TY - JOUR. T1 - Neutrophil recruitment by intradermally injected neutrophil attractant/activation protein-1. AU - Leonard, Edward J.. AU - Yoshimura, Teizo. AU - Tanaka, Shuji. AU - Raffeld, Mark. PY - 1991/5. Y1 - 1991/5. N2 - Neutrophil attractant/activation protein-1 (NAP-1) is a recently described cytokine that attracts neutrophils, but not monocytes or eosinophils. This leukocyte specificity is not absolute, in that NAP-1 attracts basophils and small numbers of lymphocytes. Our purpose was to determine in vivo effects of NAP-1, and to compare them to the reported action of the complement attractant, C5a. Intradermal injection into normal human subjects of 40 μl of NAP-1, over a concentration range of 4 × 10-8 M to 10-6 M, caused no symptoms or signs such as wheal-and-flare, itching, induration, or tenderness. However, biopsies of injection sites showed perivascular neutrophil infiltration as early as 30 min, which increased at 1 and 3 h. The mean number of neutrophils per mm2 of dermis ...
In this study we focused on the cellular infiltration in the bronchial mucosa of patients with post-infective bronchiectasis compared with corresponding bronchial biopsy specimens from normal healthy control subjects. The striking finding was an intense cellular infiltrate (with increased CD45+ cell numbers) with mononuclear cells (CD4+ T lymphocytes and macrophages), a prominent neutrophilia, and increased expression of the potent neutrophil chemoattractant IL-8. In those patients with bronchiectasis treated with inhaled steroids the T cell infiltrate (CD4+ cells) was significantly lower than in untreated patients. These findings support a role for cell mediated immune mechanisms in the pathogenesis of ongoing airways damage in bronchiectasis and its possible modulation by topical corticosteroids.. Previous immunohistological studies of bronchiectasis3 4performed in an experimental rat model of bronchiectasis and on human subjects have identified a relative increase in CD8+ T lymphocytes in ...
Interactions between the enteric pathogen Salmonella typhimurium and the luminal surface of the intestine provoke an acute inflammatory response, mediated in part by epithelial cell secretion of the chemokine IL-8 and other proinflammatory molecules. This study investigated the mechanism by which this pathogen induces IL-8 secretion in physiologically polarized model intestinal epithelia. IL-8 secretion induced by both the prototypical proinflammatory cytokine TNF-α and S. typhimurium was NF-κB dependent. However, NF-κB activation and IL-8 secretion induced by S. typhimurium, but not by TNF-α, was preceded by and required an increase in intracellular [Ca2+]. Additionally, agonists that increased intracellular [Ca2+] by receptor-dependent (carbachol) or independent (thapsigargin, ionomycin) means also induced IL-8 secretion. Furthermore, the ability of S. typhimurium mutants to induce IκB-α degradation, NF-κB translocation, and IL-8 transcription and secretion correlated precisely with ...
IL-8 is a potent neutrophil chemoattractant that has been detected in high concentrations at acutely inflamed sites in vivo. Many cell types, including peripheral blood neutrophils, produce IL-8 that can be released by a variety of pro-inflammatory stimuli. However, the functional importance of neutrophil IL-8 during exudation is not yet known. We now report that neutrophils, harvested from skin lesions on the forearms of normal human volunteers (exudative neutrophils), expressed 100-fold higher levels of cell-associated IL-8 and spontaneously released up to 50-fold more IL-8 than freshly isolated peripheral blood neutrophils from the same donor. Furthermore, cell-associated IL-8 in peripheral blood neutrophils increased 20-fold during incubation at 37 degrees C in vitro and was increased over 200-fold after treatment with the Ca2+ ionophore A23187. More than 35% of the cell-associated IL-8 could be released by stimulation with either Ca2+ ionophore A23187 or phorbol myristate acetate. IL-8 was ...
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Primary human lung cells or cell lines were cultured on a stretchable silastic membrane forming the bottom of a 12-well plexiglas® box. The box was connected to an adult ventilator and ventilated for up to 36 hours at 20 cycles/min with a pressure-volume regimen resembling that of MV. Several lung cell types were tested in this model. The alveolar macrophage was identified as the main cellular source of key inflammatory mediators, such as tumor necrosis factor, the chemokine interleukin (IL)-8, and matrix metalloproteinase-9, produced during mechanical ventilation. Mechanical ventilation also induced low levels of IL-8 secretion by human alveolar epithelial type II-like cells. Other lung cell types such as endothelial cells, bronchial cells, and fibroblasts failed to produce IL-8 in response to mechanical ventilation (1,2). Conclusions and Relevance for 3R ...
