Moreover, it was observed that nicotine decreases the production of interleukin (IL)-6 and C-C chemokine ligand (CCL)5 during Mtb infection in epithelial cells (EpCs), whereas in macrophages derived from human monocytes (MDMs) there is a decrease in IL-8, IL-6, tumor necrosis factor (TNF)-α, IL-10, CCL2, C-X-C chemokine ligand (CXCL)9 and CXCL10 only during infection with Mtb.
IL-2 rs2069762 (recessive comparison), IL-4 rs2243250 (recessive and allele comparisons), IL-6 rs1800795 (dominant, recessive and allele comparisons), IL-8rs4073 (dominant, recessive and allele comparisons), IL-10 rs1800871 (dominant, recessive and allele comparisons) and IL-10 rs1800896 (recessive comparison) polymorphisms were all significantly associated with TB in the total population.
ML2044-stimulated IL-4 and CXCL8/IL-8 achieved the highest sensitivity (85.71% and 100%) and the highest specificity (95.24% and 84.21%) for discriminating PB patients from HHCs and TB patients, respectively.
IL-6 rs1800795 (1750 cases and 2335 controls, dominant, recessive and allele comparisons), IL-8rs4073 (1125 cases and 1188 controls, dominant, recessive and allele comparisons), IL-10 rs1800871 (5528 cases and 7671 controls, dominant, recessive and allele comparisons), IL-10 rs1800872 (5269 cases and 7013 controls, dominant and allele comparisons) and IL-10 rs1800896 (7564 cases and 8952 controls, recessive comparison) polymorphisms were all significantly associated with TB in overall combined analyses.
HCWs<sup>LTB+</sup> who were highly exposed to active TB (≥3 hours per day) had significantly higher IFN-γ and IL-8 responses (p ≤ 0.02) than HCWs <sup>LTB+</sup> not in direct contact with active TB patients.
Our results with CLEC9A-knocked down cells and a CLEC9A-Fc fusion protein as blocking agents show that CLEC9A is involved in the activation of SYK and MAPK signaling in response to heat-killed M. tuberculosis H37Ra treatment, and it then promotes the production of CXCL8 and IL-1β in macrophages.
Ga(III) Nanoparticles Inhibit Growth of both Mycobacterium tuberculosis and HIV and Release of Interleukin-6 (IL-6) and IL-8 in Coinfected Macrophages.
Secretion of IL8 by peripheral blood cells was greatly stimulated upon exposure to Mycobacterium tuberculosis whole cell extract, but such enhanced secretion was not associated with the IL8rs4073 alleles.
Mycobacterium tuberculosis AtsG (Rv0296c), GlmU (Rv1018c) and SahH (Rv3248c) Proteins Function as the Human IL-8-Binding Effectors and Contribute to Pathogen Entry into Human Neutrophils.
In healthy household contacts (HHC), all the tested antigens induced significantly higher levels of IFN-γ and Interlukin-8 (IL-8) compared with those in PTB.
In addition, after stimulated with inactivated lysate of M. tuberculosis strain H37Rv, samples of peripheral blood mononuclear cells (PBMCs) from children with the rs5743618 GT genotypes showed a decreased level of Tumor Necrosis Factor-a (TNF-a) and CXC chemokine ligand 10 (CXCL10) production, invariable production of interleukin-6 (IL-6) and IL-8 and increased production of IL-10 ex vivo.
A higher prevalence of purified protein derivative reactivity was associated with the TNF-α CCA/TCG haplotype (PR 1.298, 95%CI 1.059-1.589) and with the IL-10 AT/CC diplotype (PR 1.181, 95% CI 1.024-1.362), and the presence of the IL-8rs4073 T allele was associated with protection against TB (PR 0.482, 95%CI 0.273-0.851).
H37Rv significantly increased the release of MIP-1α and IL-8 in both normals and tuberculosis patients, while S10 up regulated only the release of MIP-1α in patients.
NF-κB repressing factor downregulates basal expression and mycobacterium tuberculosis induced IP-10 and IL-8 synthesis via interference with NF-κB in monocytes.
Early secreted antigenic target of 6 kDa (ESAT-6) protein of Mycobacterium tuberculosis induces interleukin-8 (IL-8) expression in lung epithelial cells via protein kinase signaling and reactive oxygen species.
Collectively, these results suggest that differential IL-8 expression in human macrophages infected with M. tuberculosis and M. marinum may be critically associated with distinct host responses in tuberculosis.
In addition, enzyme-linked immunosorbent assay showed that IL-8 protein secretion was significantly elevated in M. tuberculosis-infected U937 cells, human primary monocytes, and monocyte-derived macrophages compared with that in M. marinum-infected cells.
Pharmacological analysis of signal transduction pathways required for mycobacterium tuberculosis-induced IL-8 and MCP-1 production in human peripheral monocytes.