Interleukin 4 as an essential factor for in vitro clonal growth of murine connective tissue-type mast cells.

Hamaguchi, Yasushi; Kanakura, Yuzuru; Fujita, Jun; Takeda, Shunichi; Nakano, Toru; Tarui, Seiichiro; Honjo, Tasuku; Kitamura, Yukihiko

doi:10.1084/jem.165.1.268

Cited by 263 publications

(105 citation statements)

References 19 publications

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“…IL-4 is involved in the isotype switching in B cells from IgG2a and 2b to produce IgG1 (in mice) and IgE (a hallmark of atopy in human asthma) (22,26). In addition, IL-4 is involved in activation of mast cells thus leading to the release of several proinflammatory cytokines and chemotactic factors that could contribute to the altered airway function (22,27,28). Using knockout mice and cytokine antagonists, it has become evident that a cytokine imbalance with predominance of Th2 cells is capable of producing an environment favorable for the development of eosinophilic inflammation, increased IgE, and AHR (22).…”

Section: Discussionmentioning

confidence: 99%

Recurrent Milk Aspiration Produces Changes in Airway Mechanics, Lung Eosinophilia, and Goblet Cell Hyperplasia in a Murine Model

et al. 2000

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Recurrent aspiration of milk into the respiratory tract has been implicated in the pathogenesis of a variety of inflammatory lung disorders including asthma. However, the lack of animal models of aspiration-induced lung injury has limited our knowledge of the pathophysiological characteristics of this disorder. This study was designed to evaluate the effects of recurrent milk aspiration on airway mechanics and lung cells in a murine model. Under light anesthesia, BALB/c mice received daily intranasal instillations of whole cow's milk (n ϭ 7) or sterile physiologic saline (n ϭ 9) for 10 d. Respiratory system resistance (Rrs) and dynamic elastance (Edyn,rs) were measured in anesthetized, tracheotomized, paralyzed and mechanically ventilated mice 24 h after the last aspiration of milk. Rrs and Edyn,rs were derived from transrespiratory and plethysmographic pressure signals. In addition, airway responses to increasing concentrations of i.v. methacholine (Mch) were determined. Airway responses were measured in terms of PD 100 (dose of Mch causing 100% increase from baseline Rrs) and Rrs,max (% increase from baseline at the maximal plateau response) and expressed as % control (mean Ϯ SE). We found recurrent milk aspiration did not affect Edyn and baseline Rrs values. However, airway responses to Mch were increased after milk aspiration when compared with control mice. These changes in airway mechanics were associated with an increased percentage of lymphocytes and eosinophils in the bronchoalveolar lavage, mucus production, and lung inflammation. Our findings suggest that recurrent milk aspiration leads to alterations in airway function, lung eosinophilia, and goblet cell hyperplasia in a murine model. Abbreviations Rrs, respiratory system resistance Edyn,rs, dynamic elastance of the respiratory system Mch, methacholine PD 100 , dose of methacholine causing 100% increase of Rrs from baseline Rrs,max, % increase from baseline at the maximal plateau response GER, gastroesophageal reflux ASM, airway smooth muscle BAL, bronchoalveolar lavage AHR, airway hyperresponsiveness NEP, neutral endopeptidase Recurrent aspiration of foreign material into the respiratory tract is a common problem in children and patients with predisposing anatomic and functional disorders such as tracheoesophageal fistula, GER, and neuromuscular disorders (1-3). As a result, it has been implicated in the etiology of a variety of pulmonary disorders (1-3). Clinically, children who aspirate may present with pneumonia, recurrent wheezing, unexplained cough, interstitial lung disease, and even apnea (1-3). Furthermore, an association between aspiration of milk and exacerbation and/or development of asthma has been suggested (4). Children with asthma commonly have GER, but it is not always clear if GER causes, exacerbates, or is the result of the asthma itself (4). In this respect, the interpretation of clinical studies represents a clinical challenge in terms of establishing a cause-effect relationship between GER, aspiration, and pulmonary sequelae (4 ...