Using thapsigargin (Tg), an agent that mobilizes calcium by directly emptying intracellular stores, we previously showed that intracellular calcium may play an important role in the regulation of intercellular adhesion molecule (ICAM)-1 gene expression induced by cytokines in human airway smooth muscle (ASM) cells. In the present study, we extended this previous observation by comparing the effect of Tg and other calcium-mobilizing G-protein-coupled receptor (GPCR) agonists on the expression of different pro-inflammatory genes in response to tumor necrosis factor (TNF)-alpha in ASM cells. We found that in resting cells, Tg (10-100 nM) or the bradykinin (BK) (1-10 muM) and thrombin (Thr) (1 U/ml) stimulated interleukin (IL)-6 secretion but had no effect on regulated on activation, normal T cells expressed and secreted (RANTES) levels. More importantly, such calcium-mobilizing agents significantly enhanced TNF-alpha-induced IL-6 secretion while RANTES secretion was abrogated. The use of ...
Rat CXCL2/MIP-2 (macrophage inflammatory protein-2) is a 69-amino acid CXC chemokine. MIP-2 is induced during acute inflammation in rat models of disease. It is a potent neutrophil chemotactic factor both |i|in vitro|/i| and|i| in vivo|/i|.
Christenson SA, van den Berge M, Faiz A, Inkamp K, Bhakta N, Bonser LR, Zlock LT, Barjaktarevic IZ, Barr RG, Bleecker ER, Boucher RC, Bowler RP, Comellas AP, Curtis JL, Han MK, Hansel NN, Hiemstra PS, Kaner RJ, Krishnanm JA, Martinez FJ, ONeal WK, Paine R, Timens W, Wells JM, Spira A, Erle DJ, Woodruff PG. An airway epithelial IL-17A response signature identifies a steroid-unresponsive COPD patient subgroup. J Clin Invest. 2019 01 02; 129(1):169-181 ...
InterPro provides functional analysis of proteins by classifying them into families and predicting domains and important sites. We combine protein signatures from a number of member databases into a single searchable resource, capitalising on their individual strengths to produce a powerful integrated database and diagnostic tool.
Power C.A., Furness R.B., Brawand C., Wells T.N.C. (1994). Cloning of a full-length cDNA encoding the neutrophil-activating peptide ENA-78 from human platelets.. Gene 151: 333 - 334. PubMed DOI:10.1016/0378-1119(94)90682-3 ...
TY - JOUR. T1 - Three forms of monocyte-derived neutrophil chemotactic factor (MDNCF) distinguished by different lengths of the amino-terminal sequence. AU - Teizo, Yoshimura. AU - Robinson, Elizabeth A.. AU - Appella, Ettore. AU - Matsushima, Kouji. AU - Showalter, Stephen D.. AU - Skeel, Alison. AU - Leonard, Edward J.. PY - 1989/1. Y1 - 1989/1. N2 - Human monocyte-derived neutrophil chemotactic factor (MDNCF) was purified from culture supernatant of lipopolysaccharide-stimulated human peripheral blood mononuclear leukocytes on a column of Sepharose-bound murine monoclonal anti-MDNCF. About 65% of the culture fluid chemotactic activity was bound to the column. The unbound 35% probably represents chemotactic activity of other cytokines in the culture fluid. More than 85% of the bound activity was eluted by pH 2.5 glycine buffer. When this material was applied to an HPLC-CM column, gradient elution produced four well-separated A280 peaks, each of which had chemotactic activity. N-terminal amino ...
Chemokine (C-C motif) ligand 5 (also CCL5) is a protein which in humans is encoded by the CCL5 gene. It is also known as RANTES (regulated on activation, normal T cell expressed and secreted). CCL5 is an 8kDa protein classified as a chemotactic cytokine or chemokine. CCL5 is chemotactic for T cells, eosinophils, and basophils, and plays an active role in recruiting leukocytes into inflammatory sites. With the help of particular cytokines (i.e., IL-2 and IFN-γ) that are released by T cells, CCL5 also induces the proliferation and activation of certain natural-killer (NK) cells to form CHAK (CC-Chemokine-activated killer) cells. It is also an HIV-suppressive factor released from CD8+ T cells[citation needed]. This chemokine has been localized to chromosome 17 in humans. RANTES was first identified in a search for genes expressed late (3-5 days) after T cell activation. It was subsequently determined to be a CC chemokine and expressed in more than 100 human diseases. RANTES expression is ...
