scholarly journals Chlamydia psittaci Plasmid-Encoded CPSIT_P7 Elicits Inflammatory Response in Human Monocytes via TLR4/Mal/MyD88/NF-κB Signaling Pathway

2020 ◽  
Vol 11 ◽  
Author(s):  
Qian Chen ◽  
Yumeng Li ◽  
Xiaoliang Yan ◽  
Zhenjie Sun ◽  
Chuan Wang ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Molecular Mechanisms ◽  
Leukemia Cell ◽  
Nuclear Factor Κb ◽  
Immunofluorescence Assay ◽  
Dominant Negative ◽  
Chlamydia Psittaci ◽  
Leukemia Cell Line ◽  
Monocytic Leukemia ◽  
Monocyte Chemoattractant Protein 1

The chlamydial plasmid, an essential virulence factor, encodes plasmid proteins that play important roles in chlamydial infection and the corresponding immune response. However, the virulence factors and the molecular mechanisms of Chlamydia psittaci are not well understood. In the present study, we investigated the roles and mechanisms of the plasmid-encoded protein CPSIT_P7 of C. psittaci in regulating the inflammatory response in THP-1 cells (human monocytic leukemia cell line). Based on cytokine arrays, CPSIT_P7 induces the expression of interleukin-6 (IL-6), interleukin-8 (IL-8), and monocyte chemoattractant protein-1 (MCP-1) in THP-1 cells. Moreover, the expression levels of IL-6, IL-8, and MCP-1 stimulated by CPSIT_P7 declined after silencing of the Toll-like receptor 4 (TLR4) gene using small interfering RNA and transfection of a dominant negative plasmid encoding TLR4 (pZERO-hTLR4). We further demonstrated that transfection with the dominant negative plasmid encoding MyD88 (pDeNy-hMyD88) and the dominant negative plasmid encoding Mal (pDeNy-hMal) could also abrogate the expression of the corresponding proteins. Western blot and immunofluorescence assay results showed that CPSIT_P7 could activate nuclear factor κB (NF-κB) signaling pathways in THP-1 cells. Altogether, our results indicate that the CPSIT_P7 induces the TLR4/Mal/MyD88/NF-κB signaling axis and therefore contributes to the inflammatory cytokine response.

Localized pancreatic NF-κB activation and inflammatory response in taurocholate-induced pancreatitis

2001 ◽  
Vol 280 (6) ◽  
pp. G1197-G1208 ◽  
Author(s):  
Eva Vaquero ◽  
Ilya Gukovsky ◽  
Vjekoslav Zaninovic ◽  
Anna S. Gukovskaya ◽  
Stephen J. Pandol
Keyword(s):  
Transcription Factor ◽  
Inflammatory Response ◽  
Pancreatic Head ◽  
Pancreatic Injury ◽  
Nuclear Factor Κb ◽  
Saline Infusion ◽  
Activator Protein 1 ◽  
Local Inflammatory Response ◽  
Monocyte Chemoattractant Protein 1 ◽  
Factor Α

Transcription factor nuclear factor-κB (NF-κB) is activated in cerulein pancreatitis and mediates cytokine expression. The role of transcription factor activation in other models of pancreatitis has not been established. Here we report upregulation of NF-κB and inflammatory molecules, and their correlation with local pancreatic injury, in a model of severe pancreatitis. Rats received intraductal infusion of taurocholate or saline, and the pancreatic head and tail were analyzed separately. NF-κB and activator protein-1 (AP-1) activation were assessed by gel shift assay, and mRNA expression of interleukin-6, tumor necrosis factor-α, KC, monocyte chemoattractant protein-1, and inducible nitric oxide synthase was assessed by semiquantitative RT-PCR. Morphological damage and trypsin activation were much greater in the pancreatic head than tail, in parallel with a stronger activation of NF-κB and cytokine mRNA. Saline infusion mildly affected these parameters. AP-1 was strongly activated in both pancreatic segments after either taurocholate or saline infusion. NF-κB inhibition with N-acetylcysteine ameliorated the local inflammatory response. Correlation between localized NF-κB activation, cytokine upregulation, and tissue damage suggests a key role for NF-κB in the development of the inflammatory response of acute pancreatitis.

LRP16 is fused to RUNX1 in monocytic leukemia cell line with t(11;21)(q13;q22)

2007 ◽  
Vol 79 (1) ◽  
pp. 25-31 ◽  
Author(s):  
Shizuka Imagama ◽  
Akihiro Abe ◽  
Momoko Suzuki ◽  
Fumihiko Hayakawa ◽  
Akira Katsumi ◽  
...  
Keyword(s):  
Cell Line ◽  
Leukemia Cell ◽  
Leukemia Cell Line ◽  
Monocytic Leukemia

scholarly journals Microfluidic Separation of Blood Cells Based on the Negative Dielectrophoresis Operated by Three Dimensional Microband Electrodes

Micromachines ◽  
2020 ◽  
Vol 11 (9) ◽  
pp. 833
Author(s):  
Tomoyuki Yasukawa ◽  
Junko Yamada ◽  
Hitoshi Shiku ◽  
Tomokazu Matsue ◽  
Masato Suzuki
Keyword(s):  
Electric Field ◽  
Blood Cells ◽  
White Blood Cells ◽  
Three Dimensional ◽  
Leukemia Cell ◽  
Leukemia Cell Line ◽  
Acute Monocytic Leukemia ◽  
Label Free ◽  
Monocytic Leukemia ◽  
Insulating Layer

A microfluidic device is presented for the continuous separation of red blood cells (RBCs) and white blood cells (WBCs) in a label-free manner based on negative dielectrophoresis (n-DEP). An alteration of the electric field, generated by pairs of slanted electrodes (separators) that is fabricated by covering parts of single slanted electrodes with an insulating layer is used to separate cells by their sizes. The repulsive force of n-DEP formed by slanted electrodes prepared on both the top and bottom substrates led to the deflection of the cell flow in lateral directions. The presence of gaps covered with an insulating layer for the electric field on the electrodes allows the passing of RBCs through gaps, while relatively large WBCs (cultured cultured human acute monocytic leukemia cell line (THP-1 cells)) flowed along the slanted separator without passing through the gaps and arrived at an edge in the channel. The passage efficiency for RBCs through the gaps and the arrival efficiency for THP-1 cells to the upper edge in the channel were estimated and found to be 91% and 93%, respectively.

Demonstration of IL-1α and IL-1β secretion by the monocytic leukemia cell line, THP-1

1989 ◽  
Vol 122 (2) ◽  
pp. 211-218 ◽  
Author(s):  
Edwin V. Gaffney ◽  
Cheryl R. Stoner ◽  
Susan E. Lingenfelter ◽  
Lisa A. Wagner
Keyword(s):  
Cell Line ◽  
Leukemia Cell ◽  
Leukemia Cell Line ◽  
Monocytic Leukemia
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