{"title":"Oxidative stress in allergic and inflammatory skin diseases.","authors":"Yoshimichi Okayama","doi":"10.2174/1568010054526386","DOIUrl":"https://doi.org/10.2174/1568010054526386","url":null,"abstract":"<p><p>The skin is exposed to endogenous and environmental pro-oxidant agents, leading to the harmful generation of reactive oxygen species (ROS). The resulting oxidative stress damages proteins, lipids, and DNA. An imbalance between ROS and antioxidants can lead to an elevated oxidative stress level. Some evidence indicates that allergic and inflammatory skin diseases like atopic dermatitis, urticaria and psoriasis are mediated by oxidative stress. For example, monocytes from patients with atopic dermatitis are primed to generate ROS in response to zymosan, a Toll-like receptor 2 (TLR2) ligand, suggesting that Staphylococcus aureus may damage lesional skin of the disease by production of ROS. Mast cells generate mainly intracellular ROS following the aggregation of FceRI; these ROS may act as secondary messengers in the induction of several biological responses. The present review summarizes the involvement of ROS in the pathogenesis of allergic and inflammatory skin diseases.</p>","PeriodicalId":86954,"journal":{"name":"Current drug targets. Inflammation and allergy","volume":"4 4","pages":"517-9"},"PeriodicalIF":0.0,"publicationDate":"2005-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2174/1568010054526386","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25271963","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Riku Korhonen, Aleksi Lahti, Hannu Kankaanranta, Eeva Moilanen
{"title":"Nitric oxide production and signaling in inflammation.","authors":"Riku Korhonen, Aleksi Lahti, Hannu Kankaanranta, Eeva Moilanen","doi":"10.2174/1568010054526359","DOIUrl":"https://doi.org/10.2174/1568010054526359","url":null,"abstract":"<p><p>Nitric oxide (NO) is recognized as a mediator and regulator of inflammatory responses. It possesses cytotoxic properties that are aimed against pathogenic microbes, but it can also have damaging effects on host tissues. NO reacts with soluble guanylate cyclase to form cyclic guanosine monophosphate (cGMP), which mediates many of the effects of NO. NO can also interact with molecular oxygen and superoxide anion to produce reactive nitrogen species that can modify various cellular functions. These indirect effects of NO have a significant role in inflammation, where NO is produced in high amounts by inducible nitric oxide synthase (iNOS) and reactive oxygen species are synthesized by activated inflammatory cells. The present review deals with NO production and signaling in inflammation, especially in relation to human neutrophils and eosinophils.</p>","PeriodicalId":86954,"journal":{"name":"Current drug targets. Inflammation and allergy","volume":"4 4","pages":"471-9"},"PeriodicalIF":0.0,"publicationDate":"2005-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2174/1568010054526359","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25249342","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Inflammatory cells and oxygen radicals.","authors":"Makoto Nagata","doi":"10.2174/1568010054526322","DOIUrl":"https://doi.org/10.2174/1568010054526322","url":null,"abstract":"<p><p>At sites of inflammation, multiple inflammatory cells including eosinophils, neutrophils, and macrophages are capable of generating reactive oxygen species (ROS), which can contribute to development of various diseases. In case of allergic inflammation, for example, the lung cells obtained by bronchoalveolar lavage (BAL) following antigen challenge generates superoxide anion at nanomolar concentrations. Eosinophils obtained from BAL following a segmental allergen challenge generate more superoxide anion than eosinophils obtained from the peripheral circulation. Such ROS may contribute not only to tissue injury but also to inflammatory reactions. For example, hydrogen peroxide can stimulate both neutrophil and eosinophil adhesion as an autocrine or paracrine mediator via the upregulation of beta2 integrin. Furthermore, ROS may alter morphological or functional properties of endothelial cells, including permeability and adhesion molecule expression. Thus, ROS can promote adhesive interaction between inflammatory and endothelial cells, which could culminate in manifestations of inflammatory diseases such as bronchial asthma.</p>","PeriodicalId":86954,"journal":{"name":"Current drug targets. Inflammation and allergy","volume":"4 4","pages":"503-4"},"PeriodicalIF":0.0,"publicationDate":"2005-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2174/1568010054526322","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25249346","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Annemieke Walker, Carol Ward, Emma L Taylor, Ian Dransfield, Simon P Hart, Christopher Haslett, Adriano G Rossi
