Intradermal challenge with interleukin-8 causes tissue oedema and neutrophil accumulation in atopic and non-atopic human subjects

1996 ◽  
Vol 26 (12) ◽  
pp. 1371-1379 ◽  
Author(s):  
J. Douglass ◽  
D. Dhami ◽  
M. Bulpitt ◽  
I. J. Lindley ◽  
J. Shute ◽  
...  
Keyword(s):  
Human Subjects ◽  
Interleukin 8 ◽  
Neutrophil Accumulation ◽  
Tissue Oedema

Intradermal challenge with interleukin-8 causes tissue oedema and neutrophil accumulation in atopic and non-atopic human subjects

1996 ◽  
Vol 26 (12) ◽  
pp. 1371-1379 ◽  
Author(s):  
J. DOUGLASS ◽  
D. DHAMI ◽  
M. BULPITT ◽  
I. J. LINDLEY ◽  
J. SHUTE ◽  
...  
Keyword(s):  
Human Subjects ◽  
Interleukin 8 ◽  
Neutrophil Accumulation ◽  
Tissue Oedema

Interleukin-8 induces neutrophil accumulation but not protease secretion in the canine trachea

1992 ◽  
Vol 263 (6) ◽  
pp. L708-L713 ◽  
Author(s):  
P. G. Jorens ◽  
J. B. Richman-Eisenstat ◽  
B. P. Housset ◽  
P. D. Graf ◽  
I. F. Ueki ◽  
...  
Keyword(s):  
Interleukin 8 ◽  
Cathepsin G ◽  
Human Neutrophils ◽  
Secretory Cells ◽  
Neutrophil Accumulation ◽  
High Concentrations ◽  
Granule Secretion ◽  
Protease Secretion

The neutrophil enzyme elastase is a potent secretagogue of airway secretory cells, and elastase is present in high concentrations in sputum of patients with hypersecretion (e.g., cystic fibrosis, bronchiectasis). Interleukin-8 (IL-8), a recently discovered cytokine with potent neutrophil chemotactic properties in vitro, is also found in the sputum of these patients. We used an isolated tracheal segment in dogs in vivo to study the effect of IL-8 in causing neutrophil accumulation, elastase release, and secretion (by measuring lysozyme concentrations) in the luminal superfusate. IL-8 caused a potent time-dependent neutrophil accumulation at between 3 and 6 h. The effect was significant at 10(-9) and maximum at 10(-8) M. No increase in free elastase, cathepsin G, or lysozyme was detected in the superfusate. Thus, in contrast to previous studies showing that ragweed antigen causes the accumulation of neutrophil elastase which in turn causes lysozyme secretion, IL-8 causes neutrophil accumulation without granule secretion (or subsequent secretagogue activity). The findings were confirmed with dog and human neutrophils in vitro.

Aprotinin Reduces Interleukin-8 Production and Lung Neutrophil Accumulation After Cardiopulmonary Bypass

1996 ◽  
Vol 83 (4) ◽  
pp. 696-700 ◽  
Author(s):  
Gary E. Hill ◽  
Roman Pohorecki ◽  
Anselmo Alonso ◽  
Stephen I. Rennard ◽  
Richard A. Robbins
Keyword(s):  
Cardiopulmonary Bypass ◽  
Interleukin 8 ◽  
Neutrophil Accumulation

scholarly journals In Vitro and In Vivo Activity of Human Interleukin-8 in Dogs

1994 ◽  
Vol 31 (1) ◽  
pp. 61-66 ◽  
Author(s):  
R. D. Zwahlen ◽  
D. Spreng ◽  
M. Wyder-Walther
Keyword(s):  
Animal Species ◽  
Shape Change ◽  
Positive Control ◽  
Intradermal Injection ◽  
Interleukin 8 ◽  
Human Beings ◽  
Neutrophil Accumulation ◽  
Canine Plasma

Interleukin-8 (IL-8), a proinflammatory cytokine produced by human monocytes, fibroblasts, and endothelial and epithelial cells, is effective not only on cells and tissues of human beings but also on those of several animal species. We investigated the importance of recombinant human IL-8 for the activation of canine neutrophils in vitro and its potential for inducing inflammation in vivo. Shape change (10-9–10-7 M IL-8) and chemotaxis (10-10–10-6 M IL-8) assays were used to determine the activation of canine neutrophils in vitro. Chemotaxis was induced by IL-8 at doses > 10-8 M with a maximum response at 10-6 M. A rapid shape change of comparable intensity was elicited by 10-9–10-7 IL-8. Thirty minutes after intradermal injection of 10-9 moles of IL-8, emigration of neutrophils could be observed and became more intense at 60 minutes and 240 minutes, respectively. Zymosan-activated canine plasma, which served as a positive control, induced a rapid, massive, and more diffuse neutrophil accumulation, whereas the reaction after IL-8 was weaker but still significant. The neutrophil accumulation after IL-8 was preferentially located in perivenular areas of the deep dermis. Recombinant human IL-8 is capable of activating canine neutrophils in vitro and is able to generate significant neutrophil accumulation in dog skin. Its activity is lower than that in human, rabbit, and rat systems.

scholarly journals Inhibitory effect of erythromycin on interleukin 8 production by 1 alpha,25-dihydroxyvitamin D3-stimulated THP-1 cells.

