bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of cysteinyl leukotriene receptor antagonist on CD11b and CD23 expression in asthmatic children
Authors: Gagro A. , Aberle N. , Rabatić S. , Ajduk J. , Jelačić J. , Dekaris D. 
Published: June 2004

SummaryBackground
Cysteinyl leukotrienes are potent pro‐inflammatory mediators that contribute to the pathophysiologic features observed in allergic asthma. Inhibitors of leukotriene receptors represent novel therapy in asthma treatment. In addition to the protection from early asthmatic responses, these drugs have recently been shown to protect from late airway responses too.Methods
We studied the effect of treatment with an oral antagonist of cysteinyl leukotriene receptors on the increased expression of the low‐affinity IgE receptor, CD23, on B cells, and of its ligands, CD11b and CD11c, on CD4+ T cells and monocytes in peripheral blood of patients with allergic asthma. In this uncontrolled open‐label study, 14 children with allergic asthma received montelukast, a cysteinyl leukotrine receptor antagonist, for a period of 6 weeks after demonstrating forced expiratory volume in 1 s (FEV1) of less than 80% of the predicted value. Samples of peripheral heparinized blood and sera were obtained before and after therapy completion. Three‐colour immunofluorescence analysis was performed, and expression of CD11b and CD11c on CD4+ T lymphocytes and monocytes as well as the expression of CD21 and CD23 on B cells were determined (n=12). Peripheral blood eosinophil count, changes in FEV1 and peak expiratory flow rate (PEFR), asthma exacerbations, and as‐needed use of β‐agonist were also monitored.Results
Montelukast improved FEV1 and PEFR, and decreased peripheral eosinophil counts in all study patients. There was no significant change in the expression of CD21 and CD23 on B cells. The expression of CD11c on CD4+ T cells and of both CD11b and CD11c on monocytes remained similar to the pretreatment expression. However, the percentage of CD11b+CD4+ T lymphocytes significantly decreased after treatment with montelukast. This was accompanied by a significant decrease in the levels of total IgE.Conclusion
The capacity of 6‐week montelukast therapy to reduce the percentage of CD11b CD4+ T cells might be a mechanism leading to the immune response modulation on this T cell subset interaction with CD23‐expressing B cells and subsequent down‐regulation of IgE synthesis.
Rosmarinic acid in perilla extract inhibits allergic inflammation induced by mite allergen, in a mouse model
Authors: Sanbongi C. , Takano H. , Osakabe N. , Sasa N. , Natsume M. , Yanagisawa R. , Inoue K.‐i. , Sadakane K. , Ichinose T. , Yoshikawa T. 
Published: June 2004

SummaryBackground
Perilla and its constituent rosmarinic acid have been suggested to have anti‐allergic activity. However, few studies have examined the effects on allergic asthma.Objective
The purpose of this study was to evaluate the effect of oral administration of perilla leaf extract, which contains high amount of rosmarinic acid, on a murine model of allergic asthma induced by house dust mite allergen.Methods
C3H/He mice were sensitized by intratracheal administration of Dermatophagoides farinae (Der f). Mice were orally treated with rosmarinic acid in perilla extract (PE) (1.5 mg/mouse/day).Results
Der f challenge of sensitized mice elicited pulmonary eosinophilic inflammation, accompanied by an increase in lung expression of IL‐4 and IL‐5, and eotaxin. Daily treatment with rosmarinic acid in PE significantly prevented the increases in the numbers of eosinophils in bronchoalveolar lavage fluids and also in those around murine airways. Rosmarinic acid in PE treatment also inhibited the enhanced protein expression of IL‐4 and IL‐5, and eotaxin in the lungs of sensitized mice. Der f challenge also enhanced allergen‐specific IgG1, which were also inhibited by rosmarinic acid in PE.Conclusion
These results suggest that oral administration of perilla‐derived rosmarinic acid is an effective intervention for allergic asthma, possibly through the amelioration of increases in cytokines, chemokines, and allergen‐specific antibody.
Mechanical strain enhances proteoglycan message in fibroblasts from asthmatic subjects
Authors: Ludwig M. S. , Ftouhi‐Paquin N. , Huang W. , Pagé N. , Chakir J. , Hamid Q. 
Published: June 2004

