7 results on '"Kraneveld, Aletta D."'
Search Results
2. Lipoproteins attenuate TLR2 and TLR4 activation by bacteria and bacterial ligands with differences in affinity and kinetics
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van Bergenhenegouwen, Jeroen, Kraneveld, Aletta D, Rutten, Lieke, Garssen, Johan, Vos, Arjan P, Hartog, Anita, Sub General Pharmacology, Sub Interdisciplinary translational Phar, Sub Immunopharmacology, Pharmacology, Sub General Pharmacology, Sub Interdisciplinary translational Phar, Sub Immunopharmacology, and Pharmacology
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0301 basic medicine ,Salmonella typhimurium ,Staphylococcus aureus ,Immunology ,Lipoproteins, VLDL ,Lymphocyte Activation ,03 medical and health sciences ,Immune system ,Antigen ,medicine ,Humans ,Antigens, Bacterial ,biology ,biology.organism_classification ,Mucus ,Small intestine ,Toll-Like Receptor 2 ,Lipoproteins, LDL ,Toll-Like Receptor 4 ,TLR2 ,030104 developmental biology ,medicine.anatomical_structure ,Apolipoproteins ,HEK293 Cells ,Biochemistry ,TLR4 ,Leukocytes, Mononuclear ,Cytokines ,lipids (amino acids, peptides, and proteins) ,Immunization ,Lipoproteins, HDL ,Bacteria ,Lipoprotein ,Research Article - Abstract
Background The small intestine is a specialized compartment were close interactions take place between host, microbes, food antigens and dietary fatty acids. Dietary fats get absorbed by epithelial cells and processed into a range of lipoprotein particles after which they are basolaterally secreted and collected in the lymphatics. In contrast to the colon, the small intestine is covered only by a thin mucus coat that allows for intimate interactions between host-cells and microbes. Lipoproteins have long been recognized as protective factors in infectious diseases via the neutralization of bacterial toxins like lipopolysaccharides. Much less attention has been given to the potential role of lipoproteins as factors contributing to the maintenance of small intestinal immune homeostasis via modulating bacteria-induced immune responses. Results Lipoproteins VLDL, LDL and HDL were found to neutralize TLR responses towards specific TLR-ligands or a selection of gram-negative and gram-positive bacteria. Attenuation of TLR2 activity was acute and only slightly improved by longer pre-incubation times of ligands and lipoproteins with no differences between bacterial-lipopeptides or bacteria. In contrast, attenuation of TLR4 responses was only observed after extensive preincubation of lipoproteins and LPS. Preincubation of bacteria and lipoproteins led only to a modest attenuation of TLR4 activity. Moreover, compared to TLR2, TLR4 activity could only be attenuated by lipoproteins over a small ligand dose range. Conclusions These results demonstrate the ability of lipoproteins VLDL, LDL and HDL to inhibit TLR responses towards bacterial-ligands and bacteria. Presence of lipoproteins was found to modulate the MAMP-induced cytokine release by primary human monocytes measured as changes in the release of IL-6, TNFα, GM-CSF and IFNγ. Using TLR2 and TLR4-reporter cells, lipoproteins were found to inhibit TLR responses with differences in affinity and kinetics. These data establish a role for lipoproteins as immunoregulatory molecules, attenuating TLR-responses and thereby positively contributing to mucosal homeostasis. Electronic supplementary material The online version of this article (doi:10.1186/s12865-016-0180-x) contains supplementary material, which is available to authorized users.
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- 2016
3. Dietary galacto-oligosaccharides prevent airway eosinophilia and hyperresponsiveness in a murine house dust mite-induced asthma model.
