TY - JOUR
T1 - Tuberculosis and cardiovascular disease
T2 - Linking the epidemics
AU - Huaman, Moises A.
AU - Henson, David
AU - Ticona, Eduardo
AU - Sterling, Timothy R.
AU - Garvy, Beth A.
N1 - Publisher Copyright:
© 2015 Huaman et al.
PY - 2015
Y1 - 2015
N2 - The burden of tuberculosis and cardiovascular disease (CVD) is enormous worldwide. CVD rates are rapidly increasing in low- and middle-income countries. Public health programs have been challenged with the overlapping tuberculosis and CVD epidemics. Monocyte/macrophages, lymphocytes and cytokines involved in cellular mediated immune responses against Mycobacterium tuberculosis are also main drivers of atherogenesis, suggesting a potential pathogenic role of tuberculosis in CVD via mechanisms that have been described for other pathogens that establish chronic infection and latency. Studies have shown a pro-atherogenic effect of antibodymediated responses against mycobacterial heat shock protein-65 through cross reaction with self-antigens in human vessels. Furthermore, subsets of mycobacteria actively replicate during latent tuberculosis infection (LTBI), and recent studies suggest that LTBI is associated with persistent chronic inflammation that may lead to CVD. Recent epidemiologic work has shown that the risk of CVD in persons who develop tuberculosis is higher than in persons without a history of tuberculosis, even several years after recovery from tuberculosis. Together, these data suggest that tuberculosis may play a role in the pathogenesis of CVD. Further research to investigate a potential link between tuberculosis and CVD is warranted.
AB - The burden of tuberculosis and cardiovascular disease (CVD) is enormous worldwide. CVD rates are rapidly increasing in low- and middle-income countries. Public health programs have been challenged with the overlapping tuberculosis and CVD epidemics. Monocyte/macrophages, lymphocytes and cytokines involved in cellular mediated immune responses against Mycobacterium tuberculosis are also main drivers of atherogenesis, suggesting a potential pathogenic role of tuberculosis in CVD via mechanisms that have been described for other pathogens that establish chronic infection and latency. Studies have shown a pro-atherogenic effect of antibodymediated responses against mycobacterial heat shock protein-65 through cross reaction with self-antigens in human vessels. Furthermore, subsets of mycobacteria actively replicate during latent tuberculosis infection (LTBI), and recent studies suggest that LTBI is associated with persistent chronic inflammation that may lead to CVD. Recent epidemiologic work has shown that the risk of CVD in persons who develop tuberculosis is higher than in persons without a history of tuberculosis, even several years after recovery from tuberculosis. Together, these data suggest that tuberculosis may play a role in the pathogenesis of CVD. Further research to investigate a potential link between tuberculosis and CVD is warranted.
KW - Atherosclerosis
KW - Cardiovascular diseases
KW - Communicable disease
KW - Epidemics
KW - Inflammation
KW - Tuberculosis
UR - http://www.scopus.com/inward/record.url?scp=85069238617&partnerID=8YFLogxK
U2 - 10.1186/s40794-015-0014-5
DO - 10.1186/s40794-015-0014-5
M3 - Artículo de revisión
AN - SCOPUS:85069238617
SN - 2055-0936
VL - 1
JO - Tropical Diseases, Travel Medicine and Vaccines
JF - Tropical Diseases, Travel Medicine and Vaccines
IS - 1
M1 - 10
ER -