Presentation is loading. Please wait.

Presentation is loading. Please wait.

Mast cell TNF receptors regulate responses to Mycoplasma pneumoniae in surfactant protein A (SP-A)−/− mice  Bethany J. Hsia, PhD, Julie G. Ledford, PhD,

Published by찬 요 Modified over 5 years ago

Similar presentations

Presentation on theme: "Mast cell TNF receptors regulate responses to Mycoplasma pneumoniae in surfactant protein A (SP-A)−/− mice  Bethany J. Hsia, PhD, Julie G. Ledford, PhD,"— Presentation transcript:

1 Mast cell TNF receptors regulate responses to Mycoplasma pneumoniae in surfactant protein A (SP-A)−/− mice  Bethany J. Hsia, PhD, Julie G. Ledford, PhD, Erin N. Potts-Kant, BS, Vinayak S. Nikam, BS, Njira L. Lugogo, MD, W. Michael Foster, PhD, Monica Kraft, MD, Soman N. Abraham, PhD, Jo Rae Wright, PhD  Journal of Allergy and Clinical Immunology  Volume 130, Issue 1, Pages e2 (July 2012) DOI: /j.jaci Copyright © 2012 American Academy of Allergy, Asthma & Immunology Terms and Conditions

2 Fig 1 Mycoplasma pneumoniae (Mp) positivity and TNF-α levels in asthmatic samples. A, TNF-α in human BAL fluid (fold over healthy subjects). ∗∗P < .01, asthmatic patients (high) versus asthmatic patients (low) and both asthma groups versus healthy subjects. B, RT-PCR for M pneumoniae–specific P1 adhesin and dilution of samples into SP-4 broth to verify M pneumoniae positivity in subjects. ∗P < .05, asthmatic patients (high) versus healthy subjects and asthmatic patients (low). C, TNF values in M pneumoniae–positive and M pneumoniae–negative samples. ∗∗P < .01. Journal of Allergy and Clinical Immunology  , e2DOI: ( /j.jaci ) Copyright © 2012 American Academy of Allergy, Asthma & Immunology Terms and Conditions

3 Fig 2 MCs in Mycoplasma pneumoniae (Mp)–infected lung tissue. Mice were instilled with saline (A) or M pneumoniae (B-E) and lungs were analyzed by means of immunohistochemistry 3 days after infection for MCs. Fig 2, C, MCs adjacent to the large airway. Fig 2, D, Extracellular MC granules (arrow). Fig 2, E, MCs in the lung parenchyma. F, Total number of tissue MCs assessed in WT versus SP-A−/− lungs (n = 5 each). ∗P < .05. Journal of Allergy and Clinical Immunology  , e2DOI: ( /j.jaci ) Copyright © 2012 American Academy of Allergy, Asthma & Immunology Terms and Conditions

4 Fig 3 Contribution of MCs to AHR and inflammation. A and B, Three days after Mycoplasma pneumoniae (Mp), AHR to methacholine challenge was measured by using the Flexivent system. Mean percentage over baseline for highest methacholine dose is shown in parentheses. ∗∗P < .01 and ^P < .01, 3 independent experiments per graph. C and D, Cells in BAL fluid 12 hours (Fig 3, C) or 72 hours (Fig 3, D) after infection. ∗P < .05 versus WT M pneumoniae unless otherwise noted. E, Total protein in BAL fluid, n ≥ 12 mice per group. Journal of Allergy and Clinical Immunology  , e2DOI: ( /j.jaci ) Copyright © 2012 American Academy of Allergy, Asthma & Immunology Terms and Conditions

5 Fig 4 AHR in WT bone marrow–derived MC–reconstituted infected mice. A, Engraftment of MCs (arrows) verified by means of immunohistochemistry in lung tissue 1 month after injection. B, Quantification of engraftment. C, AHR to methacholine challenge was measured by using the Flexivent system. Mean percentage over baseline for highest methacholine dose is shown in parentheses. ∗∗P < .01, #P < .01, and ^P < 0.05, 3 independent experiments per graph. D, TNF-α in BAL fluid 12 hours after infection. ∗P < .05 versus WT Mycoplasma pneumoniae group, n ≥ 12 mice per group. Mp, Mycoplasma pneumoniae. Journal of Allergy and Clinical Immunology  , e2DOI: ( /j.jaci ) Copyright © 2012 American Academy of Allergy, Asthma & Immunology Terms and Conditions

