Disease relevance of IL6

• CONCLUSIONS: In this clinically relevant septic shock model, alkaline phosphatase administration improved gas exchange, decreased interleukin-6 concentrations, and prolonged survival time [1].
• Plasma tumour necrosis factor-alpha and interleukin-6 concentrations were increased after LPS treatment with and without hypoxia, but not by hypoxia alone [2].
• This may involve upregulation of systemic IL-6 synthesis and transfer to gingiva in serum, resulting in enhanced IL-6 accumulation within the gingival tissues or reduced bone density allowing for a greater amount of alveolar bone loss [3].

High impact information on IL6

• Three days after intra-amniotic endotoxin exposure, preterm monocyte responses to in vitro endotoxin challenge demonstrated decreased H(2)O(2) and interleukin-6 production and decreased CD14 and major histocompatibility complex class II expression [4].
• Compared with monocytes from adult sheep, the preterm monocytes produced less H(2)O(2) and interleukin-6, and toll-like receptor 4 expression was decreased [4].
• At 5 h active inflammatory cells were in the airways producing hydrogen peroxide, and interleukin-6 and -8 were increased in the cord blood indicating both lung and systemic responses [5].
• This rapid peak in activin A preceded the release of the key inflammatory cytokines, tumor necrosis factor-alpha and interleukin-6 [6].
• Synergism of interleukin 6 and 1 alpha,25-dihydroxyvitamin D3 in induction of myeloid differentiation of human leukemic cell lines [7].

Biological context of IL6

• This is in contrast to recombinant human IL-6, which is capable of stimulating B9 cell proliferation, but not immunoglobulin production by ovine PBMC [8].
• Gene amplification by reverse transcriptase PCR with heterologous primers has been used to obtain a cDNA clone encoding the structural sequences of ovine interleukin 6 from alveolar macrophages [8].
• However, the combination of anti-Ig and recombinant ovine interleukin-6 to peripheral blood lymphocyte cultures was found to markedly and consistently enhance specific antibody production [9].
• This revealed that activin A was not released centrally in the CSF following a peripheral LPS injection, nor was TNFalpha or the activin binding protein, follistatin, but IL-6 showed a robust elevation [10].

Anatomical context of IL6

• This protein is capable of causing increased immunoglobulin production in pokeweed mitogen stimulated ovine peripheral blood mononuclear cells at concentrations of 10-100 ng/ml, but it only causes very limited replication of B9 cells, a murine IL-6 dependent cell line [8].
• Envenoming produced hepatocytes with Mallory body-like vacuoles which may be due to the increased plasmatic levels of TNF-alpha and IL6 [11].
• At 5-15 h after endotoxin, amnion/chorion cytokine mRNAs increased [12- to 26-fold for interleukin (IL)-1beta, IL-6, and IL-8 mRNA and 3-fold for tumor necrosis factor-alpha mRNA] [12].
• Plasma CM101 concentrations did not correlate with indexes of illness severity, leukocyte counts, or interleukin-6 or interleukin-8 plasma concentrations [13].
• Coincident with the influx of granulocytes and other cells there was an increase in the level of mRNA for the cytokines IL-1 alpha, IL-1 beta, IL-6 and IL-8 [14].

Associations of IL6 with chemical compounds

• Fetal and maternal blood gases and uterine electromyographic activity along with fetal and maternal circulating concentrations of prostaglandins PGE2 and PGFM, cortisol, and interleukin-6 were determined [15].
• Levels of interleukin-8, but not interleukin-6, were significantly increased in amniotic fluid from 5 hours to 15 days after intra-amniotic endotoxin injection, and interleukin-8 levels were not decreased by concurrent treatment with betamethasone [16].
• OVX animals had decreased serum levels of 17-beta-estradiol and increased serum levels of osteocalcin, IL-6, and urinary levels of deoxypyridinoline which, taken together, suggest development of osteoporosis [3].

Other interactions of IL6

• Single strand conformational polymorphisms (SSCPs) in the ovine IL1A and IL6 genes [17].
• After endotoxin treatment, interleukin-1beta and interleukin-8 messenger RNA were expressed in chorion, and interleukin-6 messenger RNA expression was localized to chorionic blood vessel epithelium [16].
• Measurement of cytokine production by the monocytic cell line Mono Mac 6 using novel immunoradiometric assays for interleukin-1 beta and interleukin-6 [18].
• Levels of GM-CSF mRNA expression in alveolar macrophages correlated with the presence of lung lesions, but there was no correlation of interleukin-10, interleukin-6, tumour necrosis factor-alpha and transforming growth factor-beta1 mRNA levels in alveolar macrophages from animals with pulmonary lesions [19].
• A significant increase in expression of interleukin-6, interleukin-10, granulocyte macrophage-colony stimulating factor (GM-CSF) and transforming growth factor-beta1 mRNA was observed in alveolar macrophages isolated from the lungs of naturally infected animals when compared with lungs of seronegative controls [19].

Analytical, diagnostic and therapeutic context of IL6

• In the treatment group, the Pao2/Fio2 ratio was higher (p < .05), blood interleukin-6 concentrations were lower (p < .05), and the survival time was longer (median time 23.8 vs. 17 .0 hrs, p < 0.05) than in the control group [1].
• In situ hybridization was used to determine the location of IL-6 and TNF alpha mRNA within resting and infected skin [14].
• Expression of mRNA for IL-6 could be detected by Northern blot analysis while mRNA for other inflammatory cytokines including IL-1 alpha, IL-1 beta, IL-8 and TNF alpha was detected using the polymerase chain reaction [14].
• Immunoradiometric assays for interleukin-1 beta and interleukin-6 were developed using affinity-purified IgG fractions from antisera initially raised for radioimmunoassay [18].
• IL-6 mRNA expression in the small intestine from T. colubriformis-immunised and naive sheep was determined by in situ hybridisation, whereas CD4(+), IgA(+), IgG(+) cells in the gut were evaluated by immunohistochemistry [20].

References