{"title":"Regulation of neutrophil apoptosis and removal of apoptotic cells.","authors":"Annemieke Walker, Carol Ward, Emma L Taylor, Ian Dransfield, Simon P Hart, Christopher Haslett, Adriano G Rossi","doi":"10.2174/1568010054526278","DOIUrl":"https://doi.org/10.2174/1568010054526278","url":null,"abstract":"<p><p>The accumulation of neutrophils during inflammation is essential for the destruction and removal of invading microorganisms. However, for resolution of inflammation to occur, neutrophils must also be removed from the inflammatory site since these cells are capable of releasing tissue toxic molecules. Neutrophil removal has been shown to occur via apoptosis and phagocyte clearance of apoptotic cells. Therefore, manipulation of these processes is likely to be a key therapeutic strategy in the management of inflammatory disease. In this review, we examine mediators of neutrophil survival and apoptosis and the signalling pathways that regulate the balance between life and death in these cells.</p>","PeriodicalId":86954,"journal":{"name":"Current drug targets. Inflammation and allergy","volume":"4 4","pages":"447-54"},"PeriodicalIF":0.0,"publicationDate":"2005-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2174/1568010054526278","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25249975","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
G M Walsh, M Al-Rabia, M G Blaylock, D W Sexton, C J A Duncan, A Lawrie
{"title":"Control of eosinophil toxicity in the lung.","authors":"G M Walsh, M Al-Rabia, M G Blaylock, D W Sexton, C J A Duncan, A Lawrie","doi":"10.2174/1568010054526296","DOIUrl":"https://doi.org/10.2174/1568010054526296","url":null,"abstract":"<p><p>The inappropriate accumulation of eosinophils and the subsequent release of their potent pro-inflammatory mediator arsenal are thought to be important contributors to the pathogenesis of asthma and other allergic diseases. It is also becoming apparent that eosinophils may play a role in the orchestration of immune responses in the asthmatic lung. There is therefore much interest in the development of strategies to limit or prevent eosinophil-induced toxicity. The mechanisms by which eosinophils accumulate in the peribronchial tissues of the lung are complex and include enhanced differentiation and release from the bone marrow, selective adhesion and transendothelial migration, directed movement in response to specific chemotactic mediators and finally prolonged survival as a consequence of delayed apoptosis. Thus it can be appreciated that there are many points at which the toxicity of eosinophils can be limited or even prevented. Important areas for potential advances in glucocorticoid (GC) development include efforts to dissociate their anti-inflammatory effects from unwanted side effects. Other areas include the development of humanized monoclonal antibodies against IL-4, IL-13 and IL-5 together with the inhibition of adhesion pathways and/or chemokines responsible for eosinophil accumulation in the asthmatic lung. Several avenues of research are currently underway in an attempt to define mechanisms by which pro-inflammatory cells such as eosinophils can be safely removed from the asthmatic lung through apoptosis induction and their subsequent ingestion by phagocytes. This review will discuss both the potential and shortcomings of these diverse approaches to limit eosinophil toxicity in the asthmatic lung.</p>","PeriodicalId":86954,"journal":{"name":"Current drug targets. Inflammation and allergy","volume":"4 4","pages":"481-6"},"PeriodicalIF":0.0,"publicationDate":"2005-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2174/1568010054526296","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25249343","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Role of oxygen radicals on bronchial asthma.","authors":"Takao Fujisawa","doi":"10.2174/1568010054526304","DOIUrl":"https://doi.org/10.2174/1568010054526304","url":null,"abstract":"<p><p>Bronchial asthma is an inflammatory disorder characterized by recruitment and activation of various inflammatory cells including eosinophils and T cells in the airway mucosa. Oxygen radicals are produced by inflammatory cells in the airways and/or inhaled directly from environmental air. There is ample evidence that oxygen radical production is increased in asthma and is closely related to the pathogenesis and that exogenous oxidants such as cigarette smoke and ozone directly cause asthma exacerbation. The mechanism by which oxygen radicals cause asthma pathology is oxidation or nitration of proteins, lipids, or DNA to cause dysfunction of these molecules. In addition, physiological antioxidant system, which is equipped to protect host from detrimental oxidants, is impaired in asthma, possibly because of inflammation. Thus, the imbalance between oxidant and antioxidant that is called oxidant stress is critical in asthma pathogenesis. Elegant technique to measure oxygen radicals and the footprints of oxidant stress in patients with asthma have been developed and give an important clue to evaluate possible involvement of oxygen radicals in individual pathophysiology. Therapeutic interventions that reduce oxidant stress and enhance antioxidant defense may be useful in the treatment of asthma.</p>","PeriodicalId":86954,"journal":{"name":"Current drug targets. Inflammation and allergy","volume":"4 4","pages":"505-9"},"PeriodicalIF":0.0,"publicationDate":"2005-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2174/1568010054526304","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25249347","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Neutrophils and eosinophils: clinical implications of their appearance, presence and disappearance in asthma and COPD.","authors":"A P Watt, B C Schock, M Ennis","doi":"10.2174/1568010054526313","DOIUrl":"https://doi.org/10.2174/1568010054526313","url":null,"abstract":"<p><p>Asthma and chronic obstructive pulmonary disease (COPD) are common chronic disorders. Traditionally, asthma has been associated with an eosinophilic inflammation and COPD with neutrophilic inflammation. In this review we will highlight the maturation, recruitment, activation, action and apoptosis of these cells. In addition we will focus on the evidence for their presence in disease and suggest potential new therapeutic interventions.