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Aerobic conditioning and allergic pulmonary inflammation in mice. II. Effects on lung vascular and parenchymal inflammation and remodeling

VIEIRA, Rodolfo P.; ANDRADE, Vanessa F. de; DUARTE, Anna Cecilia S.; SANTOS, Angela B. G. dos; MAUAD, Thais; MARTINS, Milton A.; DOLHNIKOFF, Marisa; CARVALHO, Celso R. F.
Fonte: AMER PHYSIOLOGICAL SOC Publicador: AMER PHYSIOLOGICAL SOC
Tipo: Artigo de Revista Científica
ENG
Relevância na Pesquisa
36.42%
Vieira RP, de Andrade VF, Duarte AC, dos Santos AB, Mauad T, Martins MA, Dolhnikoff M, Carvalho CR. Aerobic conditioning and allergic pulmonary inflammation in mice. II. Effects on lung vascular and parenchymal inflammation and remodeling. Am J Physiol Lung Cell Mol Physiol 295: L670-L679, 2008. First published August 29, 2008; doi: 10.1152/ajplung.00465.2007.-Recent evidence suggests that asthma leads to inflammation and remodeling not only in the airways but also in pulmonary vessels and parenchyma. In addition, some studies demonstrated that aerobic training decreases chronic allergic inflammation in the airways; however, its effects on the pulmonary vessels and parenchyma have not been previously evaluated. Our objective was to test the hypothesis that aerobic conditioning reduces inflammation and remodeling in pulmonary vessels and parenchyma in a model of chronic allergic lung inflammation. Balb/c mice were sensitized at days 0, 14, 28, and 42 and challenged with ovalbumin ( OVA) from day 21 to day 50. Aerobic training started on day 21 and continued until day 50. Pulmonary vessel and parenchyma inflammation and remodeling were evaluated by quantitative analysis of eosinophils and mononuclear cells and by collagen and elastin contents and smooth muscle thickness. Immunohistochemistry was performed to quantify the density of positive cells to interleukin (IL)-2...

Oral tolerance attenuates changes in in vitro lung tissue mechanics and extracellular matrix remodeling induced by chronic allergic inflammation in guinea pigs

NAKASHIMA, Adriane S.; PRADO, Carla M.; LANCAS, Tatiana; RUIZ, Viviane C.; KASAHARA, David I.; LEICK-MALDONADO, Edna A.; DOLHNIKOFF, Marisa; MARTINS, Milton A.; TIBERIO, Iolanda F. L. C.
Fonte: AMER PHYSIOLOGICAL SOC Publicador: AMER PHYSIOLOGICAL SOC
Tipo: Artigo de Revista Científica
ENG
Relevância na Pesquisa
36.34%
Oral tolerance attenuates changes in in vitro lung tissue mechanics and extracellular matrix remodeling induced by chronic allergic inflammation in guinea pigs. J Appl Physiol 104: 1778-1785, 2008. First published April 3, 2008; doi:10.1152/japplphysiol.00830.2007.-Recent studies emphasize the presence of alveolar tissue inflammation in asthma. Immunotherapy has been considered a possible therapeutic strategy for asthma, and its effect on lung tissue had not been previously investigated. Measurements of lung tissue resistance and elastance were obtained before and after both ovalbumin and acetylcholine challenges. Using morphometry, we assessed eosinophil and smooth muscle cell density, as well as collagen and elastic fiber content, in lung tissue from guinea pigs with chronic pulmonary allergic inflammation. Animals received seven inhalations of ovalbumin (1-5 mg/ml; OVA group) or saline (SAL group) during 4 wk. Oral tolerance (OT) was induced by offering ad libitum ovalbumin 2% in sterile drinking water starting with the 1st inhalation (OT1 group) or after the 4th (OT2 group). The ovalbumin-exposed animals presented an increase in baseline and in postchallenge resistance and elastance related to baseline, eosinophil density, and collagen and elastic fiber content in lung tissue compared with controls. Baseline and post-ovalbumin and acetylcholine elastance and resistance...

Inflammation in cancer cachexia: To resolve or not to resolve (is that the question?)