1996 ◽  
Vol 40 (6) ◽  
pp. 1548-1551 ◽  
Author(s):  
T Fujii ◽  
J Kadota ◽  
T Morikawa ◽  
Y Matsubara ◽  
K Kawakami ◽  
...  
Keyword(s):  
Lavage Fluid ◽  
Inhibitory Effect ◽  
Interleukin 8 ◽  
Neutrophil Accumulation ◽  
Monocytic Cell ◽  
Monocytic Cell Line ◽  
Dihydroxyvitamin D3 ◽  
Human Monocytic Cell Line ◽  
Human Monocytic Cell ◽  
Term Administration

We have recently reported that long-term administration of erythromycin at a low dose reduced the number of neutrophils and concentrations of interleukin 8 (IL-8) in bronchoalveolar lavage fluid in patients with chronic lower respiratory tract disease. To investigate the mechanism of action of erythromycin, we evaluated its effect on IL-8 production in the 1 alpha,25-dihydroxyvitamin D3-stimulated human monocytic cell line THP-1. Erythromycin at a concentration of 10 micrograms/ml significantly reduced IL-8 production by THP-1 cells stimulated with lipopolysaccharide (10 ng/ml) and 1% normal human serum compared with the amount produced by untreated cells (untreated cells, 2,448 pg/ml; erythromycin-treated cells, 872 pg/ml). Our results suggest that erythromycin may impair IL-8 production by alveolar macrophages, ultimately reducing neutrophil accumulation in the airspace.

Aprotinin Reduces Interleukin-8 Production and Lung Neutrophil Accumulation After Cardiopulmonary Bypass

1996 ◽  
Vol 83 (4) ◽  
pp. 696-700 ◽  
Author(s):  
Gary E. Hill ◽  
Roman Pohorecki ◽  
Anselmo Alonso ◽  
Stephen I. Rennard ◽  
Richard A. Robbins
Keyword(s):  
Cardiopulmonary Bypass ◽  
Interleukin 8 ◽  
Neutrophil Accumulation

Elevated level of circulatory sTLT1 induces inflammation through SYK/MEK/ERK signalling in coronary artery disease

2019 ◽  
Vol 133 (22) ◽  
pp. 2283-2299
Author(s):  
Apabrita Ayan Das ◽  
Devasmita Chakravarty ◽  
Debmalya Bhunia ◽  
Surajit Ghosh ◽  
Prakash C. Mandal ◽  
...  
Keyword(s):  
Risk Factors ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Chronic Inflammation ◽  
Ex Vivo ◽  
Human Subjects ◽  
Critical Role ◽  
Atherosclerotic Cardiovascular Disease ◽  
Tnf Α ◽  
Artery Disease

Abstract The role of inflammation in all phases of atherosclerotic process is well established and soluble TREM-like transcript 1 (sTLT1) is reported to be associated with chronic inflammation. Yet, no information is available about the involvement of sTLT1 in atherosclerotic cardiovascular disease. Present study was undertaken to determine the pathophysiological significance of sTLT1 in atherosclerosis by employing an observational study on human subjects (n=117) followed by experiments in human macrophages and atherosclerotic apolipoprotein E (apoE)−/− mice. Plasma level of sTLT1 was found to be significantly (P<0.05) higher in clinical (2342 ± 184 pg/ml) and subclinical cases (1773 ± 118 pg/ml) than healthy controls (461 ± 57 pg/ml). Moreover, statistical analyses further indicated that sTLT1 was not only associated with common risk factors for Coronary Artery Disease (CAD) in both clinical and subclinical groups but also strongly correlated with disease severity. Ex vivo studies on macrophages showed that sTLT1 interacts with Fcɣ receptor I (FcɣRI) to activate spleen tyrosine kinase (SYK)-mediated downstream MAP kinase signalling cascade to activate nuclear factor-κ B (NF-kB). Activation of NF-kB induces secretion of tumour necrosis factor-α (TNF-α) from macrophage cells that plays pivotal role in governing the persistence of chronic inflammation. Atherosclerotic apoE−/− mice also showed high levels of sTLT1 and TNF-α in nearly occluded aortic stage indicating the contribution of sTLT1 in inflammation. Our results clearly demonstrate that sTLT1 is clinically related to the risk factors of CAD. We also showed that binding of sTLT1 with macrophage membrane receptor, FcɣR1 initiates inflammatory signals in macrophages suggesting its critical role in thrombus development and atherosclerosis.

Sign in / Sign up

Export Citation Format

Share Document