</p>","PeriodicalId":86954,"journal":{"name":"Current drug targets. Inflammation and allergy","volume":"4 4","pages":"415-23"},"PeriodicalIF":0.0,"publicationDate":"2005-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2174/1568010054526313","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25249972","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Anti-inflammatory mechanisms of glucocorticoids targeting granulocytes.","authors":"Gaetano Caramori, Ian Adcock","doi":"10.2174/1568010054526331","DOIUrl":"https://doi.org/10.2174/1568010054526331","url":null,"abstract":"<p><p>Asthmatic inflammation involves the recruitment and activation of inflammatory cells, and changes in the structural cells of the lung and asthma are characterized by an increased expression of components of the inflammatory cascade including cytokines, chemokines, growth factors, enzymes, receptors and adhesion molecules. The increased expression of these proteins seen in asthma is generally the result of enhanced gene transcription, since many of the genes are not expressed in normal cells but are induced in a cell-specific manner during the inflammatory process. There is clear evidence that neutrophils, long thought of as being transcriptionally inert, can respond to stimuli to induce inflammatory genes. Glucocorticoids are very effective in controlling the inflammation seen in asthmatic airways. Beyond their recognized actions on eosinophil and neutrophil apoptosis, glucocorticoids have profound effects on the chemotaxis, activation and release of mediators from granulocytes (eosinophils, neutrophils and basophils). Few mechanistic studies are available in these cells, but it appears that in granulocytes, glucocorticoids target the same signaling pathways, such as nuclear factor-kappaB (NF-kappaB) and activator protein-1 (AP-1), that are important in other cells. We summarize these known mechanisms at the end of this review.</p>","PeriodicalId":86954,"journal":{"name":"Current drug targets. Inflammation and allergy","volume":"4 4","pages":"455-63"},"PeriodicalIF":0.0,"publicationDate":"2005-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2174/1568010054526331","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25249976","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Pharmacological regulation of human eosinophil apoptosis.","authors":"Hannu Kankaanranta, Eeva Moilanen, Xianzhi Zhang","doi":"10.2174/1568010054526395","DOIUrl":"https://doi.org/10.2174/1568010054526395","url":null,"abstract":"<p><p>Eosinophilic inflammation of the airways is a key characteristic of asthma. The balance between eosinophil recruitment into the lung and their removal from the lungs determines the number of eosinophils in the airways. Apoptosis or programmed cell death is of importance in the removal of eosinophils from the lungs. In asthma, eosinophil apoptosis is delayed. Glucocorticoids enhance eosinophil apoptosis, whereas beta(2)-agonists may delay apoptosis in eosinophils. Detailed knowledge on the mechanisms that regulate this process gives an opportunity to develop specific asthma therapies targeting the eosinophil. This review aims to focus on the signalling leading to or preventing apoptosis in human eosinophils as well as reviews the current evidence on the regulation of eosinophil apoptosis and/or survival in allergic diseases.</p>","PeriodicalId":86954,"journal":{"name":"Current drug targets. Inflammation and allergy","volume":"4 4","pages":"433-45"},"PeriodicalIF":0.0,"publicationDate":"2005-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2174/1568010054526395","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25249974","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
H Kimura, T Sawada, S Oshima, K Kozawa, T Ishioka, M Kato
{"title":"Toxicity and roles of reactive oxygen species.","authors":"H Kimura, T Sawada, S Oshima, K Kozawa, T Ishioka, M Kato","doi":"10.2174/1568010054526287","DOIUrl":"https://doi.org/10.2174/1568010054526287","url":null,"abstract":"<p><p>The history of studies in biology regarding reactive oxygen species (ROS) is approximately 40 years. During the initial 30 years, it appeared that these studies were mainly focused on the toxicity or microbicidal-related agents of ROS. However, recent studies have identified another action regarding oxidative signaling, other than toxicity of ROS. Basically, it is suggested that ROS are reactive, and degenerate to biomacromolecules such as DNA and proteins, leading to deterioration of cellular functions as an oxidative stress. On the other hand, recent studies have shown that ROS act as oxidative signaling in cells, resulting in various gene expressions. For example, NADPH oxidase, a major source of superoxide radicals (O(2)(-)), expresses in various tissues such as leukocytes and cardiovascular systems, and ROS derived from the enzyme play important roles in cell proliferation, differentiation, and cell death. In this review, we have focused on and described the basic properties, toxicity, and roles of ROS.</p>","PeriodicalId":86954,"journal":{"name":"Current drug targets. Inflammation and allergy","volume":"4 4","pages":"489-95"},"PeriodicalIF":0.0,"publicationDate":"2005-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2174/1568010054526287","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25249344","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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