Seelaender, Marilia Cerqueira Leite; Junior, Miguel Luiz Batista; Lira, Fábio Santos de; Silvério, Renata; Rossi-Fanelli, Filippo
Fonte: CHURCHILL LIVINGSTONE; EDINBURGH Publicador: CHURCHILL LIVINGSTONE; EDINBURGH
Tipo: Artigo de Revista Científica
ENG
Relevância na Pesquisa
36.37%
Background & aims: Cachexia is associated with poor prognosis and shortened survival in cancer patients. Growing evidence points out to the importance of chronic systemic inflammation in the aetiology of this syndrome. In the recent past, chronic inflammation was considered to result from overexpression and release of pro-inflammatory factors. However, this conception is now the focus of debate, since the importance of a crescent number of pro-resolving agents in the dissolution of inflammation is now recognised - leading to the hypothesis that chronic inflammation occurs rather due to failure in the resolution process. We intend to put forward the possibility that this may also be occurring in cancer cachexia. Methods: Recent reviews on inflammation and cachexia, and on the factors involved in the resolution of inflammation are discussed. Results: The available information suggests that indeed, inflammation resolution failure may be present in cachexia and therefore we speculate on possible mechanisms. Conclusions: We emphasise the importance of studying resolution-related mechanisms in cancer cachexia and propose the opening of a new venue for cachexia treatment. (C) 2012 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved.; FAPESP [08/54091-9...

Efeitos do resíduo da queima de óleo diesel (ROFA) e da inflamação pulmonar alérgica crônica em três linhagens de camundongos; Effects of residual diesel oil fly ash (ROFA) and pulmonary allergic chronic inflammation in tree lines of mice

Costa, Fernanda Magalhães Arantes
Fonte: Biblioteca Digitais de Teses e Dissertações da USP Publicador: Biblioteca Digitais de Teses e Dissertações da USP
Tipo: Tese de Doutorado Formato: application/pdf
Publicado em 09/01/2008 PT
Relevância na Pesquisa
36.4%
Neste estudo, foram realizados três experimentos distintos (1) analisando os efeitos da administração de material particulado em camundongos BALB/c com inflamação pulmonar alérgica crônica induzida por ovalbumina; (2) comparando camundongos AIRmax e AIRmin com inflamação pulmonar alérgica crônica induzida por ovalbumina; (3) comparando camundongos AIRmax e AIRmin que receberam material particulado (resíduo da queima de óleo diesel - ROFA) por via intranasal. Para a indução da inflamação pulmonar alérgica crônica, os camundongos foram sensibilizados com ovalbumina (OVA) através de duas injeções intraperitoneais de alérgeno com o adjuvante hidróxido de alumínio (dias 0 e 14) e quatro inalações de OVA 1% (dias 22, 24, 26 e 28). Os animais que foram expostos ao material particulado, receberam ROFA (60 ?g) nos dias 0, 2, 4 e 6 no experimento do efeito do material particulado ou nos dias dos desafios com OVA no experimento do efeito da administração de material particulado em animais com inflamação pulmonar induzida pela OVA. Os grupos controle foram tratados com solução salina 0,9 % seguindo o mesmo protocolo. Quarenta e oito horas após o último desafio, a responsividade pulmonar foi medida por broncoprovocação àr metacolina através da pletismografia de corpo inteiro...

Avaliação da função e da histopatologia pulmonar em modelo experimental de inflamação pulmonar alérgica crônica: efeitos da redução da função colinérgica em camundongos geneticamente modificados; Evaluation of lung function and histopathology in an experimental model of chronic allergic pulmonary inflammation: effects of reduced cholinergic function in genetically modified mice

Miranda, Claúdia Jeane Claudino de Pontes
Fonte: Biblioteca Digitais de Teses e Dissertações da USP Publicador: Biblioteca Digitais de Teses e Dissertações da USP
Tipo: Dissertação de Mestrado Formato: application/pdf
Publicado em 19/06/2012 PT
Relevância na Pesquisa
36.36%
INTRODUÇÃO: A Asma Brônquica é caracterizada por obstrução ao fluxo aéreo, reversível ou não, e processo inflamatório pulmonar, caracterizado principalmente por eosinofilia. A persistência da inflamação pode induzir processo de reparo pulmonar associado à redução progressiva da função pulmonar. A recente descrição do sistema colinérgico anti-inflamatório, um mecanismo neural que suprime a resposta imune inata e controla a inflamação por inibição de citocinas proinflammatórias, e a detecção de alguns de seus componentes em células de vias aéreas sugerem uma importante participação deste sistema na fisiopatologia de doenças pulmonares. O principal mediador deste sistema é a acetilcolina (ACh), que é estocada em vesículas sinápticas pelo transportador vesicular de ACh (VAChT), proteína essencial para sua liberação. OBJETIVOS: Avaliar os efeitos da deficiência colinérgica por redução da VAChT nas alterações pulmonares observadas em modelo experimental de inflamação pulmonar induzida pela exposição crônica a ovoalbumina. METODOLOGIA: A redução colinérgica foi induzida pela modificação genética nos níveis de VAChT. Camundongos machos selvagens e mutantes foram submetidos ao protocolo de sensibilização subcutânea com ovoalbumina ou salina nos dias 0...

