| Literature DB >> 29778672 |
Kamakshi Prudhula Devalraju1, Venkata Sanjeev Kumar Neela1, Ramulu Gaddam2, Arunabala Chaudhury3, Abhinav Van4, Siva Sai Krovvidi5, Ramakrishna Vankayalapati6, Vijaya Lakshmi Valluri7.
Abstract
HIV infection markedly increases the likelihood of latent tuberculosis infection progressing to active TB. Information on expression of TLR-2, myeloid differentiation factor (MyD88), IL-1R- associated kinase-4 (IRAK4) and nuclear factor kappa B (NF-kB) in HIV+LTBI+ and HIV+ patients with active TB disease is limited. We found significantly higher percentages of CD14+TLR2+ cells in PBMCs of HIV+LTBI+ patients compared to HIV-LTBI+ individuals. γ-irradiated Mtb was unable to induce MyD88, IRAK4 expression and IL-1β, MCP-1, IP-10 production in HIV+LTBI+ patients. Pleural fluids from HIV+TB+ patients had low IL-1β, MCP-1, IP-10 and high IL-10, TNF-α production. γ-irradiated Mtb stimulated CD14+ cells from HIV+TB+ patients had low IL-1β, MCP-1, IP-10 production and MyD88, IRAK4 and similar NF-kB expression compared to those from of HIV-TB+ patients. Our results suggest defective MyD88, IRAK4 but not NF-kB inhibit IL-1β, MCP-1 and IP-10 production by CD14+ cells of HIV+ individuals with LTBI and active TB disease in peripheral blood and at the site of disease.Entities:
Keywords: Cytokines; HIV; Human; Monocytes; TLR-2; Tuberculosis
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Year: 2018 PMID： 29778672 PMCID： PMC6103807 DOI： 10.1016/j.cyto.2018.05.005
Source DB: PubMed Journal: Cytokine ISSN： 1043-4666 Impact factor: 3.926