SummaryBackground
Remodelling of the asthmatic airway includes increased deposition of proteoglycan (PG) molecules. One of the stimuli driving airway remodelling may be excessive mechanical stimulation.Objective
We hypothesized that fibroblasts from asthmatic patients would respond to excessive mechanical strain with up‐regulation of message for PGs.Methods
We obtained fibroblasts from asthmatic patients (AF) and normal volunteers (NF) using endobronchial biopsy. Cells were maintained in culture until the fifth passage and then grown on a flexible collagen‐coated membrane. Using the Flexercell device, cells were then subjected to cyclic stretch at 30% amplitude at 1 Hz for 24 h. Control cells were unstrained. Total RNA was extracted from the cell layer and quantitative RT‐PCR performed for decorin, lumican and versican mRNA.Results
In unstrained cells, the expression of decorin mRNA was greater in AF than NF. With strain, NF showed increased expression of versican mRNA and AF showed increased expression of versican and decorin mRNA. The relative increase in versican mRNA expression with strain was greater in AF than NF.Conclusions
These data support the hypothesis that proteoglycan message is increased in asthmatic fibroblasts subject to mechanical strain. This finding has implications for the mechanisms governing airway wall remodelling in asthma.
Th1‐dominant shift of T cell cytokine production, and subsequent reduction of serum immunoglobulin E response by administration in vivo of plasmid expressing Txk/Rlk, a member of Tec family tyrosine kinases, in a mouse model
Authors: Takeno M. , Yoshikawa H. , Kurokawa M. , Takeba Y. , Kashiwakura J.‐i. , Sakaguchi M. , Yasueda H. , Suzuki N. 
Published: June 2004

SummaryBackground
Th1 and Th2 cells, resulting from antigenic stimulation in the presence of IL‐12 and IL‐4, respectively, are implicated in the pathology of various diseases including allergic and autoimmune diseases. Txk/Rlk is a member of Tec family tyrosine kinases. We reported that Txk acts as a Th1‐specific transcription factor in the T lymphocytes.Objective
In this study we have asked whether administration of txk expression plasmid brings about a Th1/Th2 shift in vivo of the mice, and subsequent reduction of circulating IgE.Methods
Mice were administered a txk expression plasmid with hemagglutinating virus of Japan (HVJ) envelope vector. Txk expressions in spleen cells were assessed by immunoblotting and immunocytochemical staining. Cytokine productions by the spleen cells and serum Ig concentrations were studied by ELISA.Results
Administration of a txk expression plasmid with HVJ vector induced expression of Txk in the spleen cells. The spleen cells showed enhanced Th1‐specific cytokine production; spleen cells from the txk administered mice produced more IFN‐γ as compared with those from control plasmid‐administered mice in an antigen‐specific manner. IL‐2 and IL‐4 secretions of the spleen cells were comparable between the two mouse groups. Txk administration did not reduce serum IgG concentration. It markedly reduced total IgE level and an IgG1/IgG2a ratio, reflection of Th1/Th2 balance, in sera. Furthermore, txk administration reduced ovalbumin (OVA)‐specific IgE levels in sera of the OVA sensitized mice.Conclusion
Thus, Txk enhances IFN‐γ secretion and thus modulates Th1/Th2 cytokine balance, leading to reduction of serum IgE.
Non‐linear short‐term effects of airborne pollen levels with allergenic capacity on asthma emergency room admissions in Madrid, Spain
Authors: Tobías A. , Galán I. , Banegas J. R. 
Published: June 2004

SummaryBackground
Several time‐series studies have shown positive associations between pollen levels and asthma morbidity. However, few studies have included air pollution as a potential confounder when examining this relationship, and they have only done so on a linear basis.Objective
To investigate the potential non‐linear short‐term effects of the types of pollen with allergenic capacity across the whole range of exposure on the daily number of asthma‐related hospital emergencies in Madrid for the period 1995–1998.Methods
Data were collected on the daily number of asthma emergency room admissions and daily average levels of major types of pollen with allergenic capacity: Olea, Plantago, Poaceae and Urticaceae. We used Poisson regression with generalized additive models, controlling for trend and seasonality, meteorological variables, acute respiratory infections and air pollutants. To study the non‐linear effect of pollen levels on asthma emergency room admissions, pollens were categorized into five groups defined on the basis of their respective distributions.Results
The strongest associations were registered in respect of a lag of 1 day for Urticaceae, a lag of 2 days for Plantago, and a day lag of 3 days for Poaceae. Adjustment for the different types of pollen failed to result in major changes. Non‐linearities were evident for pollen levels. The greatest increase in risk vs. the reference category (minimum value – 50th percentile) was observed for the categories between the 95th and 99th percentiles, with increases of 32.0% for Plantago, 32.2% for Poaceae and 24.6% for Urticaceae, and between the 99th percentile and the maximum value, with increases of 31.3%, 78.7% and 49.8%, respectively. Olea was not related with asthma emergency room admissions.Conclusions
Pollens with allergenic capacity in Madrid are positively associated with asthma‐related hospital emergencies. These associations remain stable when simultaneous adjustment is made for the four types of pollen and for air pollutants and meteorological variables. In terms of non‐linear effects, Poaceae register the strongest association with asthma emergency room admissions.
Presence of staphylococcal exfoliative toxin A in sera of patients with atopic dermatitis
Authors: Yagi S. , Wakaki N. , Ikeda N. , Takagi Y. , Uchida H. , Kato Y. , Minamino M. 
Published: June 2004

