Is interleukin-6 important in inflammatory bowel disease?

Koss, K; Satsangi, Jack; Welsh, Ken I.

doi:10.1038/sj.gene.6363658

Cited by 18 publications

(12 citation statements)

References 21 publications

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“…An unregulated, high-level production of IL-6 could generate an undesired inflammatory state, a circumstance that can cause various diseases. Several reports indicate that IL-6 is implicated in the pathogenesis of a number of human disorders, including rheumatoid arthritis and inflammatory bowel disease [28,29] . AC-2, a partially purified polysaccharide fraction from A camphorate could inhibit LPS-induced IL-6 gene expression, which could provide a therapeutic clue in IL-6-related diseases.…”

Section: Discussionmentioning

confidence: 99%

Modulation of inflammation-related genes of polysaccharides fractionated from mycelia of medicinal basidiomycete Antrodia camphorata

Chen²,

Chyau³

et al. 2007

Acta Pharmacologica Sinica

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Aim: To investigate the effect of water soluble‐ethanol precipitation fraction (AC‐1) and alkaline extraction‐isoelectric precipitation fraction (AC‐2) from Antrodia camphorata (Polyporaceae, Aphyllophorales) on lipopolysaccharide (LPS)‐induced gene activation in mouse macrophages. Methods: The AC‐1 and AC‐2 fractions were prepared, and their effects on LPS‐induced gene expression were monitored by Western blotting and RT‐PCR. Results: Our results indicated that AC‐2, but not AC‐1 dose‐dependently (50–200 mg/L) inhibited LPS‐induced nitric oxide production as well as the protein and the mRNA expression of the inducible nitric oxide synthase (iNOS) gene. Neither AC‐1 nor AC‐2 inhibited LPS‐induced cyclooxygenase‐2 gene expression. Using the cytokine array assay, it showed that AC‐2 also had the ability to inhibit LPS‐induced the protein expression of interleukin (IL)‐6, IL‐10, the monocyte chemoattractant protein (MCP)‐5, and regulated upon activation, normal T‐cell expressed, and presumably secreted (RANTES). Like iNOS, AC‐2 inhibiting LPS‐induced IL‐6 and IL‐10 secretion resulted from inhibiting their mRNA expression. Conclusion: It was suggested that alkaline extraction‐isoelectric precipitated the polysaccharide fraction of A camphorata and had the ability to inhibit LPS‐induced iNOS, IL‐6, IL‐10, MCP‐5, and RANTES expression in mouse macrophages.

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Section: Discussionmentioning

confidence: 99%

Modulation of inflammation-related genes of polysaccharides fractionated from mycelia of medicinal basidiomycete Antrodia camphorata

Chen²,

Chyau³

et al. 2007

Acta Pharmacologica Sinica

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“…Combinations of forward and reverse allele-specific primer were used to identify the cis / trans orientation of the alleles and thus the haplotypes in both the TNF-␣ and LT-␣ genes. For the biallelic polymorphism in intron 4 (A/G) of the IL-6 gene, we used the SSPs and conditions previously described by Koss and coworkers (25). For identification of the biallelic promotor polymorphism Ϫ 174(G/C) in the IL-6 gene we used the sequence-specific reverse primers 2133:5 Ј -AATGTGACG-TCCTTTAGCATC and 2134:5 Ј -AATGTGACGTCCTTTAGCATG in combination with the consensus forward primer 5 Ј -TCGTGCAT-GACTTCAGCTTTA at a final concentration of 7.68 ng/ l, with an expected PCR product size of 237 bp (the IL-6[ Ϫ 174] SSP-PCR sequences were kindly provided by Dr. S. E. Marshall) of the Oxford Tissue Typing Center.…”

Section: Sequence-specific Primers and Polymerase Chain Reactionmentioning

confidence: 99%

Analysis of Tumor Necrosis Factor- α , Lymphotoxin- α , Tumor Necrosis Factor Receptor II, and Interleukin-6 Polymorphisms in Patients with Idiopathic Pulmonary Fibrosis