Inflamação renal e estrese oxidativo em ratos espontaneamente hipertensos antes do desenvolvimento da hipertensão arterial e no diabetes mellitus precoce; Renal inflammation and oxidative stree in spontaneously hypertensive rats before development of hypertension and in early diabetes

Subrata Kumar Biswas
Fonte: Biblioteca Digital da Unicamp Publicador: Biblioteca Digital da Unicamp
Tipo: Tese de Doutorado Formato: application/pdf
Publicado em 01/02/2007 PT
Relevância na Pesquisa
36.39%
Hipertensão arterial sistêmica (HAS) e diabetes mellitus (DM) freqüentementecoexistem em humanos e constituem uma importante causa de nefropatia e de doença renal terminal. Tanto a HAS quanto o DM podem induzir a inflamação renal e o estresse oxidativo, os quais estão implicadosna patogênese da nefropatia. HAS, inflamação renal e estresse oxidativo são eventos altamente interdependentes; e na presença do DM a complexidade deste relacionamento aumenta. Na presente série de estudos nos propusemos investigar a relação entre HAS, inflamação renal e estresse oxidativo na ausência ou presença de DM em ratos espontaneamente hipertensos (SHR), um modelo aceito como representativo da HA primária ou essencial. Os estudos foram descritos nos seguintes artigos publicados(ou aceitos): Artigo I: Neste artigo, identificamos a anormalidade primária entre inflamação e estresse oxidativo nos rins de ratos SHR. Inflamação renal e estresse oxidativo foram quantificados em ratos SHR pré-hipertensos de 2 a 3 semanas de idade e em ratos geneticamente normotensos, Wistar-Kyoto (WKY), usados como controle. A inflamação renal e o estresse oxidativo estavam nitidamente elevados em ratos SHR de 3 semanas se comparados aos ratos WKY controles. Além disso...

Estudo do efeito da inflamação em pata de rato induzida por carragenina sobre o tendão flexor digital profundo; Effect of inflammation in rat paw induced by carrageenan on the deep digital flexor tendon

Cristiano Pedrozo Vieira
Fonte: Biblioteca Digital da Unicamp Publicador: Biblioteca Digital da Unicamp
Tipo: Dissertação de Mestrado Formato: application/pdf
Publicado em 21/02/2011 PT
Relevância na Pesquisa
36.39%
Os tendões podem ser acometidos por lesões, infecções e inflamações, seguidas ou não de ruptura, podendo ser decorrentes de atividades desportivas, como exercícios e alongamentos, ou de atividades diárias de muitos trabalhadores. Em situações patológicas a matriz extracelular (MEC) do tendão passa por um processo de reorganização de seus componentes, visando à regeneração e homeostasia do tecido. A inflamação pode ser desencadeada por diferentes fatores, entre os principais causadores desse processo estão injúrias mecânicas e químicas, agentes infecciosos, queimadura, radiação e supressão de oxigênio. Pouco é conhecido na literatura sobre as possíveis alterações que a inflamação instalada em tecidos próximos pode ocasionar em tendões. Desse modo, o presente estudo teve por objetivo analisar as alterações bioquímicas e morfológicas do tendão flexor digital profundo (TFDP) após indução da inflamação aguda em pata. Os períodos de análises foram 4 horas, período em que ocorre o pico da inflamação, 12 e 24 horas. Ratos Wistar (140-160g) foram separados em três grupos experimentais: os que receberam aplicação da carragenina (1%), os que receberam NaCl (0,9%), e os que não receberam nada...

