scholarly journals Pulmonary Endotoxin Tolerance Protects against Cockroach Allergen-Induced Asthma-Like Inflammation in a Mouse Model

2012 ◽  
Vol 158 (2) ◽  
pp. 120-130 ◽  
Author(s):  
Sudha Natarajan ◽  
Jiyoun Kim ◽  
Jacqueline Bouchard ◽  
William Cruikshank ◽  
Daniel G. Remick
Keyword(s):  
Mouse Model ◽  
Endotoxin Tolerance ◽  
Cockroach Allergen

scholarly journals Abr, a Negative Regulator of Rac, Attenuates Cockroach Allergen–Induced Asthma in a Mouse Model

2013 ◽  
Vol 191 (9) ◽  
pp. 4514-4520 ◽  
Author(s):  
Dapeng Gong ◽  
Fei Fei ◽  
Min Lim ◽  
Min Yu ◽  
John Groffen ◽  
...  
Keyword(s):  
Mouse Model ◽  
Negative Regulator ◽  
Cockroach Allergen

scholarly journals Epithelial Aryl Hydrocarbon Receptor Protects From Mucus Production by Inhibiting ROS-Triggered NLRP3 Inflammasome in Asthma

2021 ◽  
Vol 12 ◽  
Author(s):  
Xinyue Hu ◽  
Yingchun Shen ◽  
Yilin Zhao ◽  
Ji Wang ◽  
Xin Zhang ◽  
...  
Keyword(s):  
Mouse Model ◽  
Aryl Hydrocarbon Receptor ◽  
Airway Inflammation ◽  
Nlrp3 Inflammasome ◽  
Allergic Airway Inflammation ◽  
Ros Generation ◽  
Inflammasome Activation ◽  
Mucus Production ◽  
Aryl Hydrocarbon ◽  
Cockroach Allergen

BackgroundDespite long-standing recognition in the significance of mucus overproduction in asthma, its etiology remains poorly understood. Muc5ac is a secretory mucin that has been associated with reduced pulmonary function and asthma exacerbations.ObjectivesWe sought to investigate the immunological pathway that controls Muc5ac expression and allergic airway inflammation in asthma.MethodsCockroach allergen-induced Muc5ac expression and aryl hydrocarbon receptor (AhR) signaling activation was examined in the human bronchial epithelial cells (HBECs) and mouse model of asthma. AhR regulation of Muc5ac expression, mitochondrial ROS (Mito-ROS) generation, and NLRP3 inflammasome was determined by AhR knockdown, the antagonist CH223191, and AhR-/- mice. The role of NLRP3 inflammasome in Muc5ac expression and airway inflammation was also investigated.ResultsCockroach allergen induced Muc5ac overexpression in HBECs and airways of asthma mouse model. Increased expression of AhR and its downstream genes CYP1A1 and CYP1B1 was also observed. Mice with AhR deletion showed increased allergic airway inflammation and MUC5AC expression. Moreover, cockroach allergen induced epithelial NLRP3 inflammasome activation (e.g., NLRP3, Caspase-1, and IL-1β), which was enhanced by AhR knockdown or the antagonist CH223191. Furthermore, AhR deletion in HBECs led to enhanced ROS generation, particularly Mito-ROS, and inhibition of ROS or Mito-ROS subsequently suppressed the inflammasome activation. Importantly, inhibition of the inflammasome with MCC950, a NLRP3-specifc inhibitor, attenuated allergic airway inflammation and Muc5ac expression. IL-1β generated by the activated inflammasomes mediated cockroach allergen-induced Muc5ac expression in HBECs.ConclusionsThese results reveal a previously unidentified functional axis of AhR-ROS-NLRP3 inflammasome in regulating Muc5ac expression and airway inflammation.

scholarly journals Immune cells and oxidative stress in the endotoxin tolerance mouse model

2010 ◽  
Vol 43 (1) ◽  
pp. 57-67 ◽  
Author(s):  
E.S. Melo ◽  
H.V. Barbeiro ◽  
S. