| Id |
Subject |
Object |
Predicate |
Lexical cue |
| T1 |
0-144 |
Sentence |
denotes |
Interleukin-10 alters effector functions of multiple genes induced by Borrelia burgdorferi in macrophages to regulate Lyme disease inflammation. |
| T1 |
0-144 |
Sentence |
denotes |
Interleukin-10 alters effector functions of multiple genes induced by Borrelia burgdorferi in macrophages to regulate Lyme disease inflammation. |
| T2 |
145-284 |
Sentence |
denotes |
Interleukin-10 (IL-10) modulates inflammatory responses elicited in vitro and in vivo by Borrelia burgdorferi, the Lyme disease spirochete. |
| T2 |
145-284 |
Sentence |
denotes |
Interleukin-10 (IL-10) modulates inflammatory responses elicited in vitro and in vivo by Borrelia burgdorferi, the Lyme disease spirochete. |
| T3 |
285-356 |
Sentence |
denotes |
How IL-10 modulates these inflammatory responses still remains elusive. |
| T3 |
285-356 |
Sentence |
denotes |
How IL-10 modulates these inflammatory responses still remains elusive. |
| T4 |
357-517 |
Sentence |
denotes |
We hypothesize that IL-10 inhibits effector functions of multiple genes induced by B. burgdorferi in macrophages to control concomitantly elicited inflammation. |
| T4 |
357-517 |
Sentence |
denotes |
We hypothesize that IL-10 inhibits effector functions of multiple genes induced by B. burgdorferi in macrophages to control concomitantly elicited inflammation. |
| T5 |
518-707 |
Sentence |
denotes |
Because macrophages are essential in the initiation of inflammation, we used mouse J774 macrophages and live B. burgdorferi spirochetes as the model target cell and stimulant, respectively. |
| T5 |
518-707 |
Sentence |
denotes |
Because macrophages are essential in the initiation of inflammation, we used mouse J774 macrophages and live B. burgdorferi spirochetes as the model target cell and stimulant, respectively. |
| T6 |
708-901 |
Sentence |
denotes |
First, we employed transcriptome profiling to identify genes that were induced by stimulation of cells with live spirochetes and that were perturbed by addition of IL-10 to spirochete cultures. |
| T6 |
708-901 |
Sentence |
denotes |
First, we employed transcriptome profiling to identify genes that were induced by stimulation of cells with live spirochetes and that were perturbed by addition of IL-10 to spirochete cultures. |
| T7 |
902-999 |
Sentence |
denotes |
Spirochetes significantly induced upregulation of 347 genes at both the 4-h and 24-h time points. |
| T7 |
902-999 |
Sentence |
denotes |
Spirochetes significantly induced upregulation of 347 genes at both the 4-h and 24-h time points. |
| T8 |
1000-1157 |
Sentence |
denotes |
IL-10 inhibited the expression levels, respectively, of 53 and 65 of the 4-h and 24-h genes, and potentiated, respectively, at 4 h and 24 h, 65 and 50 genes. |
| T8 |
1000-1157 |
Sentence |
denotes |
IL-10 inhibited the expression levels, respectively, of 53 and 65 of the 4-h and 24-h genes, and potentiated, respectively, at 4 h and 24 h, 65 and 50 genes. |
| T9 |
1158-1368 |
Sentence |
denotes |
Prominent among the novel identified IL-10-inhibited genes also validated by quantitative real-time PCR (qRT-PCR) were Toll-like receptor 1 (TLR1), TLR2, IRAK3, TRAF1, IRG1, PTGS2, MMP9, IFI44, IFIT1, and CD40. |
| T9 |
1158-1368 |
Sentence |
denotes |
Prominent among the novel identified IL-10-inhibited genes also validated by quantitative real-time PCR (qRT-PCR) were Toll-like receptor 1 (TLR1), TLR2, IRAK3, TRAF1, IRG1, PTGS2, MMP9, IFI44, IFIT1, and CD40. |
| T10 |
1369-1759 |
Sentence |
denotes |
Proteome analysis using a multiplex enzyme-linked immunosorbent assay (ELISA) revealed the IL-10 modulation/and or potentiation of RANTES/CCL5, macrophage inflammatory protein 2 (MIP-2)/CXCL2, IP-10/CXCL10, MIP-1α/CCL3, granulocyte colony-stimulating factor (G-CSF)/CSF3, CXCL1, CXCL5, CCL2, CCL4, IL-6, tumor necrosis factor alpha (TNF-α), IL-1α, IL-1β, gamma interferon (IFN-γ), and IL-9. |
| T10 |
1369-1759 |
Sentence |
denotes |
Proteome analysis using a multiplex enzyme-linked immunosorbent assay (ELISA) revealed the IL-10 modulation/and or potentiation of RANTES/CCL5, macrophage inflammatory protein 2 (MIP-2)/CXCL2, IP-10/CXCL10, MIP-1α/CCL3, granulocyte colony-stimulating factor (G-CSF)/CSF3, CXCL1, CXCL5, CCL2, CCL4, IL-6, tumor necrosis factor alpha (TNF-α), IL-1α, IL-1β, gamma interferon (IFN-γ), and IL-9. |
| T11 |
1760-1847 |
Sentence |
denotes |
Similar results were obtained using sonicated spirochetes or lipoprotein as stimulants. |
| T11 |
1760-1847 |
Sentence |
denotes |
Similar results were obtained using sonicated spirochetes or lipoprotein as stimulants. |
| T12 |
1848-1988 |
Sentence |
denotes |
Our data show that IL-10 alters effectors induced by B. burgdorferi in macrophages to control concomitantly elicited inflammatory responses. |
| T12 |
1848-1988 |
Sentence |
denotes |
Our data show that IL-10 alters effectors induced by B. burgdorferi in macrophages to control concomitantly elicited inflammatory responses. |
| T13 |
1989-2131 |
Sentence |
denotes |
Moreover, for the first time, this study provides global insight into potential mechanisms used by IL-10 to control Lyme disease inflammation. |
| T13 |
1989-2131 |
Sentence |
denotes |
Moreover, for the first time, this study provides global insight into potential mechanisms used by IL-10 to control Lyme disease inflammation. |