A fractalkina (CX3CL1) está envolvida nas etapas iniciais de ativação da inflamação no hipotálamo de roedores obesos; Fractalkine (CX3CL1) participates in the early stages of inflammation in hypothalamus of obese

Joseane Morari
Fonte: Biblioteca Digital da Unicamp Publicador: Biblioteca Digital da Unicamp
Tipo: Tese de Doutorado Formato: application/pdf
Publicado em 27/08/2013 PT
Relevância na Pesquisa
36.4%
Nas últimas décadas tornou-se claro que indivíduos e animais obesos apresentam um quadro subclínico de inflamação sistêmica. Estudos desenvolvidos em nosso laboratório ao longo dos últimos 10 anos revelaram que a inflamação do hipotálamo está presente em roedores obesos e sua inibição por métodos genéticos e farmacológicos resulta na correção do fenótipo obeso e dos distúrbios metabólicos comumente associados à obesidade. Ácidos graxos saturados de cadeia longa presentes na dieta parecem ser os principais responsáveis pela ativação da resposta inflamatória no hipotálamo. Os primeiros sinais de inflamação podem ser detectados 24 h após a introdução de uma dieta rica neste tipo de gordura. Pelo menos dois mecanismos moleculares foram identificados como potenciais desencadeadores desta resposta inflamatória, sendo eles; a ativação de receptores TLR4, e a indução do estresse de retículo endoplasmático. Durante a exposição precoce a uma dieta rica em gordura saturada, células da micróglia localizadas no hipotálamo, tornam-se ativas e passam a expressar citocinas que, eventualmente, levam a ativação de vias inflamatórias em neurônios da região. A ativação de JNK e IKK em neurônios resulta na indução de resistência hipotalâmica à leptina e insulina...

Evaluation of metabolic syndrome and associations with inflammation and graft function in renal transplant recipients

Alencastro,Mariana Gascue de; Lemos,Joana Raquel Nunes; Bastos,Nícia Maria Romano de Medeiros; Vicari,Alessandra Rosa; Gonçalves,Luiz Felipe Santos; Manfro,Roberto Ceratti
Fonte: Sociedade Brasileira de Nefrologia Publicador: Sociedade Brasileira de Nefrologia
Tipo: Artigo de Revista Científica Formato: text/html
Publicado em 01/12/2013 EN
Relevância na Pesquisa
36.34%
INTRODUCTION: Cardiovascular disease (CVD) is a major determinant of mortality in renal transplant recipients (RTR). Metabolic syndrome (MS) and chronic inflammation are currently considered non traditional risk factors for cardiovascular disease. This study evaluates the frequency of these conditions their associations with graft function. OBJECTIVE: To evaluate the prevalence of metabolic syndrome (MS) and inflammation and their associations with graft function in renal transplant recipients. METHODS: A cross-sectional study was carried out with 200 RTR. MS was defined by the NCEP-ATP III criteria. Inflammation was assessed by CRP levels. Renal function was assessed by GFR estimation using the MDRD equation. RESULTS: MS occurred in 71 patients (35.5%). Patients with MS had higher CPR and decreased GFR levels. Inflammation was present in 99 patients (49.5%). Mean waist perimeter, body mass index, triglycerides and serum total cholesterol were significantly higher in inflamed patients. An association between MS and inflammation was demonstrated, 48 (67.6%) patients with MS were inflamed and among those without MS the rate of inflamed patients was 39.5% (51 patients) (p < 0.001). A significantly higher percentage of patients with MS in the group of patients in chronic renal disease stages III and IV was observed. CONCLUSION: In RTR there is a significant association among MS and inflammation. MS is negatively associated with graft function. The clinical implications of these findings must be evaluated in longitudinal studies.

Intestinal permeability and inflammation in patients on NSAIDs

Sigthorsson, G; Tibble, J; Hayllar, J; Menzies, I; Macpherson, A; Moots, R; Scott, D; Gumpel, M; Bjarnason, I
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /10/1998 EN
Relevância na Pesquisa
36.36%
Background—The frequency with which non-steroidal anti-inflammatory drugs (NSAIDs) increase small intestinal permeability and cause inflammation is uncertain. 
Aims—To examine small intestinal permeability and inflammation in a large number of patients on long term NSAIDs. 
Methods—Sixty eight patients receiving six different NSAIDs for over six months underwent combined absorption-permeability tests at three different test dose osmolarities (iso-, hypo-, and hyperosmolar). Two hundred and eighty six patients on 12 different NSAIDs underwent indium-111 white cell faecal excretion studies to assess the prevalence and severity of intestinal inflammation. 
Results—The iso- and hyperosmolar tests showed significant malabsorption of 3-0-methyl-D-glucose, D-xylose, and L-rhamnose. Intestinal permeability changes were significantly more pronounced and frequent with the hypo- and hyperosmolar as opposed to the iso-osmolar test. Sequential studies showed that four and nine patients (of 13) developed inflammation after three and six months treatment with NSAIDs, respectively. There was no significant difference (p>0.1) in the prevalence (54-72%) or severity of intestinal inflammation in the 286 patients taking the various NSAIDs apart from those on aspirin and nabumetone...

