Granulocyte and monocyte adsorptive apheresis induces apoptosis of neutrophils and release of a novel chemoattractant for desensitization of interleukin-8 response – In vitro and in vivo results

Cytokine ◽  
2021 ◽  
Vol 139 ◽  
pp. 155410
Author(s):  
Nobuhito Kashiwagi ◽  
Fumio Saito ◽  
Hidetaka Maegawa ◽  
Kenta Kaneda
Keyword(s):  
Interleukin 8 ◽  
Adsorptive Apheresis

scholarly journals Differential Normalization of Mucosal Interleukin-8 and Interleukin-6 Activity after Helicobacter pyloriEradication

1998 ◽  
Vol 66 (10) ◽  
pp. 4742-4747 ◽  
Author(s):  
Takafumi Ando ◽  
Kazuo Kusugami ◽  
Masahiro Ohsuga ◽  
Kenji Ina ◽  
Masataka Shinoda ◽  
...  
Keyword(s):  
Mononuclear Cells ◽  
Eradication Therapy ◽  
Interleukin 8 ◽  
Biopsy Specimens ◽  
Mucosal Tissues ◽  
H Pylori ◽  
Triple Treatment

ABSTRACT There is differential resolution of mucosal infiltration with neutrophils and mononuclear cells following successfulHelicobacter pylori eradication. We investigated the effects of H. pylori eradication on mucosal interleukin-8 (IL-8) and IL-6 activity in relation to the resolution of H. pylori-associated gastritis. Eighty-one duodenal ulcer patients with H. pyloriinfection received dual- or triple-treatment eradication therapy, and mucosal biopsy specimens obtained at the initial and follow-up endoscopic examinations were cultured in vitro for 24 h. The levels of IL-8 and IL-6 were measured by enzyme-linked immunosorbent assays. In the 42 patients in whomH. pylori eradication failed, there was little change in the numbers of neutrophils and mononuclear cells infiltrating the mucosa and in IL-8 and IL-6 activity. In the 39 patients in whom H. pylori was eradicated, there was normalization both in the numbers of infiltrating neutrophils and in mucosal IL-8 activity, which was evident within 1 month following therapy. In contrast, there was a gradual resolution of mononuclear cell infiltration over a 6-month period, accompanied by a gradual normalization in IL-6 levels. Addition of H. pylori to cultures of mucosal tissues induced a significant increase in IL-8 activity in both uninfected control subjects and patients from whom H. pylori was eradicated. However, this introduction yielded a significant increase in IL-6 activity only in the latter group. This study indicates a dichotomy in the changes of mucosal IL-8 and IL-6 activity afterH. pylori eradication. The rapid normalization of IL-8 after H. pylori eradication and the ability of H. pylori cells to stimulate IL-8 in control tissues indicate that IL-8 induction is a part of the innate (nonimmune) responses to this organism. In contrast, the results of experiments analyzing IL-6 activity in cultured mucosal tissues suggest that the gradual resolution of mucosal IL-6 activity and mononuclear infiltration after successful eradication observed in vivo may reflect gradually diminishing residual immune responses against H. pylori.

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.

The effect of recombinant interleukin-8 on eosinophils' and neutrophils' migration in vivo and in vitro

Allergy ◽  
2003 ◽  
Vol 58 (8) ◽  
pp. 795-801 ◽  
Author(s):  
M. Bochenska-Marciniak ◽  
M. Kupczyk ◽  
P. Gorski ◽  
P. Kuna
Keyword(s):  
Interleukin 8

Visna-maedi virus-induced expression of interleukin-8 gene in sheep alveolar cells following experimental in vitro and in vivo infection

1996 ◽  
Vol 147 (2-3) ◽  
pp. 191-197 ◽  
Author(s):  
I. Legastelois ◽  
G. Cordier ◽  
G. Cozon ◽  
J.-L. Cadoré ◽  
F. Guiguen ◽  
...  
Keyword(s):  
Interleukin 8 ◽  
Alveolar Cells ◽  
Induced Expression

scholarly journals In vitro and in vivo interleukin-8 production in human renal cortical epithelia