SummaryBackground
It has been reported that the toxins that Staphylococcus aureus produces are associated with the exacerbation of atopic dermatitis (AD). It has been shown in many studies that staphylococcal enterotoxin (SE) A and SEB contribute to AD by humoral immunity through IgE production as a superantigen. On the other hand, little attention has been paid to the relationship between AD and exfoliative toxin x (ETx).Objective
We investigated the toxins that are frequently detected from the skin of patients and how these toxins affect AD.Methods
S. aureus, isolated from the skin of 100 patients with mild to severe AD, were examined for the producibility of toxins by polymerase chain reaction. Serum samples were obtained from 21 patients with mild and moderate AD. The levels of SEB, ETA, total IgE, specific IgE, and specific IgG in sera were measured by ELISA.Results
SEB was most frequently detected from S. aureus on the skin of these patients as previously reported. And ETx, to which little attention has been paid so far, was frequently detected next to SEB. Furthermore, ETA was detected from the sera of almost all the AD patients. SEB was not detected at all. Although the level of ETA in the AD group was significantly higher than that of controls, ETA‐specific IgE was not detected from their sera. High levels of ETA tended to be detected from infantile patients. Although there were no significant differences in the levels of ETA‐IgG between AD and the controls, its prevalence was more than twice as high as the controls in AD.Conclusion
These results suggest that many AD patients were exposed to ETx. We conclude that ETx may contribute to exacerbation of AD, particularly in infants, by a mechanism that is not through specific IgE production, unlike SEB.
Acute infection with influenza virus enhances susceptibility to fatal pneumonia followingStreptococcus pneumoniaeinfection in mice with chronic pulmonary colonization withPseudomonas aeruginosa
Authors: SEKI M , HIGASHIYAMA Y , TOMONO K , YANAGIHARA K , OHNO H , KANEKO Y , IZUMIKAWA K , MIYAZAKI Y , HIRAKATA Y , MIZUTA Y , TASHIRO T , KOHNO S 
Published: June 2004

SUMMARYWe established a mouse model in which fatal pneumonia was induced by pneumococcal superinfection following influenza virus infection in chronic Pseudomonas aeruginosa infected mice. In this mouse model, influenza virus infection caused a significant increase in inflammatory cells, cytokines and severe tissue damage in the lungs of these P. aeruginosa infected mice, before pneumococcal infection. Intrapulmonary virus titres were significantly increased in mice with chronic P. aeruginosa infection, compared with control mice. Neutrophil function analysis showed significant reduction of myeloperoxidase (MPO) activity and lysozyme secretion by influenza virus infection in these mice. Our results suggest that influenza virus infection may play an important role in inducing pneumococcal pneumonia in chronic P. aeruginosa infected mice. Our results suggested that our mouse model is useful for investigating the pathogenesis of influenza virus infection in patients with chronic lung infection.
Dietary fructooligosaccharides up-regulate immunoglobulin A response and polymeric immunoglobulin receptor expression in intestines of infant mice
Authors: NAKAMURA Y , NOSAKA S , SUZUKI M , NAGAFUCHI S , TAKAHASHI T , YAJIMA T , TAKENOUCHI-OHKUBO N , IWASE T , MORO I 
Published: June 2004

