Mast cells play a key role in the developmentof late airway hyperresponsiveness through TNF-αin a murine model of asthma

2007 ◽  
Vol 37 (4) ◽  
pp. 1107-1115 ◽  
Author(s):  
Young-Suk Kim ◽  
Hyun-Mi Ko ◽  
Nam-In Kang ◽  
Chang-Ho Song ◽  
Xin Zhang ◽  
...  
2001 ◽  
Vol 107 (6) ◽  
pp. 1019-1024 ◽  
Author(s):  
Lynne C. Fiscus ◽  
Jenny Van Herpen ◽  
Douglas A. Steeber ◽  
Thomas F. Tedder ◽  
Mimi L.K. Tang

2008 ◽  
Vol 38 (12) ◽  
pp. 1959-1968 ◽  
Author(s):  
J. Bilsborough ◽  
E. Chadwick ◽  
S. Mudri ◽  
X. Ye ◽  
W. R. Henderson ◽  
...  

1999 ◽  
Vol 86 (1) ◽  
pp. 202-210 ◽  
Author(s):  
N. Noviski ◽  
J. P. Brewer ◽  
W. A. Skornik ◽  
S. J. Galli ◽  
J. M. Drazen ◽  
...  

Exposure to ambient ozone (O3) is associated with increased exacerbations of asthma. We sought to determine whether mast cell degranulation is induced by in vivo exposure to O3in mice and whether mast cells play an essential role in the development of pulmonary pathophysiological alterations induced by O3. For this we exposed mast cell-deficient WBB6F1- kitW/ kitW-v( kitW/ kitW-v) mice and the congenic normal WBB6F1(+/+) mice to air or to 1 or 3 parts/million O3for 4 h and studied them at different intervals from 4 to 72 h later. We found evidence of O3-induced cutaneous, as well as bronchial, mast cell degranulation. Polymorphonuclear cell influx into the pulmonary parenchyma was observed after exposure to 1 part/milllion O3only in mice that possessed mast cells. Airway hyperresponsiveness to intravenous methacholine measured in vivo under pentobarbital anesthesia was observed in both kitW/ kitW-vand +/+ mice after exposure to O3. Thus, although mast cells are activated in vivo by O3and participate in O3-induced polymorphonuclear cell infiltration into the pulmonary parenchyma, they do not participate detectably in the development of O3-induced airway hyperresponsiveness in mice.


2010 ◽  
Vol 153 (3) ◽  
pp. 223-233 ◽  
Author(s):  
Long Zhu ◽  
Lisheng Zhuo ◽  
Koji Kimata ◽  
Etsuro Yamaguchi ◽  
Hideto Watanabe ◽  
...  

2002 ◽  
Vol 109 (5) ◽  
pp. 621-628 ◽  
Author(s):  
Weilie Ma ◽  
Paul J. Bryce ◽  
Alison A. Humbles ◽  
Dhafer Laouini ◽  
Ali Yalcindag ◽  
...  

2021 ◽  
Vol 35 (S1) ◽  
Author(s):  
Niyati Borkar ◽  
Nilesh Ambhore ◽  
Venkatachalem Sathish

2005 ◽  
Vol 201 (12) ◽  
pp. 1869-1873 ◽  
Author(s):  
Joshua A. Boyce ◽  
K. Frank Austen

Mouse models of T helper type 2 (Th2) cell–biased pulmonary inflammation have elucidated mechanisms of sensitization, cell traffic, and induced airway hyperresponsiveness (AHR). Nonetheless, most mice lack intrinsic AHR, a central property of human asthma, and disparities persist regarding the contributions of eosinophils and mast cells and the sensitivity to induced AHR in the commonly used mouse strains. We suggest that these discordances, reflecting methodological and genetic differences, may be informative for understanding heterogeneity of human asthma.


2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Yun-Zhu Li ◽  
Xue-Yan Lu ◽  
Wei Jiang ◽  
Lin-Feng Li

Qingpeng ointment (QP) is a Chinese medicine which has been used in treatment of atopic dermatitis (AD) in China. AD-like lesions were induced in BALB/c mice by repeated application of 2,4-dinitrofluorobenzene (DNFB) on shaved backs. The mice were then treated for 2 weeks with QP of different concentrations and Mometasone Furoate cream (MF), respectively. Macroscopic and microscopic changes of the skin lesions were observed after the treatment. The levels of serum immunoglobulin (Ig) E, tissue interferon (IFN)-γ, and interleukin (IL)-4 and IL-17A and the levels of involucrin, filaggrin, and kallikrein7 in epidermis were measured. The results show severe dermatitis with immune profiles similar to human acute AD. A significant infiltration of CD4+T and mast cells was observed in dermis of lesion but inhibited by QP after a 2-week treatment with it. The production of IgE, IL-4 and the mRNA expression of IL-17A were also suppressed, but the level of IFN-γwas increased. MF suppressed all production of these cytokines and IgE. Accordingly, the mechanism of QP on AD might correlate with its ability of modulating the immune dysfunctions rather than suppressing them. It had no effect on expressions of involucrin and filaggrin, except that its vehicle decreased the level of kallikrein7.


2013 ◽  
Vol 14 (1) ◽  
pp. 28 ◽  
Author(s):  
Keiko Kan-o ◽  
Yuko Matsunaga ◽  
Satoru Fukuyama ◽  
Atsushi Moriwaki ◽  
Hiroko Hirai-Kitajima ◽  
...  

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