Pantelidis

Fanning

Wells

et al. 2001

Am J Respir Crit Care Med

130

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Idiopathic pulmonary fibrosis (IPF) is characterized by chronic inflammation that is associated with structural damage of the lung and fibrosis. Although the etiology of IPF is unknown, it is likely to involve an interaction between environmental and multiple genetic components. Animal models of pulmonary fibrosis have shown that proinflammatory mediators are critical at both the inflammatory and fibrotic stages of the disease. Genetic variants exist in genes encoding proinflammatory mediators, as well as in genes encoding their receptors, which makes these genes candidates for the pathogenesis of IPF. In the present study, we examined 12 biallelic polymorphisms in the genes for tumor necrosis factor (TNF)-alpha (+488[G/A], -238[G/A], -308[G/A]), lymphotoxin (LT)-alpha (+720[C/A], +365[C/G], and +249[A/G], determining haplotypes LT-alpha1 to LT-alpha4), tumor necrosis factor-receptor 2 (TNF-RII) (gb:M32315: 676[T/G], 1663[A/G], 1668[T/G], 1690[C/T]), and interleukin- (IL)-6 (promoter -174[G/C], intron 4[A/G]). We also examined the haplotypes determined by the three biallelic polymorphisms in each of the TNF-alpha and LT-alpha genes. As compared with a normal control population, the IPF group showed no significant deviations in genotype, allele, or haplotype frequencies. Surprisingly, in the IPF population, but not in the control population, an increased frequency of cocarriage of the IL-6 intron 4G and the TNF-RII 1690C alleles was observed, despite the location of the two genes on different chromosomes. Moreover, using impairment of carbon monoxide transfer (DL(CO)) adjusted for duration of dyspnea as a marker of rapidity of disease progression, we found that the IL-6 intron 4GG genotype was the only genotype independently associated with lower DL(CO) levels. These findings, if independently confirmed, will be the first to suggest that disease progression in IPF may be linked to a particular genetic marker or to functional polymorphisms in other genes near that marker.

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“…Fishman et al 24 also demonstrated that the −172C allele was significantly less frequent in a population of systemic-onset Juvenile Chronic Arthritis patients and that promoter constructs containing this allele were less transcriptionally active following LPS stimulation, 24 (although others have failed to observe differential IL-6 secretion in relation to this allele 28 ). This in vitro functional association was mirrored in the lower serum IL-6 levels observed in normal individuals who were homozygous for this allele, compared with those who carried the more common −172G allele.…”

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confidence: 99%

Allele associations reveal four prominent haplotypes at the human interleukin-6 (IL-6) locus

et al. 2000

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We have examined four polymorphic elements in the human interleukin-6 (IL-6) locus and described their allele distribution in 73 unrelated, healthy individuals from the West-of-Scotland. These comprised three single nucleotide polymorphisms (SNP) in the 5Ј promoter region of the gene and one VNTR in the 3Ј region of IL-6. A statistical consideration of the relationship between alleles at each locus was carried out. Of a total of 12 possible haplotypes observed in the population, the analysis suggested that four were prominent. These accounted for 41.1%, 28.1%, 14.4% and 3.4% respectively; in total, 87% of the haplotypes present. Frequently, these proposed haplotypes were supported by homozygosity across all four loci within individuals. We propose that these haplotypes be identified as IL6.0103, IL6.0204, IL6.0207 and IL6.0307, in recognition of their frequency in this population and the alleles that they contain. Genes and Immunity (2000) 1, 451-455.

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Is interleukin-6 important in inflammatory bowel disease?

Cited by 18 publications

References 21 publications

Modulation of inflammation-related genes of polysaccharides fractionated from mycelia of medicinal basidiomycete Antrodia camphorata

Modulation of inflammation-related genes of polysaccharides fractionated from mycelia of medicinal basidiomycete Antrodia camphorata

Analysis of Tumor Necrosis Factor- α , Lymphotoxin- α , Tumor Necrosis Factor Receptor II, and Interleukin-6 Polymorphisms in Patients with Idiopathic Pulmonary Fibrosis

Allele associations reveal four prominent haplotypes at the human interleukin-6 (IL-6) locus

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