SUMMARYWe examined whether or not dietary fructooligosaccharides (FOS) in infancy can have a beneficial effect on the mucosal immune system. Newborn BALB/c mice, accompanied by their dams until 21 days of age, were fed either a control diet based on casein [FOS(–) diet group] or a FOS(–) diet supplemented with 5% (w/w) FOS [FOS(+) diet group]. Total IgA levels in tissue extracts from the intestines of mice in the FOS(+) diet group at 38 days of age were about twofold higher (P &lt; 0·05) than those in the FOS(–) diet group in the jejunum, ileum and colon. Ileal and colonic polymeric immunoglobulin receptor (pIgR) expression in the FOS(+) diet group at 36 days of age was 1·5-fold higher than in the FOS(–) diet group (P &lt; 0·05). Consistent with these results, the ileal IgA secretion rate of the FOS(+) diet group at 37 days of age was twofold higher than that of the FOS(–) diet group (P &lt; 0·05). Moreover, the percentage of B220+IgA+ cells in Peyer's patches (PP) was significantly higher in the FOS(+) diet group than in the FOS(–) diet group (6·2%versus 4·3%, P &lt; 0·05), suggesting that isotype switching from IgM to IgA in PP B cells might be enhanced in vivo. Taken together, our findings suggest that dietary FOS increases the intestinal IgA response and pIgR expression in the small intestine as well as the colon in infant mice.
Anti-desmoglein 1 antibodies in Tunisian healthy subjects: arguments for the role of environmental factors in the occurrence of Tunisian pemphigus foliaceus
Authors: KALLEL SELLAMI M , BEN AYED M , MOUQUET H , DROUOT L , ZITOUNI M , MOKNI M , CERRUTI M , TURKI H , FEZZA B , MOKHTAR I , BEN OSMAN A , ZAHAF A , KAMOUN M R , JOLY P , MASMOUDI H , MAKNI S , TRON F , GILBERT D 
Published: June 2004

SUMMARY
Pemphigus foliaceus is an autoimmune blistering skin disease mediated by autoantibodies directed against desmoglein 1 and occurs as a sporadic form throughout the world, or as an endemic form called fogo selvagem in Brazil. Healthy subjects living in Brazilian endemic areas produce antidesmoglein 1 antibodies, suggesting the role of environmental factors in the initiation of the autoimmune response. Tunisia was described recently as an endemic area where the disease is characterized by its high rate among young people, especially women. An enzyme-linked immunosorbent assay using recombinant desmoglein 1 as antigen was used to detect antibodies against desmoglein 1 and calibrated with sera from 67 French healthy blood donors, 20 French pemphigus foliaceus patients and patients with other bullous skin diseases. When sera from 179 healthy Tunisian blood donors were tested, 31 (17%) were found positive. The desmoglein 1 binding activity of these 31 sera was confirmed in 10 cases by indirect immunofluorescence analysis and/or immunoblotting using human epidermal extract. Subclass analysis of antidesmoglein 1 antibodies showed that they were almost exclusively of the IgG2 subclass in positive normal sera and of IgG4 subclass in patients with PF. Thus, antibodies against desmoglein 1 are prevalent in normal subjects living in Tunisia which, along with their IgG2 isotype, suggests the role of the environment in the pathogenesis of this endemic type of pemphigus foliaceus and the need for additional factors to switch from a subclinical to a clinical form of the disease.
Down-regulation of CXCR-4 and CCR-5 expression by interferon-γis associated with inhibition of chemotaxis and human immunodeficiency virus (HIV) replication but not HIV entry into human monocytes
Authors: CREERY D , WEISS W , LIM W T , AZIZ Z , ANGEL J B , KUMAR A 
Published: June 2004

