Synergism between interleukin-1? and tumor necrosis factor-? in production by 3T3 cells of a chemotactic factor for rat polymorphonuclear leukocytes

Nakagawa, Hideo; Miyai, Hisato; Hirata, Michinori; Watanabe, Kimitsuna; Onuma, Izumi

doi:10.1007/bf00916761

Cited by 10 publications

(4 citation statements)

References 11 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It seems that IL1-b and TNF-a act synergistically to induce the neutrophil migration, since antibodies against each cytokine almost blocked the chemotactic activity of the supernatant. A synergic effect of these cytokines has been described [52,53]. The antibodies against IL-1b and TNF-a did not affect the chemotactic activity of the IL-1b-stimulated macrophage supernatants.…”

Section: Discussionmentioning

confidence: 93%

“…The theory that indirect mechanisms are involved in this migration is supported by the fact that the IL-1b-induced neutrophil recruitment in mice is attenuated by capsaicin treatment, as well by the blockage of tachykinin, neurokinin-1, and CGRP-1 receptors, indicating the participation of the neurogenic mediators [22,23]. Furthermore, IL-1b can stimulate the release of neutrophil chemotactic mediators, such as cytokine-induced neutrophil chemoattractant (CINC) [24], IL-8 [25], TNF-a [26], and LTB 4 [27Y28].…”

Section: Introductionmentioning

confidence: 96%

See 1 more Smart Citation

Neutrophil Migration Induced by IL-1β Depends upon LTB4 Released by Macrophages and upon TNF-α and IL-1β Released by Mast Cells

et al. 2007

View full text Add to dashboard Cite

In the present study, we investigate whether mast cells and macrophages are involved in the control of IL-1beta-induced neutrophil migration, as well as the participation of chemotactic mediators. IL-1beta induced a dose-dependent neutrophil migration to the peritoneal cavity of rats which depends on LTB(4), PAF and cytokines, since the animal treatment with inhibitors of these mediators (MK 886, PCA 4248 and dexamethasone respectively) inhibited IL-1beta-induced neutrophil migration. The neutrophil migration induced by IL-1beta is dependent on mast cells and macrophages, since depletion of mast cells reduced the process whereas the increase of macrophage population enhanced the migration. Moreover, mast cells or macrophages stimulated with IL-1beta released a neutrophil chemotactic factor, which mimicked the neutrophil migration induced by IL-1beta. The chemotactic activity of the supernatant of IL-1beta-stimulated macrophages is due to the presence of LTB(4), since MK 886 inhibited its release. Moreover, the chemotactic activity of IL-1beta-stimulated mast cells supernatant is due to the presence of IL-1beta and TNF-alpha, since antibodies against these cytokines inhibited its activity. Furthermore, significant amounts of these cytokines were detected in the supernatant. In conclusion, our results suggest that neutrophil migration induced by IL-1beta depends upon LTB(4) released by macrophages and upon IL-1beta and TNFalpha released by mast cells.

show abstract

Section: Discussionmentioning

confidence: 93%

Section: Introductionmentioning

confidence: 96%

Neutrophil Migration Induced by IL-1β Depends upon LTB4 Released by Macrophages and upon TNF-α and IL-1β Released by Mast Cells

et al. 2007

View full text Add to dashboard Cite

show abstract

“…The steroids inhibit the production of a variety of cytokines including TNF-a, IL-i, IL-6, and IL-8 (17,18). IL-i and TNF-a are known to induce the mRNA expression of IL-S in a variety of human cells (19,20). However, synthetic glucocorticoids used as anti-inflammatory drugs inhibit the IL-S induction at the transcription level (16,17).…”

Section: Resultsmentioning

confidence: 99%

Inhibitory Effects of Oriental Herbal Medicines on IL-8 Induction in Lipopolysaccharide-Activated Rat Macrophages