6 Fig 5 TNF-α production from Mycoplasma pneumoniae (Mp)–stimulated MCs. Nonstimulated (NS) or M pneumoniae–stimulated (multiplicity of infection, 100:1) bone marrow–derived MCs with and without SP-A (40 μg/mL) were analyzed over 14 hours (A) or 1 hour (B). Supernatants were analyzed for TNF-α release by means of ELISA; cell pellets were assessed by using RT-PCR for TNF-α transcription. ∗P < .05. Data are representative of 3 independent experiments. Journal of Allergy and Clinical Immunology  , e2DOI: ( /j.jaci ) Copyright © 2012 American Academy of Allergy, Asthma & Immunology Terms and Conditions

7 Fig 6 Contribution of MC TNF-R to AHR and mucus. Mice were engrafted with TNF-α−/− or TNF-R−/− bone marrow–derived MCs. A, AHR to methacholine challenge was measured by using the Flexivent system. Mean percentage over baseline for highest methacholine dose is shown in parentheses. ∗∗, ^, #, $P < .01, 3 independent experiments per graph, n ≥ 12 mice per group. B and C, PAS-stained airways in infected mice (original magnification ×10) were scored. ∗∗∗P < .001, ∗∗P < .01, and ∗P < .05; n = 7-12 sections per group. Mp, Mycoplasma pneumoniae. Journal of Allergy and Clinical Immunology  , e2DOI: ( /j.jaci ) Copyright © 2012 American Academy of Allergy, Asthma & Immunology Terms and Conditions

8 Fig 7 Contribution of MCs to Mycoplasma pneumoniae (Mp) clearance. M pneumoniae burden in lung tissue at day 3 was measured by using RT-PCR for the M pneumoniae–specific P1 adhesin gene relative to β-actin and is expressed as fold over WT M pneumoniae–infected mice. ∗P < .05, n ≥ 12 mice per group. Journal of Allergy and Clinical Immunology  , e2DOI: ( /j.jaci ) Copyright © 2012 American Academy of Allergy, Asthma & Immunology Terms and Conditions

9 Fig 8 Protective role of SP-A against Mycoplasma pneumoniae (Mp)–induced AHR. SP-A binds M pneumoniae in the large airway and prevents overcolonization. If SP-A is dysfunctional, more M pneumoniae burden results in TNF-α overproduction from epithelial cells, alveolar macrophages(AMs), and/or neutrophils (PMNs). TNF-α encounters tissue MCs in the submucosa, which are stimulated through the TNF-R to release mediators that contribute to high levels of AHR. Journal of Allergy and Clinical Immunology  , e2DOI: ( /j.jaci ) Copyright © 2012 American Academy of Allergy, Asthma & Immunology Terms and Conditions

10 Fig E1 AHR in KitW-sh/W-sh–engrafted mice. Mice were engrafted with MCs for 1 month. AHR to methacholine challenge was assessed by using the Flexivent system. ∗∗P < .01. Mp, Mycoplasma pneumoniae. Journal of Allergy and Clinical Immunology  , e2DOI: ( /j.jaci ) Copyright © 2012 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Download ppt "Mast cell TNF receptors regulate responses to Mycoplasma pneumoniae in surfactant protein A (SP-A)−/− mice  Bethany J. Hsia, PhD, Julie G. Ledford, PhD,"

Similar presentations

Serum amyloid P attenuates M2 macrophage activation and protects against fungal spore–induced allergic airway disease  Ana Paula Moreira, PhD, Karen A.

Serum amyloid P attenuates M2 macrophage activation and protects against fungal spore–induced allergic airway disease  Ana Paula Moreira, PhD, Karen A.
Exposure to allergen and diesel exhaust particles potentiates secondary allergen- specific memory responses, promoting asthma susceptibility  Eric B. Brandt,

Exposure to allergen and diesel exhaust particles potentiates secondary allergen- specific memory responses, promoting asthma susceptibility  Eric B. Brandt,
Surface availability of beta-glucans is critical determinant of host immune response to Cladosporium cladosporioides  Rachael A. Mintz-Cole, PhD, Eric.