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Verheijden, Kim A. T., Willemsen, Linette E. M., Braber, Saskia, Leusink-Muis, Thea, Delsing, Dianne J. M., Garssen, Johan, Kraneveld, Aletta D., and Folkerts, Gert
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ASTHMA ,EOSINOPHILIA ,HOUSE dust mites ,OLIGOSACCHARIDES ,BUDESONIDE ,AIRWAY (Anatomy) - Abstract
Background: Allergic asthma is strongly associated with the exposure to house dust mite (HDM) and is characterized by eosinophilic pulmonary inflammation and airway hyperresponsiveness (AHR). Recently, there is an increased interest in using dietary oligosaccharides, also known as prebiotics, as a novel strategy to prevent the development of, or reduce, symptoms of allergy. Aim: We investigated the preventive capacity of dietary galacto-oligosaccharides (GOS) compared to an intra-airway therapeutic treatment with budesonide on the development of HDM-induced allergic asthma in mice. Methods: BALB/c mice were intranasally sensitized with 1 μg HDM on day 0 followed by daily intranasal challenge with PBS or 10 μg HDM on days 7 to 11. Two weeks prior to the first sensitization and throughout the experiment mice were fed a control diet or a diet containing 1% GOS. Reference mice were oropharyngeally instilled with budesonide (500 μg/kg) on days 7, 9, 11, and 13, while being fed the control diet. On day 14, AHR was measured by nebulizing increasing doses of methacholine into the airways. At the end of the experiment, bronchoalveolar lavage fluid (BALF) and lungs were collected. Results: Sensitization and challenge with HDM resulted in AHR. In contrast to budesonide, dietary intervention with 1% GOS prevented the development of AHR. HDM sensitization and challenge resulted in a significant increase in BALF leukocytes numbers, which was suppressed by budesonide treatment and dietary intervention with 1% GOS. Moreover, HDM sensitization and challenge resulted in significantly enhanced concentrations of IL-6, CCL17, IL-33, CCL5 and IL-13 in lung tissue. Both dietary intervention with 1% GOS or budesonide treatment significantly decreased the HDMinduced increased concentrations of CCL5 and IL-13 in lung tissue, while budesonide also reduced the HDM-enhanced concentrations of IL-6 and CCL17 in lung tissue. Conclusion: Not only did dietary intervention with 1% GOS during sensitization and challenge prevent the induction of airway eosinophilia and Th2-related cytokine and chemokine concentrations in the lung equally effective as budesonide treatment, it also prevented AHR development in HDM-allergic mice. GOS might be useful for the prevention and/or treatment of symptoms in asthmatic disease. [ABSTRACT FROM AUTHOR]
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- 2015
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4. Bifidobacterium breve and Lactobacillus rhamnosus treatment is as effective as budesonide at reducing inflammation in a murine model for chronic asthma.
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Sagar, Seil, Morgan, Mary E., Si Chen, Vo, Arjan P., Garssen, Johan, van Bergenhenegouwen, Jeroen, Boon, Louis, Georgiou, Niki A., Kraneveld, Aletta D., and Folkerts, Gert
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T cells ,GLUCOCORTICOID receptors ,BRONCHOCONSTRICTION ,ANTI-inflammatory agents ,ALLERGY treatment ,ASTHMA - Abstract
Background: Asthma is estimated to affect as many as 300 million people worldwide and its incidence and prevalence are rapidly increasing throughout the world, especially in children and within developing countries. Recently, there has been a growing interest in the use of potentially beneficial bacteria for allergic diseases. This study is aimed at exploring the therapeutic effects of long-term treatment with two different beneficial bacterial strains (Bifidobacterium breve M-16 V and Lactobacillus rhamnosus NutRes1) and a glucocorticoid (budesonide), as a reference treatment, on inflammatory response in a murine model for chronic allergic asthma. Methods: To mimic the chronic disease in asthmatic patients, we used the murine ovalbumin-induced asthma model combined with prolonged allergen exposure. Airway function; pulmonary airway inflammation; airway remodelling, mRNA expression of pattern recognition receptors, Th-specific cytokines and transcription factors in lung tissue; mast cell degranulation; in vitro T cell activation; and expression of Foxp3 in blood Th cells were examined. Results: Lactobacillus rhamnosus reduced lung resistance to a similar extent as budesonide treatment in chronically asthmatic mice. Pulmonary airway inflammation, mast cell degranulation, T cell activation and airway remodelling were suppressed by all treatments. Beneficial bacteria and budesonide differentially modulated the expression of toll-like receptors (TLRs), nod-like receptors (NLRs), cytokines and T cell transcription factors. Bifidobacterium breve induced regulatory T cell responses in the airways by increasing Il10 and Foxp3 transcription in lung tissue as well as systemic by augmenting the mean fluorescence intensity of Foxp3 in blood CD4+ T cells. Conclusion: These findings show that Bifidobacterium breve M-16 V and Lactobacillus rhamnosus NutRes1 have strong anti-inflammatory properties that are comparable to budesonide and therefore may be beneficial in the treatment of chronic asthma. [ABSTRACT FROM AUTHOR]
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- 2014
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5. Cigarette smoke induces β2-integrin-dependent neutrophil migration across human endothelium.
- Author
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Overbeek, Saskia A., Braber, Saskia, Henricks, Paul A. J., Kleinjan, Marije, Kamp, Vera M., Georgiou, Niki A., Garssen, Johan, Kraneveld, Aletta D., and Folkerts, Gert
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PHYSIOLOGICAL effects of tobacco ,INTEGRINS ,NEUTROPHILS ,ENDOTHELIUM ,OBSTRUCTIVE lung diseases ,BRONCHOALVEOLAR lavage - Abstract
Background: Cigarette smoking induces peripheral inflammatory responses in all smokers and is the major risk factor for neutrophilic lung disease such as chronic obstructive pulmonary disease. The aim of this study was to investigate the effect of cigarette smoke on neutrophil migration and on β2-integrin activation and function in neutrophilic transmigration through endothelium.Methods and Results: Utilizing freshly isolated human PMNs, the effect of cigarette smoke on migration and β2-integrin activation and function in neutrophilic transmigration was studied. In this report, we demonstrated that cigarette smoke extract (CSE) dose dependently induced migration of neutrophils in vitro. Moreover, CSE promoted neutrophil adherence to fibrinogen. Using functional blocking antibodies against CD11b and CD18, it was demonstrated that Mac-1 (CD11b/CD18) is responsible for the cigarette smoke-induced firm adhesion of neutrophils to fibrinogen. Furthermore, neutrophils transmigrated through endothelium by cigarette smoke due to the activation of β2-integrins, since pre-incubation of neutrophils with functional blocking antibodies against CD11b and CD18 attenuated this transmigration.Conclusion: This is the first study to describe that cigarette smoke extract induces a direct migratory effect on neutrophils and that CSE is an activator of β2-integrins on the cell surface. Blocking this activation of β2-integrins might be an important target in cigarette smoke induced neutrophilic diseases. [ABSTRACT FROM AUTHOR]- Published
- 2011
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6. Inflammatory changes in the airways of micecaused by cigarette smoke exposure are onlypartially reversed after smoking cessation.