1992 ◽  
Vol 41 (1) ◽  
pp. 191-198 ◽  
Author(s):  
Robert L. Schmouder ◽  
Robert M. Strieter ◽  
Roger C. Wiggins ◽  
Stephen W. Chensue ◽  
Steven L. Kunkel
Keyword(s):  
Interleukin 8

The Biologic Role of Interleukin-8: Functional Analysis and Expression of CXCR1 and CXCR2 on Human Eosinophils

Blood ◽  
1999 ◽  
Vol 93 (2) ◽  
pp. 694-702
Author(s):  
Holger Petering ◽  
Otto Götze ◽  
Daniela Kimmig ◽  
Regina Smolarski ◽  
Alexander Kapp ◽  
...  
Keyword(s):  
Allergic Inflammation ◽  
Allergic Diseases ◽  
Interleukin 8 ◽  
Cytokine Activation ◽  
Cc Chemokines ◽  
Eosinophil Granulocytes ◽  
In Vitro Effects

Chemokines play an important role in attracting granulocytes into sites of inflammation. Two chemokine subfamilies differ in their biologic activity for different granulocyte subsets. Whereas CXC chemokines such as interleukin-8 (IL-8) activate predominantly neutrophils, CC chemokines such as RANTES and eotaxin activate predominantly eosinophils. However, controversial results have been published in the past regarding the biologic role of IL-8 in eosinophil activation, particularly in allergic diseases. In this study, we investigated the functional evidence and expression of both IL-8 receptors, CXCR1 and CXCR2, on highly purified human eosinophils. In the first set of experiments, a chemotaxis assay was performed showing that IL-8 did not induce chemotaxis of eosinophils. In addition, and in contrast to neutrophils and lymphocytes, IL-8 did not induce a rapid and transient release of cytosolic free Ca2+([Ca2+]i) in eosinophils, even after preincubation with TH1- and TH2-like cytokines. To investigate whether neutrophil contamination might be responsible for the reported IL-8 effects on eosinophils, neutrophils were added to highly purified eosinophils from the same donor in different concentrations. Interestingly, as little as 5% of neutrophil contamination was sufficient to induce an increase of [Ca2+]iafter stimulation with IL-8. Flow cytometry experiments with monoclonal antibodies against both IL-8 receptors demonstrated no expression of CXCR1 and CXCR2 on eosinophils before or after cytokine activation. Reverse transcriptase-polymerase chain reaction experiments showed that eosinophils, in contrast to neutrophils and lymphocytes, did not express mRNA for CXCR1 and CXCR2. In summary, this study clearly demonstrates that CXCR1 and CXCR2 are not expressed on human eosinophils, even after priming with different bioactive cytokines. Because the CXC chemokine IL-8 did not induce in vitro effects on human eosinophils, IL-8 may also not contribute in vivo to the influx of eosinophil granulocytes into sites of allergic inflammation. Our results suggest that CC chemokines such as eotaxin, eotaxin-2, and MCP-4 are predominant for the activation of eosinophils.

scholarly journals Loss of S100A9 (MRP14) Results in Reduced Interleukin-8-Induced CD11b Surface Expression, a Polarized Microfilament System, and Diminished Responsiveness to Chemoattractants In Vitro

2003 ◽  
Vol 23 (3) ◽  
pp. 1034-1043 ◽  
Author(s):  
Marie-Pierre Manitz ◽  
Basil Horst ◽  
Stephan Seeliger ◽  
Anke Strey ◽  
Boris V. Skryabin ◽  
...  
Keyword(s):  
Calcium Binding ◽  
Inflammatory Diseases ◽  
Three Dimensional ◽  
Collagen Matrix ◽  
Interleukin 8 ◽  
In Vivo Models ◽  
Migration Assay ◽  
Microfilament System