Surface availability of beta-glucans is critical determinant of host immune response to Cladosporium cladosporioides  Rachael A. Mintz-Cole, PhD, Eric.
Sejal Saglani, MD, Stephen Lui, PhD, Nicola Ullmann, MD, Gaynor A

Sejal Saglani, MD, Stephen Lui, PhD, Nicola Ullmann, MD, Gaynor A
Russell S. Traister, MD, PhD, Crystal E. Uvalle, BS, Gregory A

Russell S. Traister, MD, PhD, Crystal E. Uvalle, BS, Gregory A
IL-4 induces IL-13–independent allergic airway inflammation

IL-4 induces IL-13–independent allergic airway inflammation
Weiguo Chen, PhD, Umasundari Sivaprasad, PhD, Aaron M

Weiguo Chen, PhD, Umasundari Sivaprasad, PhD, Aaron M
Effective prevention and therapy of experimental allergic asthma using a GATA-3– specific DNAzyme  Serdar Sel, MD, Michael Wegmann, PhD, Tanja Dicke, MSc,

Effective prevention and therapy of experimental allergic asthma using a GATA-3– specific DNAzyme  Serdar Sel, MD, Michael Wegmann, PhD, Tanja Dicke, MSc,
Let-7 microRNA–mediated regulation of IL-13 and allergic airway inflammation  Manish Kumar, MSc, Tanveer Ahmad, MSc, Amit Sharma, PhD, Ulaganathan Mabalirajan,

Let-7 microRNA–mediated regulation of IL-13 and allergic airway inflammation  Manish Kumar, MSc, Tanveer Ahmad, MSc, Amit Sharma, PhD, Ulaganathan Mabalirajan,
The sphingosine-1-phosphate/sphingosine-1-phosphate receptor 2 axis regulates early airway T-cell infiltration in murine mast cell–dependent acute allergic.

The sphingosine-1-phosphate/sphingosine-1-phosphate receptor 2 axis regulates early airway T-cell infiltration in murine mast cell–dependent acute allergic.
Allergy prevention starts before conception: Maternofetal transfer of tolerance protects against the development of asthma  Tobias Polte, PhD, Christian.

Allergy prevention starts before conception: Maternofetal transfer of tolerance protects against the development of asthma  Tobias Polte, PhD, Christian.
Ting-ting Zhang, MSc, Klaus Okkenhaug, PhD, Baher F

Ting-ting Zhang, MSc, Klaus Okkenhaug, PhD, Baher F
Frank Kirstein, PhD, Natalie E

Frank Kirstein, PhD, Natalie E
Lack of autophagy induces steroid-resistant airway inflammation

Lack of autophagy induces steroid-resistant airway inflammation
Exposure to allergen and diesel exhaust particles potentiates secondary allergen- specific memory responses, promoting asthma susceptibility  Eric B. Brandt,

Exposure to allergen and diesel exhaust particles potentiates secondary allergen- specific memory responses, promoting asthma susceptibility  Eric B. Brandt,
Pentraxin 3 deletion aggravates allergic inflammation through a TH17-dominant phenotype and enhanced CD4 T-cell survival  Jyoti Balhara, MSc, Lianyu Shan,

Pentraxin 3 deletion aggravates allergic inflammation through a TH17-dominant phenotype and enhanced CD4 T-cell survival  Jyoti Balhara, MSc, Lianyu Shan,
Autocrine hemokinin-1 functions as an endogenous adjuvant for IgE-mediated mast cell inflammatory responses  Tina L. Sumpter, PhD, Chin H. Ho, MD, Anna.

Autocrine hemokinin-1 functions as an endogenous adjuvant for IgE-mediated mast cell inflammatory responses  Tina L. Sumpter, PhD, Chin H. Ho, MD, Anna.
Restoration of T-box–containing protein expressed in T cells protects against allergen- induced asthma  Jung Won Park, MD, Hyun Jung Min, MS, Jung Ho Sohn,

Restoration of T-box–containing protein expressed in T cells protects against allergen- induced asthma  Jung Won Park, MD, Hyun Jung Min, MS, Jung Ho Sohn,
Leukocyte nicotinamide adenine dinucleotide phosphate-reduced oxidase is required for isocyanate-induced lung inflammation  Si-Yen Liu, PhD, Wei-Zhi Wang,

Leukocyte nicotinamide adenine dinucleotide phosphate-reduced oxidase is required for isocyanate-induced lung inflammation  Si-Yen Liu, PhD, Wei-Zhi Wang,
Allergic airway disease is unaffected by the absence of IL-4Rα–dependent alternatively activated macrophages  Natalie E. Nieuwenhuizen, PhD, Frank Kirstein,

Allergic airway disease is unaffected by the absence of IL-4Rα–dependent alternatively activated macrophages  Natalie E. Nieuwenhuizen, PhD, Frank Kirstein,

Similar presentations

Ads by Google