Inflammatory cytokines induce synthesis and secretion of gro protein and a neutrophil chemotactic factor but not beta 2-microglobulin in human synovial cells an
Results In C57BL/6 mice, gefitinib decreased Cxcl1 and Cxcl2 expression by gastric epithelial cells, myeloperoxidase-positive inflammatory cells in the mucosa and epithelial DNA damage induced by H. pylori infection. Similar reductions in chemokines, inflammatory cells and DNA damage occurred in infected EgfrΔepi versus Egfrfl/fl control mice. In H. pylori-infected transgenic insulin-gastrin (INS-GAS) mice and gerbils, gefitinib treatment markedly reduced dysplasia and carcinoma. Gefitinib blocked H. pylori-induced activation of mitogen-activated protein kinase 1/3 (MAPK1/3) and activator protein 1 in gastric epithelial cells, resulting in inhibition of chemokine synthesis. MAPK1/3 phosphorylation and JUN activation was reduced in gastric tissues from infected wild-type and INS-GAS mice treated with gefitinib and in primary epithelial cells from EfgrΔepi versus Egfrfl/fl mice. Epithelial EGFR activation persisted in humans and mice after H. pylori eradication, and gefitinib reduced gastric ...
These studies demonstrate that GM-CSF is a neutrophil chemotactic agent. The concentration of GM-CSF needed to achieve maximal chemotaxis is comparable to that of the potent neutrophil chemoattractant IL-8 and less than the other known chemoattractants that we studied. We believe that GM-CSF induction of neutrophil chemotaxis has been previously unrecognized because the stimulatory effect occurs in a narrow range of concentrations (Fig. 3⇑A) and requires an extended incubation interval of at least 30 min. Results reported by Harakawa et al. (44) agreed with our finding that GM-CSF produces an early stimulation of neutrophil chemokinesis, but observations were not reported past 15 min, which may have been insufficient to recognize an effect on chemotaxis. Other earlier studies provided contradictory data on the effect of GM-CSF on neutrophil migration. In a checkerboard assay using polycarbonate filters, Wang et al. (45) demonstrated that GM-CSF induced chemotaxis in neutrophils, while Kharazmi ...
Chemokines are a large group of chemotactic cytokines that play an important pathogenic role in inflammatory diseases and autoimmune disorders by enhancement of leukocyte recruitment and activation at inflammatory sites [3-6]. ENA-78 is a CXC chemokine that attracts neutrophils during inflammation [7].. In this work, serum levels of ENA-78 were significantly higher in autistic children than healthy control children (P , 0.001). In addition, 69.35% of autistic children had increased serum levels of ENA-78. This study was the first to investigate serum levels of ENA-78 in autistic children. ENA-78 is an inflammatory C-X-C chemokine that is encoded by the CXCL5 gene [28]. Its levels are elevated in myriad inflammatory conditions [29-32].. ENA-78 is an α chemokine which is produced concomitantly with IL-8 and melanoma growth stimulating activity [7]. The main stimuli for secretion of chemokines, including ENA-78, are the early signals elicited during innate immune response such as bacterial ...
A potential new strategy to developing new drugs to control inflammation without serious side effects has been found by Georgia State University researchers and international colleagues.. Jian-Dong Li, director of Georgia States Center for Inflammation, Immunity and Infection, and his team discovered that blocking a certain pathway involved in the biological process of inflammation will suppress it.. Inhibiting a molecule called phosphodiesterase 4B, or PDE4B, suppresses inflammation by affecting a key gene called CLYD, a gene that serves as a brake on inflammation.. The research was published in the journal Nature Communications.. Li explained the process of overactive inflammation using a police analogy.. When a pathogen - such as bacteria or viruses -- infects a patient, he said, it triggers an alarm to which the police of immune system respond. In turn, it triggers neutrophil attractant called cytokines to respond, leading to inflammation that serves to help rid the body of the ...
