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IL7 — IL8

Text-mined interactions from Literome

Lottaz et al., J Invest Dermatol 2001 : We hypothesize that inhibition of this pathway prevents secretion of interleukin-1, thereby downregulating interleukin-1 dependent autocrine induction of interleukin-8
Prause et al., Eur J Pharmacol 2003 : Pharmacological modulation of interleukin-17 induced GCP-2-, GRO-alpha- and interleukin-8 release in human bronchial epithelial cells ... We found that interleukin-17 ( 1-1000 ng/ml ) increased the release of GCP-2, GRO-alpha and interleukin-8 in a concentration dependent manner
Waehre et al., J Am Coll Cardiol 2003 (Coronary Artery Disease) : Our main findings were : 1 ) gene expression of several chemokines ( i.e., macrophage inflammatory protein [MIP ] -1alpha, MIP-1beta, and interleukin [ IL]-8 ) and chemokine receptors ( i.e., CC chemokine receptor [ CCR]1, CCR2, CCR4, and CCR5 ) was markedly increased among CAD patients compared with healthy control subjects ; 2 ) treatment with atorvastatin and simvastatin markedly reduced the mRNA levels of some of these chemokines ( i.e., MIP-1alpha, MIP-1beta, IL-8 ) and receptors ( i.e., CCR1 and CCR2 ), with the most pronounced effect in the atorvastatin group ; and 3 ) statin therapy reduced the spontaneous release of IL-8 and MIP-1alpha from PBMCs in CAD patients
Vittori et al., J Allergy Clin Immunol 1992 : Protective effect of nedocromil sodium on the interleukin-1 induced production of interleukin-8 in human bronchial epithelial cells
Uchiyama et al., Am J Obstet Gynecol 1992 : These results indicate that interleukin-8-like chemotactic factor participates in the cervical ripening at term pregnancy and that the production of this factor is controlled effectively by interleukin-1
Soloff et al., Endocrinology 2004 : In situ analysis of interleukin-1 induced transcription of cox-2 and il-8 in cultured human myometrial cells
Wuyts et al., J Heart Lung Transplant 2004 : N-acetylcysteine inhibits interleukin-17 induced interleukin-8 production from human airway smooth muscle cells : a possible role for anti-oxidative treatment in chronic lung rejection ?
Standiford et al., J Immunol 1992 : In addition, IL-7 significantly potentiated the production of IL-8 from LPS-, TNF-, and IL-1 treated peripheral blood monocytes
Hirota et al., Rheumatol Int 1992 : Production of interleukin 8 by cultured synovial cells in response to interleukin 1 and tumor necrosis factor
Hashmi et al., Coron Artery Dis 2006 (Angina, Unstable) : Role of interleukin-17 and interleukin-17 induced cytokines interleukin-6 and interleukin-8 in unstable coronary artery disease
Darbonne et al., J Clin Invest 1991 : Their binding of IL-8 is rapidly reversible and does not result in receptor internalization, although bound IL-8 is resistant to extraction by pH 3 buffer at 5 degrees C. 125I-IL-8 binding to red cells was not inhibited by epidermal growth factor or interleukin 1, but was inhibited by monocyte chemotactic peptide-1, which is not a neutrophil chemotaxin, but is a member of the same family of polypeptides as IL-8
Larsen et al., Biochem Biophys Res Commun 1991 : 1,25 ( OH ) 2-D3 is a potent regulator of interleukin-1 induced interleukin-8 expression and production
Hua et al., Molecular oral microbiology 2010 (Periodontal Diseases) : Furthermore, as little as 2 µg ml(-1) mPE was sufficient to inhibit interleukin-1ß induced secretion of interleukin-8 in both gingival epithelial cells and THP-1 cells
Vindeløv et al., Growth Horm IGF Res 2011 (Adenoma...) : Interleukin-8 production from human somatotroph adenoma cells is stimulated by interleukin-1ß and inhibited by growth hormone releasing hormone and somatostatin
Strieter et al., Am J Respir Cell Mol Biol 1990 : The induction of AMO derived IL-8 by tumor necrosis factor (TNF), lipopolysaccharide (LPS), and interleukin-1 ( IL-1 beta ) was shown to be both dose and time dependent
Ng et al., J Biol Chem 1994 : Although tumor necrosis factor (TNF) and interleukin-1 ( IL ) induce the expression of the IL-8 , TNF stimulated gene 6, and plasminogen activation inhibitor-2 genes and the activation of NF-kappa B with nearly identical kinetics, the two cytokines differ significantly in the induction of the IL-6 gene in all primary fibroblasts tested
Elner et al., Exp Eye Res 1996 : In this study, we examined the ability of interleukin-7 to induce RPE derived monocyte chemotactic protein-1 and interleukin-8 and assessed the potentiating effects of interleukin-7 on interleukin-1 beta- and tumor necrosis factor-alpha induced RPE monocyte chemotactic protein-1 and interleukin-8 production ... Interleukin-7 potentiated tumor necrosis factor-alpha induced RPE monocyte chemotactic protein-1 steady-state mRNA expression at all doses of interleukin-7 while only high dose interleukin-7 ( 100 ng ml-1 ) enhanced tumor necrosis factor-alpha induced RPE interleukin-8 steady-state gene expression ... This is one of the first reports demonstrating : ( 1 ) interleukin-7 induction of monocyte chemotactic protein-1 in any cell type, and ( 2 ) interleukin-7 induction of interleukin-8 in resident, tissue based cells
Krakauer et al., J Infect Dis 1998 : Interleukin-8 production by human monocytic cells in response to staphylococcal exotoxins is direct and independent of interleukin-1 and tumor necrosis factor-alpha