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Braber, Saskia, Henricks, Paul A. J., Nijkamp, Frans P., Kraneveld, Aletta D., and Folkerts, Gert
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AIRWAY (Anatomy) ,RESPIRATORY obstructions ,PULMONARY emphysema ,LUNG diseases ,SMOKING ,DISEASE risk factors - Abstract
Background: Tobacco smoking irritates and damages the respiratory tract and contributes to a higher risk of developing lung emphysema. At present, smoking cessation is the only effective treatment for reducing the progression of lung emphysema, however, there is hardly anything known about the effects of smoking cessation on cytokine and chemokine levels in the airways. To the best of our knowledge, this is the first reported in vivo study in which cytokine profiles were determined after cessation of cigarette smoke exposure. Methods: The severity of airway remodeling and inflammation was studied by analyzing alveolar enlargement, heart hypertrophy, inflammatory cells in the bronchoalveolar lavage fluid (BALF) and lung tissue and by determining the cytokine and chemokine profiles in the BALF of A/J mice exposed to cigarette smoke for 20 weeks and 8 weeks after smoking cessation. Results: The alveolar enlargement and right ventricle heart hypertrophy found in smoke-exposed mice remained unchanged after smoking cessation. Although the neutrophilic inflammation in the BALF of cigarette smokeexposed animals was reduced after smoking cessation, a sustained inflammation in the lung tissue was observed. The elevated cytokine (IL-1α and TNF-α) and chemokine (CCL2 and CCL3) levels in the BALF of smoke-exposed mice returned to basal levels after smoking cessation, while the increased IL-12 levels did not return to its basal level. The cigarette smoke-enhanced VEGF levels did not significantly change after smoking cessation. Moreover, IL- 10 levels were reduced in the BALF of smoke-exposed mice and these levels were still significantly decreased after smoking cessation compared to the control animals. Conclusion: The inflammatory changes in the airways caused by cigarette smoke exposure were only partially reversed after smoking cessation. Although smoking cessation should be the first step in reducing the progression of lung emphysema, additional medication could be provided to tackle the sustained airway inflammation. [ABSTRACT FROM AUTHOR]
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- 2010
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7. Cigarette smoke regulates the expression of TLR4 and IL-8 production by human macrophages.
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Sarir, Hadi, Mortaz, Esmaeil, Karimi, Khalil, Kraneveld, Aletta D., Rahman, Irfan, Caldenhoven, Eric, Nijkamp, Frans P., and Folkerts, Gert
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CIGARETTE smoke ,OBSTRUCTIVE lung diseases ,CYTOKINES ,MACROPHAGES ,INTERLEUKIN-8 - Abstract
Background: Toll-like receptors (TLRs) are present on monocytes and alveolar macrophages that form the first line of defense against inhaled particles. The importance of those cells in the pathophysiology of chronic obstructive pulmonary disease (COPD) has well been documented. Cigarette smoke contains high concentration of oxidants which can stimulate immune cells to produce reactive oxygen species, cytokines and chemokines. Methods: In this study, we evaluated the effects of cigarette smoke medium (CSM) on TLR4 expression and interleukin (IL)-8 production by human macrophages investigating the involvement of ROS. Results and Discussion: TLR4 surface expression was downregulated on short term exposure (1 h) of CSM. The downregulation could be explained by internalization of the TLR4 and the upregulation by an increase in TLR4 mRNA. IL-8 mRNA and protein were also increased by CSM. CSM stimulation increased intracellular ROS-production and decreased glutathione (GSH) levels. The modulation of TLR4 mRNA and surface receptors expression, IRAK activation, IκB-α degradation, IL-8 mRNA and protein, GSH depletion and ROS production were all prevented by antioxidants such as N-acetyl-L-cysteine (NAC). Conclusion: TLR4 may be involved in the pathogenesis of lung emphysema and oxidative stress and seems to be a crucial contributor in lung inflammation. [ABSTRACT FROM AUTHOR]
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- 2009
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