CCL5 is an 8kDa protein classified as a chemotactic cytokine or chemokine. CCL5 is chemotactic for T cells, eosinophils, and basophils, and plays an active role in recruiting leukocytes into inflammatory sites. With the help of particular cytokines (i.e., IL-2 and IFN-γ) that are released by T cells, CCL5 also induces the proliferation and activation of certain natural-killer (NK) cells to form CHAK (CC-Chemokine-activated killer) cells.[6] It is also an HIV-suppressive factor released from CD8+ T cells[citation needed]. This chemokine has been localized to chromosome 17 in humans.[5]. RANTES was first identified in a search for genes expressed late (3-5 days) after T cell activation. It was subsequently determined to be a CC chemokine and expressed in more than 100 human diseases. RANTES expression is regulated in T lymphocytes by Kruppel like factor 13 (KLF13).[7][8][9][10] RANTES, along with the related chemokines MIP-1alpha and MIP-1beta, has been identified as a natural HIV-suppressive ...
Human IL-16 (hIL-16) is a homotetrameric cytokine with chemotactic properties towards cells expressing the CD4 receptor. This chemotactic cytokine plays an important role in attracting cells of the immune system to the site where CD8+ T-cells were activated for example by a foreign antigen. In addition to the chemotactic activity, hIL-16 also induces expression of IL-2 receptor, increasing the responsiveness to IL-2 and therefore implying a role for specific expansion of the CD4+ T-cell population in an area of induced inflammation. In this report we describe the cloning, sequencing and the expression of feline IL-16 (fIL-16). At the nucleotide level, fIL-16 shows 84.6 and 84.5%, on the amino acid level 93 and 91.5% identity to the human and African green monkey (agm) IL-16, respectively. ...
Methods Quiescent cultured RASMCs were pretreated with E2 or vehicle for 24 hours before tumor necrosis factor (TNF)-α was added. After 6 hours of treatment, total RNA was extracted from cells using TRIzol reagent, and SYBR green real-time RT-PCR was used to detect expression of CINC-2 mRNA. Conditioned media was collected and concentrated to measure CINC-2 protein level by ELISA. To assess neutrophil chemotactic activity of conditioned media, in vitro chemotaxis assays were performed using differentiated HL-60 cells in a 96-well modified Boyden chamber appropriate for the evaluation of leukocyte chemotaxis. The nonselective ER antagonist ICI-182780 was given to cells 2 hours prior to E2 incubation to study the mechanism of E2 effect. ...
Primobolan side effects is a selective agonist of beta2-adrenergic receptors. At therapeutic doses it acts on beta2-adrenergic receptors of smooth muscles of the bronchi, providing pronounced bronchodilator effect, prevents and relieves bronchospasm, increases lung capacity. It prevents the release of histamine, slow reacting substances from mast cells and neutrophil chemotactic factors. It is a small …. Read more ...
Primobolan side effects is a selective agonist of beta2-adrenergic receptors. At therapeutic doses it acts on beta2-adrenergic receptors of smooth muscles of the bronchi, providing pronounced bronchodilator effect, prevents and relieves bronchospasm, increases lung capacity. It prevents the release of histamine, slow reacting substances from mast cells and neutrophil chemotactic factors. It is a small …. Read more ...
Inhibition of LPS induced sputum neutrophil percentage. The reduction in sputum neutrophil percentage caused by active treatments compared to placebo are shown;
CXCL5 protein is expressed in E. coli, processed, refolded and purified to yield the native, secreted form of the mature chemokine. C-X-C motif chemokine 5 (CXCL5) or epithelial-derived neutrophil-activating peptide 78 (ENA-78) is a protein that in humans
HSV-1 infected keratinocytes release IL-1αPrimary human keratinocytes were treated with medium only, 25 μg ml-1 poly(I:C), or HSV-1 as indicated. After one ho
Abstract: : Purpose: Adenovirus infection of the cornea manifests as punctate epithelial keratitis, geographic epithelial erosions, and delayed-onset subepithelial corneal infiltrates. We have previously shown that (1)adenovirus type 19 (Ad19) infection of human corneal fibroblasts (HCF) induces expression of the neutrophil chemokine interleukin-8 (IL-8); (2) Ad19 infection of HCF induces tyrosine phosphorylation of the intracellular signaling protein c-src; and (3) phosphorylation of c-src is necessary for the expression of IL-8 by Ad19-infected HCF. These data suggest that Ad19 induces IL-8 expression in HCF by a signaling cascade involving c-src. In the experiments described herein, we sought to determine whether adenovirus infection of HCF might induce other host responses dependent on c-src associated signaling pathways. Methods: HCF were derived from donor corneas and infected for one hour with Ad19, or mock-infected with virus-free media. Parallel experiments were performed with the ...
