Interleukin‐10 and pentoxifylline inhibit C‐reactive protein‐induced tissue factor gene expression in peripheral human blood monocytes

Ramani, Mohamed; Khechai, F.; Ollivier, Véronique; Ternisien, Catherine; Bridey, Françoise; Hakim, Jacques; Prost, Dominique de

doi:10.1016/0014-5793(94)01236-9

Cited by 32 publications

(15 citation statements)

References 19 publications

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“…Furthermore, macrophages in atherosclerotic plaques express TF (32). Anti-inflammatory cytokines, such as IL-10 and transforming growth factor beta, inhibit or suppress monocyte TFA (14,18,20,24,29,30).It is well known that pro-and anti-inflammatory cytokines each control the other's production (5, 33). TNF-␣ and IL-1, which are examples of the earliest cytokines produced by monocytes upon appropriate stimulation (15, 28), are able to stimulate monocyte IL-10 production (15,27,28,40).…”

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“…Monocytes can be stimulated by various agents, such as endotoxin, phorbol ester, lipoteichoic acid, and C-reactive protein, to express TF molecules on their membranes, thereby generating TF activity (TFA) (9,25,26,30,31). We have shown that monocytes also express TFA when they adhere in vitro to fibrin matrixes containing bacteria, in particular bacteria that are known to cause the endovascular disease bacterial endocarditis (BE) (1)(2)(3)(4)38).…”

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Interleukin-10 Regulates the Tissue Factor Activity of Monocytes in an In Vitro Model of Bacterial Endocarditis

et al. 2001

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Monocytes are important effector cells in the pathogenesis of bacterial endocarditis since they provide the tissue factor that activates the coagulation system and maintains established vegetations. Monocytes secrete cytokines that can modulate monocyte tissue factor activity (TFA), thereby affecting the formation and maintenance of vegetations. In this study, we show that monocytes cultured for 4 h on a Streptococcus sanguis-infected fibrin matrix mimicking the in vivo vegetational surface express high levels of TFA. This was accompanied by secretion of the proinflammatory cytokines tumor necrosis factor alpha (TNF-␣), interleukin-1␣ (IL-1␣), and IL-1␤. After a 24-h incubation period the anti-inflammatory cytokine IL-10 could also be detected. Our data show that, whereas TNF-␣ and IL-1 have a minor role in the induction of TFA by monocytes cultured on a fibrin matrix, TNF-␣ but not IL-1 plays an important role in the induction of IL-10 by these cells. In turn, our data show that IL-10 is an important factor in the downregulation of monocyte TFA. In summary, we conclude that IL-10 is an important factor in the control of monocyte TFA in endocardial vegetations.Tissue factor (TF), a transmembrane glycoprotein, is the most important factor in the initiation of the extrinsic coagulation pathway (25). Monocytes can be stimulated by various agents, such as endotoxin, phorbol ester, lipoteichoic acid, and C-reactive protein, to express TF molecules on their membranes, thereby generating TF activity (TFA) (9,25,26,30,31). We have shown that monocytes also express TFA when they adhere in vitro to fibrin matrixes containing bacteria, in particular bacteria that are known to cause the endovascular disease bacterial endocarditis (BE) (1-4, 38). With respect to the pathogenesis of BE, Drake and coworkers (13) have shown that in vivo TF is a crucial factor in the formation of an endocardial fibrin clot, called endocardial vegetation, in which the infecting microorganisms and blood cells are embedded (33). In a rabbit model of BE it was found that the TF needed to maintain the endocardial vegetation is generated by monocytes that settle from the circulation onto the infected endocardial lesion (2,3,6,38).Monocyte TFA can be regulated by cytokines. Proinflammatory cytokines, such as tumor necrosis factor alpha (TNF-␣) and interleukin-1 (IL-1), induce TFA on monocytes (15,17,18,22,24,25). Monocytes isolated from patients with atherosclerosis, a disease in which TNF-␣ and IL-1 play a significant role, express TF on their membranes (24). Furthermore, macrophages in atherosclerotic plaques express TF (32). Anti-inflammatory cytokines, such as IL-10 and transforming growth factor beta, inhibit or suppress monocyte TFA (14,18,20,24,29,30).It is well known that pro-and anti-inflammatory cytokines each control the other's production (5, 33). TNF-␣ and IL-1, which are examples of the earliest cytokines produced by monocytes upon appropriate stimulation (15, 28), are able to stimulate monocyte IL-10 production (15,27,28,40). In turn, IL...

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Interleukin-10 Regulates the Tissue Factor Activity of Monocytes in an In Vitro Model of Bacterial Endocarditis

et al. 2001

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“…Hence, it is possible that LFA-1 expressed on platelets directly participates in blood coagulation during endotoxemia. However, endogenous IL-10 neutralization markedly increases numbers of platelets in the liver of LFA-1 -/-mice following low-dose LPS challenge, and an inhibitory role of IL-10 in fibrin formation has been reported [98][99][100][101][102]. Therefore, it seems more likely that higher levels of IL-10 increase resistance of LFA-1 -/-mice to low-dose LPS-induced shock/liver injury by impairing the blood coagulation cascade (Fig.…”

Section: Which Type Of Cells Is the Source Of Tnf-α And Il-10 In The mentioning

confidence: 88%

New Aspects of the Role of LFA-1 in Bacterial Infection

Emoto

2005

CIR

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Leukocyte function-associated antigen (LFA)-1 (CD11a/CD18) is considered to play a pivotal role in a broad range of cellular events, ranging from firm adhesion of leukocytes to endothelial cells initiating leukocyte transmigration and extravasation to functional activation of various inflammatory cells promoting type 1-immune responses. Yet, recent studies argue against the role of LFA-1 in these inflammatory responses. Additionally, recent advances establish LFA-1 as a crucial molecule in regulation of pro-inflammatory and anti-inflammatory cytokine network and in control of granulopoiesis. Thus, it seems likely that LFA-1 plays more complicated/unique roles than originally thought.

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“…This population may also be divided into two separate groups of early and late onset preeclampsia. Pentoxifylline down regulates pro-inflammatory cytokines such as TNF-a, IL-1b, IL-6 and IFN-c and decreases serum levels of CRP, which were all elevated in preeclampsia [4,22,[25][26][27][28]35,83,84]. Therefore, to follow the course of the disease, assessment of the patients for these factors seems to be a necessity.…”

Section: Hypothesis/ideamentioning

confidence: 97%