and increased cardiovascular risk. Gut microbiota (GM) dysbiosis has been linked with chronic inflammation associated with MS in a general non-infected population. However, no studies concerning GM have been performed in HIV-infected patients with MS. The aim of this study was to analyze bacterial translocation, inflammation, and GM composition in HIV-infected patients with and without MS. A total of 51 HIV-infected patients were recruited and classified according to the presence of MS (40 patients without MS and 11 with MS). Markers of bacterial translocation, inflammation, and cardiovascular risk were measured and GM was analyzed using 16S rRNA gene deep sequencing. No differences were observed among both HIV-infected groups in the bacterial translocation markers LBP and sCD14. A tendency to increase the inflammatory markers IL-6 (p = 0.069) and MCP-1 (p = 0.067) was observed in those patients suffering from MS. An increase in the cardiovascular risk markers PAI-1 (p = 0.007) and triglycerides/HDL cholesterol ratio (p < 0.0001) was also found in the MS group. No significant changes were observed at phylum level although a decrease in the abundance of seven genera and seven bacterial species, including some anti-inflammatory bacteria, was observed in HIV-infected patients with MS. To summarize, the presence of MS was not accompanied by major changes in GM, although the reduction observed in some anti-inflammatory bacteria may be clinically useful to develop strategies to minimize inflammation and its future deleterious consequences in these HIV-infected patients.
journal_name
J Physiol Biochemjournal_title
Journal of physiology and biochemistryauthors
Villanueva-Millán MJ,Pérez-Matute P,Recio-Fernández E,Lezana Rosales JM,Oteo JAdoi
10.1007/s13105-019-00673-9subject
Has Abstractpub_date
2019-08-01 00:00:00pages
299-309issue
3eissn
1138-7548issn
1877-8755pii
10.1007/s13105-019-00673-9journal_volume
75pub_type
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