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Section: Discussionmentioning

confidence: 99%

Recurrent Milk Aspiration Produces Changes in Airway Mechanics, Lung Eosinophilia, and Goblet Cell Hyperplasia in a Murine Model

et al. 2000

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“…Eosinophils and mast cells are prominent cellular constituents of schistosome granulomas, and IL-13 and IL-4 clearly play important roles in regulating their development, differentiation, and recruitment to sites of inflammation. 12,24,33,34 Therefore, the cellular composition of the granuloma could have a significant impact on the development of fibrosis in these mice. Eosinophils and mast cells are widely believed to be important effector cells in a variety of Th2-mediated allergic and infectious diseases.…”

Section: Discussionmentioning

confidence: 99%

Studies of murine schistosomiasis reveal interleukin-13 blockade as a treatment for established and progressive liver fibrosis

et al. 2001

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In several allergic, autoimmune, and infectious diseases, fibrosis is a major cause of morbidity and mortality. Here, using a model of infection-induced liver fibrosis, we show that interleukin (IL)-13 is required at all stages of Schistosomiasis mansoni infection to induce fibrosis. IL-4 production was preserved in IL-13-deficient mice, yet failed to significantly contribute to the fibrotic response in either acute or chronic infection. Significant fibrosis develops in all infected mice, although the magnitude of the response varies widely in inbred mice. C3H/HeN, BALB/c, and C57BL/6 mice develop high, intermediate, and low levels of fibrosis, respectively. Despite these differences, IL-13 antagonism resulted in a marked amelioration of fibrosis in all strains. The fibrotic mechanism in the high-and low-responder strains was unrelated to their tissue eosinophil or mast cell responses, but did correlate with their patterns of IL-13, IL-10, and interferon gamma (IFN-␥) mRNA expression. Indeed, severe fibrosis correlated with a high IL-13 and low IFN-␥/IL-10 mRNA response. Because fibrotic diseases are typically progressive disorders, an important issue was to determine whether IL-13 inactivation might be used to treat an established and ongoing fibrotic disease. Here, IL-13 antagonism was highly efficacious, even after fibrosis and the Th2 cytokine response were firmly established. These studies demonstrate the central role played by IL-13 in fibrogenesis and suggest that therapeutic approaches aimed at disrupting the IL-13 pathway will be highly effective at preventing fibrotic disease caused by chronic Th2-mediated inflammatory reactions. (HEPATOLOGY 2001;34:273-282.)

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“…Mast cells were derived from bone marrow from both MIF ϩ/ϩ and MIF Ϫ/Ϫ mice in the presence of murine IL-3 (PeproTech) as previously reported (12). PWM-stimulated mast cells were prepared by differentiating bone marrow cells in medium containing PWM-stimulated, splenocyte-conditioned medium as described (13).…”

Section: Preparation Of Lung Dendritic Cells Splenocytes Cd4 ϩ T Cementioning

confidence: 99%

Cutting Edge: Deficiency of Macrophage Migration Inhibitory Factor Impairs Murine Airway Allergic Responses

Wang

Huang

Wolters

et al. 2006

The Journal of Immunology

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Increased levels of macrophage migration inhibitory factor (MIF) in serum, sputum, and bronchioalveolar lavage fluid (BALF) from asthmatic patients and time/dose-dependent expression of MIF in eosinophils in response to phorbol myristate acetate suggest the participation of MIF in airway inflammation. In this study, we examined inflammation in OVA-sensitized mouse lungs in wild-type and MIF-deficient mice (MIF−/−). We report increased MIF in the lung and BALF of sensitized wild-type mice. MIF−/− mice demonstrated significant reductions in serum IgE and alveolar inflammatory cell recruitment. Reduced Th1/Th2 cytokines and chemokines also were detected in serum or BALF from MIF−/− mice. Importantly, alveolar macrophages and mast cells, but not dendritic cells or splenocytes, from MIF−/− mice demonstrated impaired CD4+ T cell activation, and the reconstitution of wild-type mast cells in MIF−/− mice restored the phenotype of OVA-induced airway inflammation, revealing a novel and essential role of mast cell-derived MIF in experimentally induced airway allergic diseases.

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Interleukin 4 as an essential factor for in vitro clonal growth of murine connective tissue-type mast cells.

Cited by 263 publications

References 19 publications

Recurrent Milk Aspiration Produces Changes in Airway Mechanics, Lung Eosinophilia, and Goblet Cell Hyperplasia in a Murine Model

Recurrent Milk Aspiration Produces Changes in Airway Mechanics, Lung Eosinophilia, and Goblet Cell Hyperplasia in a Murine Model

Studies of murine schistosomiasis reveal interleukin-13 blockade as a treatment for established and progressive liver fibrosis

Cutting Edge: Deficiency of Macrophage Migration Inhibitory Factor Impairs Murine Airway Allergic Responses

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