Inflammation enhances myeloid-derived suppressor cell cross-talk by signaling through Toll-like receptor 4

Bunt, Stephanie K.; Clements, Virginia K.; Hanson, Erica M.; Sinha, Pratima; Ostrand-Rosenberg, Suzanne
Fonte: The Society for Leukocyte Biology Publicador: The Society for Leukocyte Biology
Tipo: Artigo de Revista Científica
EN
Relevância na Pesquisa
36.36%
Myeloid-derived suppressor cells (MDSC) are potent inhibitors of anti-tumor immunity that facilitate tumor progression by blocking the activation of CD4+ and CD8+ T cells and by promoting a type 2 immune response through their production of IL-10 and down-regulation of macrophage production of IL-12. MDSC accumulate in many cancer patients and are a significant impediment to active cancer immunotherapies. Chronic inflammation has been shown recently to enhance the accumulation of MDSC and to increase their suppression of T cells. These findings led us to hypothesize that inflammation contributes to tumor progression through the induction of MDSC, which create a favorable environment for tumor growth. As chronic inflammation also drives type 2 immune responses, which favor tumor growth, we asked if inflammation mediates this effect through MDSC. We find that IL-1β-induced inflammation increased IL-10 production by MDSC and induces MDSC, which are more effective at down-regulating macrophage production of IL-12 as compared with MDSC isolated from less-inflammatory tumor microenvironments, thereby skewing tumor immunity toward a type 2 response. Inflammation heightens MDSC phenotype by signaling through the TLR4 pathway and involves up-regulation of CD14. Although this pathway is well-recognized in other myeloid cells...

Altered eosinophil profile in mice with ST6Gal-1 deficiency: an additional role for ST6Gal-1 generated by the P1 promoter in regulating allergic inflammation

Nasirikenari, Mehrab; Chandrasekaran, E. V.; Matta, Khushi L.; Segal, Brahm H.; Bogner, Paul N.; Lugade, Amit A.; Thanavala, Yasmin; Lee, James J.; Lau, Joseph T. Y.
Fonte: The Society for Leukocyte Biology Publicador: The Society for Leukocyte Biology
Tipo: Artigo de Revista Científica
EN
Relevância na Pesquisa
36.36%
Cumulative evidence indicates that the sialyltransferase ST6Gal-1 and the sialyl-glycans, which it constructs, are functionally pleiotropic. Expression of the ST6Gal-1 gene is mediated by six distinct promoter/regulatory regions, and we hypothesized that these promoters may be used differentially to produce ST6Gal-1 for different biologic purposes. To examine this hypothesis, we compared a mouse with a complete deficiency in ST6Gal-1 (Siat1 null) with another mouse that we have created previously with a disruption only in the P1 promoter (Siat1ΔP1). We noted previously greater neutrophilic inflammation associated with ST6Gal-1 deficiency. Here, we report that ST6Gal-1-deficient mice also have significantly elevated eosinophilic responses. Upon i.p. thioglycollate elicitation, eosinophils accounted for over 20% of the total peritoneal inflammatory cell pool in ST6Gal-1-deficient animals, which was threefold greater than in corresponding wild-type animals. A principal feature of allergic respiratory inflammation is pulmonary eosinophilia, we evaluated the role of ST6Gal-1 in allergic lung inflammation. Using OVA and ABPA experimental models of allergic airways, we showed that ST6Gal-1 deficiency led to greater airway inflammation characterized by excessive airway eosinophilia. The severity of airway inflammation was similar between Siat1ΔP1 and Siat1 null mice...