ABSTRACT The S100A9 (MRP14) protein is abundantly expressed in myeloid cells and has been associated with various inflammatory diseases. The S100A9-deficient mice described here were viable, fertile, and generally of healthy appearance. The myelopoietic potential of the S100A9-null bone marrow was normal. S100A8, the heterodimerization partner of S100A9 was not detectable in peripheral blood cells, suggesting that even a deficiency in both S100A8 and S100A9 proteins was compatible with viable and mature neutrophils. Surprisingly, the invasion of S100A9-deficient leukocytes into the peritoneum and into the skin in vivo was indistinguishable from that in wild-type mice. However, stimulation of S100A9-deficient neutrophils with interleukin-8 in vitro failed to provoke an up-regulation of CD11b. Migration upon a chemotactic stimulus through an endothelial monolayer was markedly diminished in S100A9-deficient neutrophils. Attenuated chemokinesis of the S100A9-deficient neutrophils was observed by using a three-dimensional collagen matrix migration assay. The altered migratory behavior was associated with a microfilament system that was highly polarized in unstimulated S100A9-deficient neutrophils. Our data suggest that loss of the calcium-binding S100A9 protein reduces the responsiveness of the neutrophils upon chemoattractant stimuli at least in vitro. Alternative pathways for neutrophil emigration may be responsible for the lack of any effect in the two in vivo models we have investigated so far.

scholarly journals Presence of autoantibodies to interleukin-8 or neutrophil-activating peptide-2 in patients with heparin-associated thrombocytopenia

Blood ◽  
1996 ◽  
Vol 88 (2) ◽  
pp. 410-416 ◽  
Author(s):  
J Amiral ◽  
A Marfaing-Koka ◽  
M Wolf ◽  
MC Alessi ◽  
B Tardy ◽  
...  
Keyword(s):  
Cell Activation ◽  
Interleukin 8 ◽  
Enzyme Linked Immunosorbent Assay ◽  
Platelet Factor ◽  
Elisa System ◽  
Platelet Aggregometry ◽  
Test Result

Eighty-seven patients with heparin-associated thrombocytopenia (HAT) showed either a positive heparin platelet aggregometry test result and/or the presence of antibodies to heparin-platelet factor 4 (H-PF4) complexes by enzyme-linked immunosorbent assay (ELISA). Fifteen of these patients lacked antibodies to H-PF4, and plasma from these patients was analyzed for the presence of antibodies to PF4-related chemokines, Neutrophil-activating peptide-2 (NAP-2) and interleukin-8 (IL-8). Of these 15 patients, 6 showed antibodies to IL-8 and 3 to the platelet basic protein (PBP)-derived protein, NAP-2. Antibodies to IL-8 and NAP-2 were not observed in control patients (n = 38), patients with HAT and H-PF4 autoantibodies (n = 72), patients with autoimmune diseases (n = 21), or patients with non-HAT thrombocytopenia (n = 30). Five of these nine patients with anti-IL-8 or anti-NAP-2 developed thrombosis during heparin treatment, which is not statistically different from the patients with H-PF4 antibodies. The existence of autoantibodies to IL-8 and NAP-2 in HAT patients highlights the significance of chemokines in the pathogenesis of HAT. The contribution of heparin in vitro was minimal in patients with anti-IL-8 and anti-NAP- 2 antibodies, suggesting a biologic difference from the majority of patients with HAT and anti-PF4 antibodies. It may be that antibodies to IL-8 and NAP-2 have weaker affinity for heparin and that the ELISA system may not reflect in vivo heparin-chemokine complex formation. Alternatively, antichemokine autoantibodies may predate heparin exposure, and the role of heparin in initiating HAT may be to mobilize the chemokines and to target them to platelets, neutrophils, or endothelial cells. Subsequent chemokine-binding autoantibodies then lead to cell activation resulting in thrombocytopenia and thrombosis.

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