SUMMARYAlterations in the expression of CXCR4 and CCR5, the co-receptors for HIV entry, may be associated with susceptibility of monocytic cells to HIV infection. Interferon (IFN)-γ has been shown to inhibit HIV replication in monocytic cells, but the molecular mechanism involved is not well understood. To determine if IFN-γ regulates HIV replication by altering CXCR-4/CCR-5 expression and hence virus entry into monocytic cells, we investigated the effects of IFN-γ on CXCR-4 and CCR-5 expression and its biological implications with respect to HIV entry, replication and chemotaxis towards the CXCR-4 and CCR-5 ligands SDF-1 and MIP-1α, respectively. IFN-γ decreased CXCR-4 and CCR-5 expression on monocytes derived from HIV-negative adults, HIV-positive adults and HIV-negative cord blood. This down-regulation of chemokine receptor expression did not result in a corresponding change in mRNA expression but was associated with elevated levels of the endogenously produced chemokines SDF-1 and RANTES. Furthermore, IFN-γ inhibited chemotaxis in response to SDF-1 and MIP-1α, inhibited HIV replication, but failed to inhibit virus entry in monocytic cells. These results suggest that although IFN-γ-induced down-regulation of CXCR-4 and CCR-5 expression is associated with an inhibition of SDF-1-/MIP-1α-mediated chemotaxis, IFN-γ-induced inhibition of HIV replication may be mediated at levels subsequent to the virus entry.
Oligoclonal expansion of circulating and tissue-infiltrating CD8+ T Cells with killer/effector phenotypes in juvenile dermatomyositis syndrome
Authors: MIZUNO K , YACHIE A , NAGAOKI S , WADA H , OKADA K , KAWACHI M , TOMA T , KONNO A , OHTA K , KASAHARA Y , KOIZUMI S 
Published: June 2004

SUMMARYAlthough triggering by infectious agents and abnormal immune responses may play some role in the pathogenesis of juvenile dermatomyositis syndrome (JDMS), the precise mechanism of muscle destruction and vascular damage is largely unknown. In this study, we tried to elucidate the role of cytotoxic T cells in two patients with JDMS, who were diagnosed based on the characteristic symptoms, laboratory data, MRI findings and electromyographic patterns. Peripheral blood T cell phenotypes were determined by flow cytometry, using mAbs against specific T cell receptor (TCR) Vβs. Complementarity-determining region3 (CDR3) size analysis was performed by gene scanning of CDR3 polymerase chain reaction (PCR) amplification products specific for each Vβ. Subsequently, CDR3 nucleotide sequences were obtained after cloning of the predominant products. The distribution of lymphocytes infiltrating the muscle tissue was analysed by immunohistochemistry. In both patients examined, a unique combination of TCR Vβ repertoires was increased within the CD8+ T cells. These subpopulations expressed a characteristic phenotype, indicating that they are memory/effector T cells with killer functions. At the same time, immunohistological and molecular biological examinations of the biopsied muscle samples revealed that identical CD8+ T cell clones with identical phenotypes/TCR Vβ infiltrated within the inflammatory tissue, in particular around vessels. These findings indicate that oligoclonal expansion of CD8+ T cells plays a central role in the pathogenesis of muscle injury in the juvenile form of dermatomyositis syndrome and may provide a useful clinical parameter of disease activity and responsiveness to anti-inflammatory therapy.
Murine viral hepatitis involves NK cell depletion associated with virus-induced apoptosis
Authors: LEHOUX M , JACQUES A , LUSIGNAN S , LAMONTAGNE L 
Published: June 2004

SUMMARYMouse hepatitis virus type 3 (MHV3), a coronavirus, is an excellent animal model for the study of immunological disorders related to acute and chronic hepatitis. In this study, we have verified if the fulminant hepatitis induced by MHV3 could be related to an impairment of innate immunity. Groups of three C57BL/6 mice were infected with the pathogenic L2-MHV3 or attenuated YAC-MHV3 viruses, and the natural killer (NK) cell populations from liver, spleen and bone marrow were analysed. The percentage of intrahepatic NK1·1+T cell receptor (TCR)− cells did not increase while NK1·1+TCRinter cells decreased in both L2-MHV3- and YAC-MHV3-infected mice. Concurrently, splenic and myeloid NK1·1+ cells decreased in L2-MHV3-infected mice. However, the cytotoxic activity of NK cells increased in liver and decreased in bone marrow from pathogenic L2-MHV3-infected mice while no modification was detected in YAC-MHV3-infected mice. Flow cytometric analysis revealed that both normal and larger splenic or myeloid NK cells decreased more in pathogenic L2-MHV3-infected mice than in attenuated YAC-MHV3-infected mice. In vitro viral infections of interleukin (IL)-15-stimulated lymphoid cells from liver and bone marrow revealed that L2-MHV3 induced higher decreases in cell viability of NK1·1+ cells than the YAC-MHV3 variant. The NK cell decreases were due to the viral permissivity leading to cytopathic effects characterized by cell rounding, syncytia formation and apoptosis. Larger NK+ syncytia were observed in L2-MHV3-infected cells than in YAC-MHV3-infected cells. These results suggest that NK cell production is impaired by viral infection favouring fulminant hepatitis.