Enterococcus faecalis Overcomes Foreign Body-Mediated Inflammation To Establish Urinary Tract Infections

Guiton, Pascale S.; Hannan, Thomas J.; Ford, Bradley; Caparon, Michael G.; Hultgren, Scott J.
Fonte: American Society for Microbiology Publicador: American Society for Microbiology
Tipo: Artigo de Revista Científica
Publicado em /01/2013 EN
Relevância na Pesquisa
36.36%
Urinary catheterization elicits major histological and immunological changes that render the bladder susceptible to microbial invasion, colonization, and dissemination. However, it is not understood how catheters induce these changes, how these changes act to promote infection, or whether they may have any protective benefit. In the present study, we examined how catheter-associated inflammation impacts infection by Enterococcus faecalis, a leading cause of catheter-associated urinary tract infection (CAUTI), a source of significant societal and clinical challenges. Using a recently optimized murine model of foreign body-associated UTI, we found that the implanted catheter itself was the primary inducer of inflammation. In the absence of the silicone tubing implant, E. faecalis induced only minimal inflammation and was rapidly cleared from the bladder. The catheter-induced inflammation was only minimally altered by subsequent enterococcal infection and was not suppressed by inhibitors of the neurogenic pathway and only partially by dexamethasone. Despite the robust inflammatory response induced by urinary implantation, E. faecalis produced biofilm and high bladder titers in these animals. Induction of inflammation in the absence of an implanted catheter failed to promote infection...

Gene Dosage-Dependent Negative Regulatory Role of β-Arrestin-2 in Polymicrobial Infection-Induced Inflammation

Sharma, Deepika; Malik, Ankit; Lee, Eunhee; Britton, Robert A.; Parameswaran, Narayanan
Fonte: American Society for Microbiology Publicador: American Society for Microbiology
Tipo: Artigo de Revista Científica
Publicado em /08/2013 EN
Relevância na Pesquisa
36.36%
β-arrestin-2 (β-arr2) is a scaffolding protein of the arrestin family with a wide variety of cellular functions. Recent studies have demonstrated differential roles for β-arr2 in inflammation following endotoxemia and cecal ligation and puncture (CLP) models of sepsis. Because CLP-induced inflammation involves response to fecal contents and necrotic cecum in addition to microbial challenge, in this study, we examined the role of β-arr2 in an exclusively polymicrobial infection (PMI) model. In addition, we examined the role of gene dosage of β-arr2 in polymicrobial sepsis. Our studies demonstrate that β-arr2 is a negative regulator of systemic inflammation in response to polymicrobial infection and that one allele is sufficient for this process. Our results further reveal that loss of β-arr2 leads to increased neutrophil sequestration and overt inflammation specifically in the lungs following polymicrobial infection. Consistent with this, specific NF-κB and mitogen-activated protein kinase (MAPK) signaling pathways were differentially activated in the β-arr2 knockout (KO) mice lungs compared to the wild type (WT) following PMI. Associated with enhanced inflammation in the KO mice, PMI-induced mortality was also significantly higher in KO mice than in WT mice. To understand the differential role of β-arr2 in different sepsis models...

Dendritic cell-derived osteoclasts and inflammation-induced bone loss; development and regulation

Alnaeeli, Mawadda ; Teng, Yen-Tung Andy
Fonte: Universidade de Rochester Publicador: Universidade de Rochester
Tipo: Tese de Doutorado Formato: Number of Pages:xv, 220 leaves
ENG
Relevância na Pesquisa
36.42%
Thesis (Ph. D.)--University of Rochester. School of Medicine and Dentistry. Dept. of Microbiology and Immunology, 2008. ; Inflammation-induced osteoclastogensis is a well established osteo-immunological phenomenon associated with dys-regulated bone remodeling, whereby the frequency and activity of osteoclasts (OC) become elevated under inflammatory conditions, in response to several stimuli including osteogenic cytokines signaling. OC are bone-resorbing cells, thus considered to be central players during inflammation-induced bone loss. They are derived from precursors of the monocyte/ macrophage lineage, in response to receptor activator of NF-κB ligand (RANKL) and macrophage-colony stimulating factor (M-CSF). Inflammation-induced osteoclastogenesis can lead to irreversible bone destruction and physical disability, and may be the result of several factors including infections, metabolic bone disorders, or autoimmunity. Dendritic cells (DC) are innate immune effectors, and as antigen presenting cells, they are critically involved in regulating adaptive immune responses, including T-cell immunity. Additionally, DC share common progenitors with OC and infiltrate bone adjacent tissues during inflammation, where their interactions with T-cells constitute a key component of the inflammatory infiltrate at active disease sites in human and experimental rheumatoid arthritis and periodontitis. The work presented in this thesis is focused on the characterization of DC-derived OC (DDOC) development and phenotype...

