Regulation of lipopolysaccharide-induced tumor necrosis factor production by cyclosporin A in mice primed with muramyl dipeptide

Contel, Carole Le; Beigneux, Anne P.; Huang, Jian; Parant, M

doi:10.1111/j.1574-695x.1995.tb00160.x

Cited by 3 publications

(6 citation statements)

References 25 publications

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“…IL-1ra partially antagonized LPS-induced cytokine release in monocytes from BCG-treated individuals (21). TNF-␣ gene expression and blood levels of TNF-␣ are also upregulated by BCG treatment in mice (22,23). In fact, serum levels of TNF-␣ after an intraperitoneal injection of LPS were over 200 times higher in mice that had been inoculated with BCG 2 weeks before than in uninfected mice (18).…”

Section: Discussionmentioning

confidence: 99%

Proinflammatory Cytokine Expression Contributes to Brain Injury Provoked By Chronic Monocyte Activation

Sirén

McCarron

Wang

et al. 2001

Mol Med

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Background: We have proposed that an increased interaction between monocyte/macrophages and blood vessel endothelium predisposes subjects to strokes. The effect of chronic monocyte activation on the development of cerebral infarcts was thus studied in rats after provocation of a modified local Swartzman reaction, in brain vasculature. Materials and Methods: Two weeks after an IV bolus of bacillus Calmette-Guérin (BCG), we studied spontaneous superoxide production, integrin expression, endothelial adhesion of monocytes and the neurological symptoms, brain histology, and cytokine immunoreactivity after a provocative dose of LPS (30-300 g/rat i.c.v.). Results: Monocyte migration into the brain was stimulated by BCG priming. The incidence of paralysis and death in response to LPS was markedly increased in BCGprimed rats. Histological evaluation of the brains of neurologically impaired and moribund animals revealed

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Section: Discussionmentioning

confidence: 99%

Proinflammatory Cytokine Expression Contributes to Brain Injury Provoked By Chronic Monocyte Activation

Sirén

McCarron

Wang

et al. 2001

Mol Med

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“…Pettipher et al (1996) also found that propranolol had the same effect as adrenalectomy, suggesting that effects of adrenalectomy on TNF-a were due to loss of adrenaline, not Cort. Other groups found that adrenalectomy either increased (Le Contel et al 1995) or had no effect (Morrow et al 1993, Meltzer et al 2003 on LPS-induced plasma TNF-a. With respect to IL-6, several groups reported that adrenalectomy increases LPS-induced plasma IL-6 (Morrow et al 1993, Schöbitz et al 1993, Le Contel et al 1995.…”

Section: ###mentioning

confidence: 99%

“…Other groups found that adrenalectomy either increased (Le Contel et al 1995) or had no effect (Morrow et al 1993, Meltzer et al 2003 on LPS-induced plasma TNF-a. With respect to IL-6, several groups reported that adrenalectomy increases LPS-induced plasma IL-6 (Morrow et al 1993, Schöbitz et al 1993, Le Contel et al 1995. However, two of these studies did not examine whether Cort could reverse the effects of adrenalectomy (Morrow et al 1993, Le Contel et al 1995.…”

Section: ###mentioning

confidence: 99%

“…With respect to IL-6, several groups reported that adrenalectomy increases LPS-induced plasma IL-6 (Morrow et al 1993, Schöbitz et al 1993, Le Contel et al 1995. However, two of these studies did not examine whether Cort could reverse the effects of adrenalectomy (Morrow et al 1993, Le Contel et al 1995. The study by Schöbitz et al (1993) did report that Cort reversed effects of adrenalectomy; however, their data show that there were no significant differences in plasma Cort between control, adrenalectomized, and adrenalectomized C Cort replacement groups at the time LPS-induced IL-6 was measured.…”

Section: ###mentioning

confidence: 99%

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Effects of endogenous glucocorticoid secretion on the interleukin-6 response to bacterial endotoxin in pregnant and non-pregnant rats

