Disease relevance of IL8

• In this study, we investigated IL8 mRNA expression following visna-maedi virus infection [1].
• These data indicate that a chemotactic substance immunoreactive to interleukin-8 antibody is formed as a result of unilateral lung ischemia in sheep in vivo and is a possible mediator of PMN inflammation in this model [2].
• Of these mediators LTB4, ZAP, IL-1 alpha, TNF-alpha, IFN-gamma, and IL-8 have been reported to induce neutrophil accumulation in skin of sheep, and in the current study E. coli endotoxin was a potent inducer of 111In-labeled neutrophil accumulation and plasma leakage in skin [3].
• Differential expression of sheep beta-defensin-1 and -2 and interleukin 8 during acute Mannheimia haemolytica pneumonia [4].
• No differences between R and S lines were found in numbers of neutrophils accumulating in acute inflammatory lesions induced by activated complement, leukotriene B4, interleukin (IL)-1 beta, tumour necrosis factor-alpha, IL-8 or endotoxin from Pseudomonas aeruginosa [5].

High impact information on IL8

• Cultured rabbit pleural mesothelial cells incubated with crocidolite asbestos also released chemotactic activity for neutrophils, which was inhibited significantly by the anti-IL-8 antibody [6].
• Homology-based PCR yielded a single cDNA fragment with a nucleotide sequence 88% identical to that of a corresponding region of human IL-8 cDNA [6].
• To determine whether rabbit pleural mesothelial cells synthesize IL-8, we generated a probe for rabbit IL-8 mRNA by amplifying cDNA prepared from stimulated pleural mesothelial cells using the polymerase chain reaction (PCR) and primers based on homologous sequences in human and sheep IL-8 cDNAs [6].
• In vitro infection with visna-maedi virus at low multiplicity of alveolar macrophages from uninfected sheep also strongly induced the expression of IL-8 mRNA and the accumulation of IL-8 in the extracellular medium [7].
• The level of IL-8 mRNA induced by treatment with live or inactivated virus could be severely reduced by pretreatment of the macrophages with genistein but not with staurosporine, suggesting the involvement of a tyrosine-kinase signaling pathway [7].

Biological context of IL8

• The inferred amino acid sequence has 78, 82, 84 and 67% similarity with human, rabbit, porcine and guinea-pig IL-8, respectively [8].
• Isolation stress in sheep: effects on neutrophil gene expression of CD18, IL8 and C5a receptors [9].
• Analysis of AM culture supernatants incubated with the combination of pigments showed significant increases in leukotriene B4 and interleukin-8, and blocking these mediators separately or together reduced AM supernatant-induced neutrophil chemotaxis [10].
• The alpha chemokine interleukin-8 (IL-8) was detected in cell free bronchoalveolar lavage fluid from naturally infected animals, confirmed by RT-PCR, presenting typical lesions of maedi and elevated total alveolar cell counts [11].
• Insemination increased IL-8 gene expression in progesterone-synchronized ewes [12].

Anatomical context of IL8

• Northern analysis of total RNA using an ovine IL8-specific probe demonstrated that the IL8 gene is upregulated in alveolar macrophages as a consequence of in vitro infection and in alveolar cells from experimentally infected animals [1].
• At 5 h, the epithelial cells in large airways expressed heat shock protein 70, and alveolar interleukin-8 was increased [13].
• Indicators of inflammation (white blood cells, hydrogen peroxide production, and IL-1beta and IL-8 cytokine mRNA expression in cells from the alveolar wash) qualitatively indicated less injury in the high PCO(2) group, although the differences were not significant [14].
• Betamethasone treatment can suppress the initial inflammation in the amnion-chorion, but interleukin-8 levels and inflammatory cells in amniotic fluid were not suppressed 5 and 15 days after betamethasone treatment, presumably because of the slow clearance of bioactive endotoxin from the amniotic fluid [15].
• 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 [15].

Associations of IL8 with chemical compounds

• Coinjection of actinomycin D did not abrogate recruitment of neutrophils to skin sites receiving LTB4; thus neither induction of endothelial adhesion molecules nor synthesis of IL-8 was necessary for LTB4 to exhibit inflammatory activity in vivo [3].
• Co-inoculation of M. haemolytica with xylitol, an osmotic agent, did not alter mRNA levels of SBD-1, SBD-2 or IL-8 [4].
• Chemotaxis was evaluated on a modified Boyden chamber using a nitrate cellulose filter and both Zymosan activated serum (ZAS) and interleukin-8 (IL-8) as chemoattractants [16].
• IL-8 gene expression in the luminal epithelium varied throughout the oestrous cycle and was highest at oestrus and at day 5 of the oestrous cycle [12].
• In ewes artificially induced to ovulate, either by the withdrawal of progesterone pessaries after treatment for 12 days, or by two i.m. injections of prostaglandin 9 days apart, IL-8 gene expression at oestrus was significantly lower than it was at natural oestrus [12].

Other interactions of IL8

• Higher cytokine expression was measured in sheep with pyogranulomas in the draining lymph nodes as compared to those without, especially for interleukin-1 beta and interleukin-8 [17].
• Plasma gastrin, interleukin-8 and tumor necrosis factor-alpha were also determined [18].

Analytical, diagnostic and therapeutic context of IL8

• By analogy with the most prevalent form of hIL-8, a 72 amino acid form of oIL-8 was expressed as a fusion protein containing glutathione-S-transferase and purified by affinity chromatography on a glutathione-Sepharose column yielding 8 mg IL-8/L broth culture [8].
• Using a semi-quantitative RT-PCR method, we showed that various levels of IL8 mRNA are expressed by alveolar cells from infected animals and that they correlate with the intensity of the lesions [1].
• With the radiolabeled PCR product as a probe, we demonstrated rapid induction of IL-8 mRNA expression in pleural mesothelial cells exposed to asbestos [6].
• IL-1beta, IL-6, and IL-8 mRNA in cells from bronchoalveolar lavage fluid were increased by antenatal endotoxin exposure but not changed by ventilation [19].
• In situ hybridization showed that macrophages were the predominant cell type expressing IL-8 mRNA [11].

References