Inhibition of cytokine production by a new inotropic agent, vesnarinone, in human lymphocytes, T cell line, and monocytic cell line

Life Sciences ◽  
1994 ◽  
Vol 54 (1) ◽  
pp. PL11-PL16 ◽  
Author(s):  
Tetsuo Shioi ◽  
Akira Matsumori ◽  
Shigeo Matsui ◽  
Shigetake Sasayama
Keyword(s):  
T Cell ◽  
Cell Line ◽  
Cytokine Production ◽  
Human Lymphocytes ◽  
Inotropic Agent ◽  
Monocytic Cell ◽  
Monocytic Cell Line ◽  
New Inotropic Agent

scholarly journals Interleukin-10 Modulates Proinflammatory Cytokines in the Human Monocytic Cell Line THP-1 Stimulated withBorrelia burgdorferi Lipoproteins

2000 ◽  
Vol 68 (12) ◽  
pp. 6663-6669 ◽  
Author(s):  
P. K. Murthy ◽  
Vida A. Dennis ◽  
Barbara L. Lasater ◽  
Mario T. Philipp
Keyword(s):  
Cell Line ◽  
Inflammatory Cytokines ◽  
Cytokine Production ◽  
Interleukin 10 ◽  
Monocytic Cell ◽  
Monocytic Cell Line ◽  
Human Monocytic Cell Line ◽  
Tnf Α ◽  
Human Monocytic Cell ◽  
Kinetics Of

ABSTRACT We determined previously that lipoproteins of Borrelia burgdorferi stimulate inflammatory and anti-inflammatory cytokines (interleukin-10 [IL-10]) in monocytes. IL-10 could have an effect on innate and acquired immune responses to B. burgdorferi and influence the magnitude of the infectious inoculum and disease outcome. To understand the mechanism(s) of IL-10 action during early infection, when innate immunity expressed chiefly by skin macrophages is key, we investigated the effect of exogenous and endogenous IL-10 on the production of the macrophage-derived cytokines IL-6, IL-1β, IL-12, and tumor necrosis factor alpha (TNF-α). We used the THP-1 human monocytic cell line and recombinant lipidated OspA (L-OspA) as the model target cell and stimulant, respectively. To determine the kinetics of cytokine production by THP-1 cells, we stimulated them with L-OspA and also with heat-killed B. burgdorferi cells (HBb) and lipopolysaccharide (LPS). Exogenous IL-10 dampened production of inflammatory cytokines, as elicited by lipoproteins. The inhibition of endogenous IL-10 function by anti-IL-10 antibody reduced the production of IL-12 and IL-6 but not that of IL-1β and TNF-α. An inspection of the kinetics of cytokine production clarified this finding. TNF-α was produced prior to, and IL-β was produced at the same time as, IL-10, whereas IL-6 and IL-12 were produced later. HBb, LPS, and L-OspA yielded similar kinetics of cytokine production. This result reinforces the notion that lipoproteins are the functional molecules in HBb and perhaps in vivo. It indicates also that signaling pathways utilized by LPS and lipoproteins may be extensively shared. The results are consistent with a major role played by IL-10 in controlling the initial phase of infection with this spirochete.

Surfactant protein A regulates cytokine production in the monocytic cell line THP-1

1997 ◽  
Vol 272 (5) ◽  
pp. L996-L1004 ◽  
Author(s):  
S. G. Kremlev ◽  
T. M. Umstead ◽  
D. S. Phelps
Keyword(s):  
Cell Line ◽  
Cytokine Production ◽  
Protein A ◽  
Surfactant Protein ◽  
Surfactant Protein A ◽  
Tnf Alpha ◽  
Enzyme Linked Immunosorbent Assay ◽  
Mrna Levels ◽  
Monocytic Cell ◽  
Monocytic Cell Line

Surfactant lipids inhibit cytokine production by immune cells, and surfactant protein A (SP-A) stimulates it. By enzyme-linked immunosorbent assay and mRNA blotting, we studied proinflammatory cytokine production by the monocytic cell line THP-1. SP-A caused increases in tumor necrosis factor (TNF)-alpha within 1 h, peaking at 4 h and then declining. Interleukin (IL)-1 beta increased and stayed elevated for 24 h. SP-A stimulated IL-8 also, peaking at 4 h, rapidly declining, and peaking again at 24 h. SP-A-dependent changes were detected for IL-6, but at higher SP-A doses. mRNA levels for TNF-alpha and IL-1 beta increased in response to SP-A, peaking within 2 h. The increases in TNF-alpha mRNA and protein induced by SP-A were inhibited by surfactant lipids. For IL-1 beta and IL-8, the lipids either had no inhibitory influence or inhibited less than for TNF-alpha. This suggests that the ability of macrophages to participate in inflammatory reactions is enhanced by SP-A alone or by mixtures of lipids and SP-A containing more SP-A than in normal surfactant, as occurs in many conditions leading to inflammation.

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