Luheshi²,

Boksa

2011

Journal of Endocrinology

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Glucocorticoids (GCs) are released in response to immune activation by the bacterial endotoxin, lipopolysaccharide (LPS). However, GC secretion in response to immune activation and other stressors is attenuated at term of pregnancy. GCs are important modulators of the immune response, and both pro-and anti-inflammatory effects are described. Here, we examined whether GC secretion in response to LPS is maintained in earlier pregnancy before term, and investigated the role of endogenous GCs in modulating LPS-induced circulating cytokines, interleukin-6 (IL-6) and tumor necrosis factor-a (TNF-a), in pregnant compared to non-pregnant female rats. Plasma corticosterone (Cort) and ACTH responses to LPS were well maintained in pregnant rats at embryonic days 15/16 (E15/16) and E18/19 compared to non-pregnant rats. At E19, maternal LPS administration increased fetal plasma Cort and decreased testosterone in male fetuses. In non-pregnant animals, pretreatment with the GC synthesis inhibitor, metyrapone, inhibited the LPS-induced increase in IL-6, and the IL-6 response was restored by Cort replacement, indicating that LPS induction of IL-6 is Cort-dependent. In E15 pregnant animals, metyrapone had no effect on LPS-induced IL-6 levels, indicating that LPS-induction of IL-6 is not dependent on Cort. These contrasting patterns of IL-6 induction in nonpregnant and pregnant animals were reflected in levels of hypothalamic Socs3 mRNA, an indicator of IL-6 signaling pathway activation. In both non-pregnant and pregnant rats, LPS-induced plasma TNF-a responses were inhibited by metyrapone but not re-instated by Cort replacement. It is suggested that altered GC regulation of IL-6 may be required to sustain specialized functions of IL-6 during pregnancy.

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“…Furthermore, previous studies in humans and mice have shown that CsA could inhibit the pro-inflammatory cytokines IL-1β, IL-6, IL-8, TNF-α, and IFN-γ and increase the production of anti-inflammatory cytokines IL-4 and IL-10 in response to LPS stimulation [19,[59][60][61][62][63][64]. Recently Hu and colleagues, using a pregnant rat model, have demonstrated that CsA significantly ameliorates the clinical signs of LPS-induced pre-eclampsia and inhibits the inflammatory response [59].…”

Section: Introductionmentioning

confidence: 99%

Immunosuppressant Cyclosporin A-Based Regulation of Lipopolysaccharide-Triggered Pro- and Anti-Inflammatory Cytokines in the Genital Tract of Female Rabbits

Yang¹,

Wu²,

X³

et al. 2018

Preprint

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In this study, we evaluated the effects of Cyclosporine A (CsA) on Lipopolysaccharide (LPS)-induced cytokine production in the genital tract of female rabbits. Twelve sexually mature and healthy female rabbits were randomly divided into four groups (n = 3 each). The rabbits in the LPS group were given an intrauterine infusion of Escherichia coli LPS (4 mg/kg body weight (BW)). Rabbits in the CsA group were given CsA (20 mg/kg BW). Rabbits in the LPS + CsA group were given LPS (4 mg/kg BW) and CsA (20 mg/kg BW). The control group received only LPS and CsA carrier. The gene expression and protein levels of pro- and anti-inflammatory cytokines were observed using qRT-PCR and immuno-histochemical (IHC) assay, respectively. Our study showed that IL-1β, IL-6, IL-8, TNF-α, IFN-γ, IL-4, IL-10, IL-13, and TGF-β were expressed in female genital organs. The LPS challenge increased the mRNA expression of IL-6 and TNF-α in the uterine body and IL-1β in the uterotubal junction compared to the control group. CsA increased the basal mRNA expression of anti-inflammatory cytokines (i.e., IL-4 in the uterine body, uterotubal junction, and oviductal ampulla; IL-10 in the cervix, oviductal isthmus, and ampulla; and TGF-β in the uterotubal junction and oviductal ampulla) and pro-inflammatory cytokines (i.e., IL-6 and IL-8 in the cervix; IL-1β in the oviductal isthmus; TNF-α in the oviductal ampulla; and IFN-γ in the uterine body compared to the control group). In addition, CsA inhibited the mRNA expression of pro-inflammatory cytokines, such as IL-6 in the uterine body, uterotubal junction, and oviductal isthmus; TNF-α in the uterine body; and IFN-γ in the uterotubal junction and oviductal isthmus induced by the LPS challenge. The IHC assay showed the LPS-induced increase in protein production of IL-6 in the uterine body and oviductal isthmus. CsA increased the protein production of IL-10 in the cervix, uterine body, oviductal ampulla, and isthmus. Moreover, CsA decreased the protein production of IL-6 in the uterine body and oviductal isthmus induced by LPS.

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Regulation of lipopolysaccharide-induced tumor necrosis factor production by cyclosporin A in mice primed with muramyl dipeptide

Cited by 3 publications

References 25 publications

Proinflammatory Cytokine Expression Contributes to Brain Injury Provoked By Chronic Monocyte Activation

Proinflammatory Cytokine Expression Contributes to Brain Injury Provoked By Chronic Monocyte Activation

Effects of endogenous glucocorticoid secretion on the interleukin-6 response to bacterial endotoxin in pregnant and non-pregnant rats

Immunosuppressant Cyclosporin A-Based Regulation of Lipopolysaccharide-Triggered Pro- and Anti-Inflammatory Cytokines in the Genital Tract of Female Rabbits

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