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International Journal of Inflammation
Volume 2018, Article ID 2157434, 6 pages
Research Article

Impaired Inflammatory Response to LPS in Type 2 Diabetes Mellitus

1Group of Cell Technologies, Institute of Molecular Biology, National Academy of Sciences, Yerevan, Armenia
2Laboratory of Molecular and Cellular Immunology, Institute of Molecular Biology, National Academy of Sciences, Yerevan, Armenia
3Russian-Armenian (Slavonic) University, Yerevan, Armenia

Correspondence should be addressed to Gayane Manukyan; moc.liamg@naykunam.ayag

Received 12 October 2017; Accepted 14 December 2017; Published 14 January 2018

Academic Editor: B. L. Slomiany

Copyright © 2018 Lusine Khondkaryan et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Type 2 diabetes mellitus (T2DM) is a severe health problem worldwide, reaching epidemic levels. High susceptibility to infections of T2DM patients indicates dysregulated immune responses to pathogens. However, innate immune responses, including monocyte functions, in T2DM are poorly investigated. Therefore, in this study we aimed to assess lipopolysaccharide- (LPS-) induced immune responses of circulating monocytes from T2DM patients. The results showed that monocytes from T2DM were hyporesponsive to LPS challenge as reflected by significantly suppressed secretion of TNFα () and expression of CD11b () and TLR4 () compared to those in monocytes from healthy subjects. Furthermore, LPS-induced IL-10 levels were similar in diabetic and healthy supernatants, while expression levels of CD163 were found to be downregulated on monocytes from T2DM () suggesting impaired ability of monocytes to switch their phenotype to anti-inflammatory. Taken together, our results suggest compromised function of monocytes in T2DM, which may explain, at least partly, high incidence of infection in these patients.