Animal model of silicosis and silica-induced inflammation

Wang, He; Peng, X. D.; Lawson, G.
Fonte: Australian Institute of Environmental Health Publicador: Australian Institute of Environmental Health
Tipo: Artigo de Revista Científica
Publicado em //2006 EN
Relevância na Pesquisa
36.37%
Animal models are useful in studies of the mechanism of silica-induced effects and the testing of potentially effective drugs because such experiments cannot be carried out directly on humans. Different animal species might react differently in response to silica exposure. Rats appear to be the most ideal animal species for studying silicainduced effects because of both strong fibrogenic and carcinogenic reactions. Moreover, the different responses of various species to silica exposure might assist in understanding the mechanisms of silica induced lung damage in humans. Many studies have been conducted to elucidate the mechanism of silica-induced acute inflammation. These studies indicate that silica is a strong inflammatory agent and can induce an overt and rapid inflammatory response. Silica-induced pulmonary inflammation persists, evolving into the destruction of normal lung structure and function. It is well known that silica particles persist in the lung, but persistence of inflammation might be attributed to not only the persistent particles but also to the infiltrated inflammatory cells. Continued recruitment of inflammatory cells and the defective clearance of the infiltrated cells might be more important in the persistence of inflammation. After silica exposure...

The effect of azithromycin on acute and chronic inflammation in an in vivo experimental model.

Du Bois, A. H.
Fonte: Universidade de Adelaide Publicador: Universidade de Adelaide
Tipo: Tese de Doutorado
Publicado em //2013
Relevância na Pesquisa
36.41%
Background: Macrolide antibiotics have been found to have both antimicrobial and antiinflammatory properties. They may be useful adjuncts in the treatment of conditions in which both these factors play a role, such as periodontitis. Objectives: The aim of this study was to evaluate the effect of azithromycin in a rat model of experimentally induced acute and chronic inflammation. Material and methods: Polyurethane sponges loaded with either heat killed Porphyromonas gingivalis (HKPG), Mycobacterium tuberculosis (HKTB) or Phosphate Buffered Saline (PBS) were surgically implanted into the fore flanks of rats. To determine any acute inflammatory effects animals received azithromycin 4 days prior to surgery, while to determine the effects on chronic inflammation animals did not receive azithromycin until day 25 post operatively. The control groups did not receive azithromycin. The sponges were retrieved at days 7, 14, 21, 35 and 49, wet weights recorded and then processed for histological evaluation of acute and chronic inflammation and fibrosis. Additionally, immunohistochemical staining was used to identify macrophages using CD163 and CD68 macrophage markers at days 21 and 35. Biochemical analyses were used to determine serum levels of C-reactive protein (CRP) and hydroxyproline (HP) content in the retrieved sponges. Results: No differences were found between wet and dry weights of sponges for any of the groups. Acute Inflammation: A trend for lower inflammation and infiltration scores was observed for all azithromycin treated groups compared to untreated groups...

Die Bedeutung des Adenosinrezeptors A1 für die LPS-induzierte akute pulmonale Inflammation; The role of adenosine receptor A1 in LPS-induced acute pulmonary inflammation

Ngamsri, Kristian-Christos
Fonte: Universidade de Tubinga Publicador: Universidade de Tubinga
Tipo: Dissertação
DE_DE
Relevância na Pesquisa
36.36%
Die Migration neutrophiler Granulozyten (PMNs) in die Lunge ist ein zentraler pathophysiologischer Mechanismus in der frühen Phase der akuten respiratorischen Insuffizienz (Acute Respiratory Distress Syndrome, ARDS). Dabei vermittelt extrazelluläres Adenosin über vier Adenosinrezeptoren (AR) (A1, A2a, A2b und A3) wichtige pro- und anti-inflammatorische Effekte. In diesen Arbeiten untersuchten wir im murinen ARDS-Model, die Rolle von Adenosinrezeptor A1 bei der LPS-induzierten pulmonalen Inflammation. Mittels durchflusszytometrischer Verfahren bestimmten wir die Migration von PMNs in der Lunge. Desweiteren untersuchten wir die LPS-induzierten mikrovaskuläre Permeabilität, Freisetzung inflammatorischer Mediatoren und Effekte von pharmakologischen Modulatoren. Für unsere in vivo Versuche nutzten wir Wildtyp- (WT, C57/Bl6) und A1-gendefiziente Mäuse (A1AR-/-). Wir haben auch chimäre Mäuse generiert, welche A1AR entweder auf hämatopoetischen oder auf nicht hämatopoetischen Zellen exprimierten. Die Rolle des A1AR in der PMN-Migration wurde ebenfalls in vitro untersucht und auch deren Effekte bei dem LPS-induzierten zytoskelettalen Remodelling. Unsere Daten zeigen, dass die pharmakologische Aktivierung von A1AR zu einer reduzierten PMN-Migration...