Schizophrenia patients typically exhibit cognitive impairments that directly affect their daily functioning, but are not effectively treated by current antipsychotics. Maternal immune activation (MIA) during pregnancy, which can be triggered by a variety of infectious agents, has been associated with the development of schizophrenia in adult offspring. Epidemiological evidence indicates that elevated maternal levels of the chemokine interleukin- 8 (IL-8) during MIA contribute to the neurodevelopmental alterations underlying the disorder. The present experiments used an animal model of neurodevelopmental disorders to study the effects of MIA and chemokine receptor antagonism on the behavior of rat offspring, with behavioral tests chosen to examine cognitive functions that are typically impaired in human schizophrenia patients. The viral mimetic polyinosinic-polycytidylic acid (polyI:C) (4.0 mg/kg, i.v.) was injected into pregnant Long-Evans (LE) dams on gestational day (GD) 15. Dams were also ...
TY - JOUR. T1 - Increased expression of epidermal interleukin-8 receptor in psoriasis. Downregulation by FK-506. AU - Schulz, B. S.. AU - Michel, G.. AU - Wagner, S.. AU - Suss, R.. AU - Angerpoitner, T.. AU - Kemeny, L.. AU - Ruzicka, T.. PY - 1994/12/1. Y1 - 1994/12/1. N2 - IL-8 is a chemotactic cytokine with proinflammatory and growth promoting activities. Recently it has been shown to influence several functions of keratinocytes, including HLA-DR expression, chemotaxis and proliferation by binding to a specific receptor. Since psoriasis vulgaris is characterized by epidermal hyperproliferation and infiltration of inflammatory cells, we investigated the expression of IL-8 and its receptor in normal and psoriatic epidermis using semiquantitative reverse-transcriptase-PCR. In addition the mRNA levels of the protooncogenes c-ras, c-raf, c-myc and HER-2 were also investigated as potential growth promoting stimuli in psoriatic epidermis. IL-8 mRNA was only detected in lesional psoriatic epidermis, ...
Bronchial Epithelial Cell Medium-basal-phenol red free https://www.sciencepro.com.br/produtos/sc-3211-b-prf https://www.sciencepro.com.br/@@site-logo/logo-novo.png ...
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Dirofilaria immitis neutrophil chemotactic factor: aa sequence given in first source; isolated from the adult worm; GenBank D11438
AIM Behcets disease (BD) is a systemic immunoinflammatory disorder and the aetiopathogenesis is to be specified. Cytokines play a role in immune response and in many inflammatory diseases. The aim of this case-control study is to investigate serum pro-inflammatory cytokine tumour necrosis factor (TNF)-alpha, interleukin-1beta (IL-1beta), soluble IL-2 receptor (sIL-2R), IL-6, and chemokine IL-8 levels in patients with BD. We also determined the end product of lipid peroxidation (malondialdehyde (MDA)) in BD patients as an index for oxidative stress. ...
Chemokine ligand 5 is a small cytokine belonging to the CXC chemokine family that is also known as epithelial-derived neutrophil-activating peptide 78.
Recombinant Human CXCL5 (ENA-78) (ELISA Std.) - CXCL5 is a member of the CXC family of chemokines, also known as epithelial activated peptide 78 (ENA-78).
Interleukins are naturally occurring proteins that help the bodys immune system. The different types of interleukins all serve to...
It is a formaldehyde-free, next generation smoothing system that uses the latest advances in science, along with only the finest ingredients, to create a product that delivers the results of a traditional keratin smoothing treatment without the harmful chemicals ...
有多种机制认为病毒感染与过敏性炎症相互作用,从而导致下呼吸道功能障碍、喘息和哮喘。首先,潜在的过敏性炎症可以直接增强气道对鼻病毒感染的反应性。此外,病毒感染可损害气道上皮的屏障功能,导致气道壁对气传过敏原的吸收增加和炎症反应增强,而潜在的过敏性炎症也可能导致病毒复制增强。值得注意的是,鼻病毒感染和变应原均可促进气道上皮细胞产生IL-33, IL-33是最近发现的一种先天细胞因子,可促进2型气道炎症和重塑。据报道,这种类固醇耐药途径在难以控制哮喘的儿童中上调。有趣的是,IL-33多聚物与中晚期发作的喘息有关,而中晚期发作的喘息与早期生活中的过敏反应密切相关。 另一种先天上皮细胞因子IL-25也由鼻病毒诱导,在过敏患者鼻病毒感染的情况下,IL-25可能加重过敏性气道炎症 ...
