Anti-Inflammatory Cytokines

Opal, Steven M.; DePalo, Vera A.

doi:10.1378/chest.117.4.1162

Cited by 1,407 publications

(1,024 citation statements)

References 103 publications

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“…In fact, IL-6 could facilitate wound healing, for its slight anti-inflammatory activity [23,24]: it down-regulates the synthesis of IL-1 and TNF and have little effect on the synthesis of anti-inflammatory cytokines such as IL-10 and transforming growth factor-β (TGF-β) [24].…”

Section: Discussionmentioning

confidence: 99%

Colonization by human fibroblasts of polypropylene prosthesis in a composite form for hernia repair

Canuto

Saracino

Oraldi

et al. 2012

Hernia

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Purpose: Abdominal wall hernia is one of the commonest surgical disorders world-wide and there is no single gold-standard operative technique to repair it. In an effort to improve techniques and technologies to reinforce hernia repair, synthetic meshes are employed. In this study a new prosthesis (named composite) formed of two polypropylene layers, one macroporous (named mesh) and one transparent (named film) was examined to evaluate its capability to enable cell proliferation without inducing cell death. Inflammatory processes were also examined.Methods: Human fibroblasts BJ were seeded on multiwells, on which composite or film had been placed. After 7, 14 and 21 days, cell growth and viability, deposition of collagen, and release of IL-6, IL-1β and TNF-α were evaluated.Results: The "in vitro" protocol showed the composite to be colonized by human fibroblasts on the polypropylene macroporous mesh side; no cell growth occurred on the film. The slowdown of cell growth observed between 14 and 21 days was accompanied by an increase of type I collagen deposition and marked fibroblast activity. Inflammatory cytokines initially increased, followed by their reduction beginning at 14 days.Conclusions: The new prosthesis comprising two polypropylene layers of differing morphologies can be colonized by fibroblasts on the side facing the abdominal wall, whereas no cell growth occurs on the side facing the viscera. The transient inflammation, observed at early experimental times, is probably important for the healing process.

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Section: Discussionmentioning

confidence: 99%

Colonization by human fibroblasts of polypropylene prosthesis in a composite form for hernia repair

Canuto

Saracino

Oraldi

et al. 2012

Hernia

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“…IL-4 exerts its effects on cells of different lineages such as fibroblasts, endothelial cells (Lowenthal et al 1988), microglia (Chao et al 1993) and astrocytes (Brodie and Goldreich 1994;. IL-4 provides support for the development of humoral immune responses through the induction of T-helper type 2 (Th2) cell differentiation (Opal and DePalo 2000).…”

Section: Discussionmentioning

confidence: 99%

Dual Effect of Central Injection of Recombinant Rat Interleukin-4 on Lipopolysaccharide-Induced Sickness Behavior in Rats

Bluthé

Lestage

Rees

et al. 2002

Neuropsychopharmacology

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Systemic administration of the bacterial endotoxin lipopolysaccharide (LPS) has profound depressive effects on behavior that are mediated by the inducible expression of pro-inflammatory cytokines, such as interleukin-1 (IL-1), IL-6 and tumor necrosis factor ␣ (TNF), in the brain. To assess the regulatory effects of the anti-inflammatory cytokine IL-4 on LPS-induced sickness behavior, rats injected intra-peritoneally (i.p.) with LPS were administered intracerebroventricularly (i.c.v.) with When an organism becomes sick during the course of an infection, several changes occur, which are mediated by the central nervous system (CNS). These changes include regulated increases in body temperature, sleep, activation of the hypothalamo-pituitary-adrenocortical (HPA) axis, decreases in locomotor activity, feeding, drinking, and social interactions, and alterations in brain neurotransmitters. They are due to the release of pro-inflammatory cytokines such as interleukin-1 (IL-1), IL-6 and tumor necrosis factor-alpha (TNF-␣ ) by activated monocytes and macrophages Dinarello 2000;Gabay and Kushner 1999;Krueger et al. 1999;Mulla and Buckingham 1999;Rothwell 1997;Turrin and Plata-Salaman 2000). The same effects can be obtained by systemic administration of the cytokine-inducer lipopolysaccharide (LPS), a component of the cell wall of Gram-negative bacteria (Cabrera et al. 2000;Francis et al. 2000;Lacosta et al. 1999;Ma et al. 2000;MohanKumar et al. 2000;Roth and de Souza 2001;Swiergel and Dunn 1999;Yirmiya 1996;Yirmiya et al. 2001). Peripherally released cytokines act on the brain by inducing the expression and release of cytokines in the central nervous system (Eriksson et al. 2000;Konsman et al. 1999;Layé et al. 2000;Quan et al. 2000). LPS induces the expression of not only pro-inflammatory but also anti-inflammatory cytokines such as IL-10 and IL-13 in the brain (Wong et al. 1997 Laman et al. 1998;Liedtke et al. 1998; Woodroofe and Cuzner 1993). Anti-inflammatory cytokines have the ability to suppress the synthesis of IL-1, TNF, and other cytokines in peripheral immune and non-immune cells (Dinarello 1997;Marie and Cavaillon 1997).There has been a recent surge of interest in the behavioral effects of cytokines in neuropsychopharmacology. Several reasons account for that, including the fact that cytokine-induced sickness behavior is not the result of weakness and physical debilitation but appears to be the expression of a previously unrecognized motivational state that is triggered by peripheral immune stimuli and reorganizes the organism's priorities (Dantzer 2001). In addition, the possibility of an intersection between sickness behavior and depression has raised new and important issues in psychopathology.If sickness behavior is the ineluctable result of the brain action of those proinflammatory cytokines that are released at the periphery during the course of an innate immune response or even in response to exteroceptive stressors, it becomes important to find out how this behavior is regulated. The production and ac...

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“…Among others, interleukin 4 (IL4) acts as a regulator to counter-play the inflammatory immune processes. 4 Usually, IL4 is secreted by lymphocytes of the Th2 lineage, 5 whereas the IL4 locus appears silenced in Th1 cells. Because of its immune response regulating role, IL4 is an obvious candidate gene for potential association in MS. We focus here on the IL4 promoter polymorphism À589C/T, since numerous studies have shown association of this single nucleotide polymorphism (SNP) with various inflammatory diseases, including asthma, atopy, brucellosis and rheumatoid arthritis, [6][7][8][9][10][11] and because earlier deletion expression assays hinted to a functional role of this SNP.…”

Section: Introductionmentioning

confidence: 99%

Sex specifically associated promoter polymorphism in multiple sclerosis affects interleukin 4 expression levels

et al. 2007

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The interleukin 4 promoter polymorphism À589 C/T (rs2243250) was genotyped in 869 multiple sclerosis (MS) patients and 595 healthy blood donors. Sex-specific MS association was evident whereas two flanking polymorphisms showed insignificant P values. In dual luciferase assays of cultured Jurkat cells the cloned promoter comprising the À589 T allele leads to higher expression as compared to the respective construct with the C allele. Together these findings may be discussed functionally as contributing to the genetic predisposition and to the pathogenesis in MS.

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Anti-Inflammatory Cytokines

Cited by 1,407 publications

References 103 publications

Colonization by human fibroblasts of polypropylene prosthesis in a composite form for hernia repair

Colonization by human fibroblasts of polypropylene prosthesis in a composite form for hernia repair

Dual Effect of Central Injection of Recombinant Rat Interleukin-4 on Lipopolysaccharide-Induced Sickness Behavior in Rats

Sex specifically associated promoter polymorphism in multiple sclerosis affects interleukin 4 expression levels

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