Abnormal inflammation in a rat model of spontaneous fetal loss leads to maternal coagulopathies associated with placental haemostatic alterations

FALCON, BANI JADIEL
Fonte: Quens University Publicador: Quens University
Tipo: Tese de Doutorado
EN; EN
Relevância na Pesquisa
36.37%
Spontaneous foetal loss is the most common complication of pregnancy, affecting up to 20% of recognized pregnancies and recurring in 1-3% of cases. Abnormal maternal inflammation and systemic maternal coagulopathies are associated with foetal loss; however, the causal role of inflammation in the development of obstetric coagulopathies has not been determined. Further, questions remain as to whether maternal systemic coagulopathies are associated with placental haemostatic alterations and what role these local alterations play in foetal outcome. We hypothesized that abnormal maternal inflammation during pregnancy is causally linked to maternal coagulopathies and that these coagulopathies are associated with impaired utero-placental blood flow preceding foetal death. To induce inflammation-mediated fetal death, we administered lipopolysaccharide (LPS; 100-µg/kg) to Wistar rats on gestational day 14.5 and characterized the systemic maternal coagulation status 1hr post LPS administration using thromboelastograpy. Utero-placental haemostatic alterations were analyzed by periodic acid Schiff staining (PAS) and immunohistochemistry for fibrin/fibrinogen. Spiral arteriole peak flow velocity was determined by Doppler ultrasound. To determine causality between abnormal maternal inflammation...

Rho-kinase inhibition attenuates airway responsiveness, inflammation, matrix remodeling, and oxidative stress activation induced by chronic inflammation

Possa, Samantha Souza; Charafeddine, Homar Toledo; Righetti, Renato Fraga; Silva, Patricia Angeli da; Almeida-Reis, Rafael; Saraiva-Romanholo, Beatriz Mangueira; Perini, Adenir; Prado, Carla Maximo; Leick-Maldonado, Edna Aparecida; Martins, Milton A.; Lop
Fonte: AMER PHYSIOLOGICAL SOC; BETHESDA Publicador: AMER PHYSIOLOGICAL SOC; BETHESDA
Tipo: Artigo de Revista Científica
ENG
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Possa SS, Charafeddine HT, Righetti RF, da Silva PA, Almeida-Reis R, Saraiva-Romanholo BM, Perini A, Prado CM, Leick-Maldonado EA, Martins MA, Tiberio ID. Rho-kinase inhibition attenuates airway responsiveness, inflammation, matrix remodeling, and oxidative stress activation induced by chronic inflammation. Am J Physiol Lung Cell Mol Physiol 303: L939-L952, 2012. First published September 21, 2012; doi:10.1152/ajplung.00034.2012.-Several studies have demonstrated the importance of Rho-kinase in the modulation of smooth muscle contraction, airway hyperresponsiveness, and inflammation. However, the effects of repeated treatment with a specific inhibitor of this pathway have not been previously investigated. We evaluated the effects of repeated treatment with Y-27632, a highly selective Rho-kinase inhibitor, on airway hyperresponsiveness, oxidative stress activation, extracellular matrix remodeling, eosinophilic inflammation, and cytokine expression in an animal model of chronic airway inflammation. Guinea pigs were subjected to seven ovalbumin or saline exposures. The treatment with Y-27632 (1 mM) started at the fifth inhalation. Seventy-two hours after the seventh inhalation, the animals' pulmonary mechanics were evaluated, and exhaled nitric oxide (E-NO) was collected. The lungs were removed...