TNF can contribute to multiple features of ovalbumin-induced allergic inflammation of the airways in mice

Nakae, Susumu; Lunderius, Carolina; Ho, Lien H.; Schäfer, Beatrix; Tsai, Mindy; Galli, Stephen J.

doi:10.1016/j.jaci.2006.11.701

Cited by 90 publications

(71 citation statements)

References 47 publications

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“…This increased bronchial hyperresponsiveness to methacholine in BALB/c mice could also be explained by increased mast cell numbers found in the lung tissue of those mice since the degranulation of these cells induces a release of mediators such as histamine, leukotrienes, and TNF-α [22]. Those mediators markedly increase vascular permeability, followed by inflammatory cell recruitment, and further release of pro-inflammatory mediators, but they also act directly on smooth muscle cells and consequently increase bronchial hyperreactivity [23][24][25]. Mast cells are also a major source of IL-4, which is increased in those mice after allergen exposure [26].…”

Section: Discussionmentioning

confidence: 99%

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Mouse models of asthma: a comparison between C57BL/6 and BALB/c strains regarding bronchial responsiveness, inflammation, and cytokine production

et al. 2009

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Objective Animal models of asthma mimic major features of human disease. Since the genetic background of experimental animals might affect hyperresponsiveness and inflammation, we studied its potential influence and the mechanisms leading to differences in strains. MethodsWe applied a mouse model of allergic asthma to BALB/c and C57BL/6 mice.Results BALB/c mice displayed greater levels of airway reactivity to methacholine than C57BL/6 mice. Moreover, BALB/c mice exhibited higher numbers of mast cells in lung tissue when compared to C57BL/6. On the contrary, eosinophil and neutrophil counts in bronchoalveolar lavage fluid (BALF) as well as peribronchial eosinophilia were greater in C57BL/6. IL (Interleukin)-4, IL-5, IL-13, and CCL11 levels measured in wholelung extracts were higher in BALB/c, while, in sharp contrast, CCL11 and CCL5 levels were higher in BALF of C57BL/6 mice. ConclusionsWe observed phenotypic differences between C57BL/6 and BALB/c mice in an asthma model with different distributions of pro-inflammatory cytokines and inflammatory cells.

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Section: Discussionmentioning

confidence: 99%

“…Penh was measured for 3 min in baseline conditions. Mice were then exposed to the inhalation of PBS and subsequent increasing doses of MCh (3,6,12,24, and 48 g/l) during 1 min. Every aerosol was separated by a 15-min recovery period in order to allow airway Penh to go back to baseline level.…”

Section: Bronchial Airway Responsiveness Measurementmentioning

confidence: 99%

Mouse models of asthma: a comparison between C57BL/6 and BALB/c strains regarding bronchial responsiveness, inflammation, and cytokine production

et al. 2009

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“…47,48 Because TNF-α expression preceded increases in SP-D levels during the allergic airway response, we tested whether this cytokine can contribute to upregulation of SP-D production without allergic sensitization. Interestingly, mice specifically overexpressing TNF-α in alveolar type II cells [43][44][45] had increased SP-D levels.…”

Section: Discussionmentioning

confidence: 99%

Surfactant protein D inhibits TNF-α production by macrophages and dendritic cells in mice

Hortobagyi

Kierstein

Krytska

et al. 2008

Journal of Allergy and Clinical Immunology

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“…Presence of inflammatory cells can be confirmed by Hematoxylin & Eosin stain (Figure 2A) and presence of mucus production can be assessed by Periodic-acid-Schiff stain ( Figure 2B ). Altogether this will confirm induction of airway allergic inflammation following OVA challenge of OVA-sensitized mice 8 . In contrast, lung sections from Saline treated mice are expected to be free of any inflammation along with absence of any mucus production.…”

Section: Representative Resultsmentioning

confidence: 64%

Analysis of Pulmonary Dendritic Cell Maturation and Migration during Allergic Airway Inflammation

Kushwah

2012

JoVE

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Dendritic cells (DCs) are the key players involved in initiation of adaptive immune response by activating antigen-specific T cells. DCs are present in peripheral tissues in steady state; however in response to antigen stimulation, DCs take up the antigen and rapidly migrate to the draining lymph nodes where they initiate T cell response against the antigen 1,2 . Additionally, DCs also play a key role in initiating autoimmune as well as allergic immune response 3 .DCs play an essential role in both initiation of immune response and induction of tolerance in the setting of lung environment 4 . Lung environment is largely tolerogenic, owing to the exposure to vast array of environmental antigens 5 . However, in some individuals there is a break in tolerance, which leads to induction of allergy and asthma. In this study, we describe a strategy, which can be used to monitor airway DC maturation and migration in response to the antigen used for sensitization. The measurement of airway DC maturation and migration allows for assessment of the kinetics of immune response during airway allergic inflammation and also assists in understanding the magnitude of the subsequent immune response along with the underlying mechanisms.Our strategy is based on the use of ovalbumin as a sensitizing agent. Ovalbumin-induced allergic asthma is a widely used model to reproduce the airway eosinophilia, pulmonary inflammation and elevated IgE levels found during asthma 6,7 . After sensitization, mice are challenged by intranasal delivery of FITC labeled ovalbumin, which allows for specific labeling of airway DCs which uptake ovalbumin. Next, using several DC specific markers, we can assess the maturation of these DCs and can also assess their migration to the draining lymph nodes by employing flow cytometry. Video LinkThe 2. In order to prepare OVA-Alum mixture, take Alum in a tube and add OVA solution in a dropwise fashion while vortexing the tube at a ratio of 1:1. Stir the mixture for 30 minutes and use right away after mixing. 3. Using a 1 ml syringe, inject 0.2 ml of the mixture into mouse peritoneal cavity and repeat the injection again after 2 weeks.1. 7 days after the second injection of OVA-Alum, mice are ready to be challenged intranasally with OVA-FITC. 2. Prepare a solution of OVA-FITC (Sigma) using sterile PBS at a concentration of 1 mg/ml and store in aliquots at -80°C. 3. Place a sterile gauze at the bottom of a 50 ml falcon tube and in a chemical hood, add 5 ml of Aerrane onto the gauze. In order to anesthetize mice, direct the animal into the tube for approximately 5-10 seconds. 4. Hold the anesthetized animal in an upright position and using sterile pipette tips, pipette 100 μl of the OVA-FITC solution onto the nares of mice in a drop-wise fashion. 5. Repeat intranasal challenge with OVA-FITC for the next two days.

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TNF can contribute to multiple features of ovalbumin-induced allergic inflammation of the airways in mice

Cited by 90 publications

References 47 publications

Mouse models of asthma: a comparison between C57BL/6 and BALB/c strains regarding bronchial responsiveness, inflammation, and cytokine production

Mouse models of asthma: a comparison between C57BL/6 and BALB/c strains regarding bronchial responsiveness, inflammation, and cytokine production

Surfactant protein D inhibits TNF-α production by macrophages and dendritic cells in mice

Analysis of Pulmonary Dendritic Cell Maturation and Migration during Allergic Airway Inflammation

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