Инфламмасома - важный компонент нативного иммунитета. Она представляет собой макромолекулярный комплекс, включающий сенсорные элементы, адапторные белки и зимоген каспазы-1. Под действием продуктов распада тканей и патогенных микроорганизмов инфламмасома активируется и превращает про-IL-1b и про-IL-18 в активные интерлейкины. Активация инфламмасом отмечена при многих воспалительных заболеваниях и служит мишенью для терапевтических воздействий. В настоящем обзоре обсуждается вклад инфламмасом в патогенез социально-значимых заболеваний ...
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Description: Description of target: C-X-C motif chemokine 5 is a protein that in humans encoded by the CXCL5 gene. The protein encoded by this gene, CXCL5 is a small cytokine belonging to the CXC chemokine family that is also known as epithelial-derived neutrophil-activating peptide 78 (ENA-78). It is produced following stimulation of cells with the inflammatory cytokines interleukin-1or tumor necrosis factor-alpha. Expression of CXCL5 has also been observed in eosinophils, and can be inhibited with the type II interferon IFN-gamma. This chemokine stimulates the chemotaxis of neutrophils possessing angiogenic properties. It elicits these effects by interacting with the cell surface chemokine receptor CXCR2. The gene for CXCL5 is encoded on four exons and is located on humanchromosome 4 amongst several other CXC chemokine genes. CXCL5 has been implicated in connective tissue remodeling. CXCL5 plays a role in reducing sensitivity to sunburn pain in some subjects, and is a potential target which ...
The presence of neutrophils in the synovial joint of patients with rheumatoid arthritis (RA) is thought to be due to the activity of chemotactic factors released by activated cells in the joint. We have shown in this report, for the first time, the abundance of one such factor, interleukin 8 (IL 8), in the synovial fluid of patients both with RA and other non-RA joint diseases, and the spontaneous production of IL 8 mRNA by RA synovial cells in culture. There was no correlation between the levels of chemotactic activity and IL 8 protein, suggesting that other factors with similar neutrophil chemotactic activity are also present in the synovial fluid exudate. In support of this concept neither the level of chemotactic activity nor IL 8 protein levels correlated with neutrophil or leukocyte infiltration, indicating that the mechanism of migration into the inflammatory environment of the joint is complex. Such migration is likely to be due to a number of chemotactic signals in addition to IL 8, which may
Chemokine (C-X-C motif) ligand 1 (CXCL1) is a small cytokine belonging to the CXC chemokine family that was previously called GRO1 oncogene, GROα, KC, Neutrophil-activating protein 3 (NAP-3) and melanoma growth stimulating activity, alpha (MSGA-α). In humans, this protein is encoded by the CXCL1 gene.
SEA080Hu, ELISA Kit for Interleukin 8 (IL8), Homo sapiens (Human), Sandwich ELISA, CXCL8, AMCF-I, GCP1, K60, LECT, LUCT, LYNAP, MDNCF, MONAP, NAF, NAP1, SCYB8, TSG1, B-ENAP, Neutrophil-Activating Protein 1, Granulocyte Chemotactic Protein 1, Designed by Cloud-Clone Corp.
In this series of experiments we have demonstrated that the stimulated release of IL-6 and IL-8 from cultures obtained from controls and smokers without airflow obstruction is amplified by 5% CSE pretreatment, but this was not apparent in the COPD group. Our results also show cellular immunosuppressive effects of 5% CSE in the COPD cultures. These findings suggest that COPD PBECs are more susceptible to the immunosuppressive effects of CSE which may explain, in part, the increased susceptibility of this particular group to respiratory infections.. In our experiments, 5% CSE reduced the expression of TLR-4. Similar findings were recently reported using a human bronchial epithelial cell line, where CSE treatment led to a downregulation of TLR-4 expression, which was associated with a corresponding increase in the release of IL-8. Internalisation of the receptor was proposed as the mechanism, as there was a parallel increase in the expression of TLR-4 in permeabilised cells [4]. However, the ...
An all-on-chip method enables rapid neutrophil chemotaxis assay directly from a few microliters of blood for both cell migration research and clinical sample test.
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