Lee

Min

et al. 1995

Planta Med

Self Cite

View full text Add to dashboard Cite

Cytokine-induced neutrophil chemoattractant (CINC), a rat interleukin-8 (IL-8), was quantitated by using a sensitive ELISA. The CINC was induced up to 20 ng/ml from basal 1-2 ng/ml in lipopolysaccharide (LPS)-activated peritoneal macrophages. This CINC induction was significantly inhibited by steroidal anti-inflammatory drugs including dexamethasone, but not by non-steroidal drugs including indomethacin at all. Nine out of 59 herbal medicines which are frequently used in Korean traditional prescriptions for inflammatory diseases exhibited more than 50% of inhibition on the CINC induction by their total methanol extracts with 0.1 mg/ml as a final concentration. The active 9 total extracts were prepared from radix of Aralia continentalis, rhizoma of Cnidium officinale, rhizoma of Coptis chinensis, tuber of Fritillaria verticillata, radix of Saussurea lappa, tuber of Sparganium stoloniferum, flower of Syzygium aromaticum, semen of Trichosanthes kirilowii, and herba of Tripterygium regelii. These total extracts were sequentially fractionated with dichloromethane, ethyl acetate, butanol, and water. Among the solvent-fractionated extracts with 0.05 mg/ml as a final concentration, more than 50% of inhibition on the CINC induction was exhibited by the dichloromethane fraction of Aralia continentalis; the water fraction of Fritillaria verticillata; the dichloromethane fraction of Saussurea lappa; the dichloromethane, ethyl acetate, and butanol fractions of Syzygium aromaticum; the dichloromethane, ethyl acetate, and water fractions of Trichosanthes kirilowii; and the dichloromethane and ethyl acetate fractions of Tripterygium regelii.

show abstract

“…The present results should be considered in light of previous studies of the effects of IL-1 and TNF on diverse mesenchymal cell responses. To compliment their individual pleiotropic affects, IL-1 and TNF have been shown to interact with other cytokines, as well as with each other, in an additive and sometimes supra-additive manner (Branch et al, 1989;Seelentag et al, 1987;Nakagawa et al, 1989;Leizer et al, 1990;Elias et al, 1988;Wankowicz et al, 1988;Male and Pryce, 1988;Brach et al, 1992;Hoang et al, 1989;Chantry et al, 1989;Tanner et al, 1992;Stashenko et al, 1987;Mandrup-Poulsen et al, 1987;Brox-meyer et al, 1986). In particular, Wankowicz et al (1988) found that IL-1 and TNF synergistically stimulated leukocyte migration during inflammation and Stashenko et al (1987) found that IL-la and TNFa stimulated bone resorption with apparently supra-additive kinetics.…”

Section: Kinetics Of Myeloid-csf Production By a Stromal-derived Cellmentioning

confidence: 99%

IL‐1α and TNFα act synergistically to stimulate production of myeloid colony‐stimulating factors by cultured human bone marrow stromal cells and cloned stromal cell strains

Caldwell

Emerson

1994

Journal Cellular Physiology

View full text Add to dashboard Cite

Human bone marrow stromal cells repond to stimulation by the monokines IL-1 and TNF by producing colony-stimulating factors such as GM-CSF and G-CSF. In this study we show that I L -l a and TNFa act synergistically to stimulate GM-CSF and G-CSF production by cultured marrow stromal cells. We further show that I L -l a and TNFa synergistically stimulate production of GM-CSF and G-CSF by a clonal stroma-derived cell strain. Although IL-1 and TNF share many of the same biological activities, we show that I L -l a and TNFa have an unequal ability to induce myeloid-CSF production by both cultures, with I L -l a being the more potent inducer. We found that induction by I L -l a and TNFa was independent of cell proliferation. The effect of I L -l a and TNFa on production of the two myeloidCSFs by the clonal cells was significantly greater than the unfractionated passaged strornal cultures, having the greater effect on G-CSF production. The clonally derived stromal cells constitutively produced colony-stimulating activity, in particular GM-CSF, at levels easily detected by ELISA. These findings show that, in addition to the overlapping and additive activities of IL-la and TNFa, they can interact synergistically. Our findings further suggest that a small subpopulation of stroma cells may be the major producer of G-CSF in the marrow microenvironment during immune response. o 1994 ~i l e y -~i s s , Inc.

show abstract

Synergism between interleukin-1? and tumor necrosis factor-? in production by 3T3 cells of a chemotactic factor for rat polymorphonuclear leukocytes

Cited by 10 publications

References 11 publications

Neutrophil Migration Induced by IL-1β Depends upon LTB4 Released by Macrophages and upon TNF-α and IL-1β Released by Mast Cells

Neutrophil Migration Induced by IL-1β Depends upon LTB4 Released by Macrophages and upon TNF-α and IL-1β Released by Mast Cells

Inhibitory Effects of Oriental Herbal Medicines on IL-8 Induction in Lipopolysaccharide-Activated Rat Macrophages

IL‐1α and TNFα act synergistically to stimulate production of myeloid colony‐stimulating factors by cultured human bone marrow stromal cells and cloned stromal cell strains

Contact Info

Product

Resources

About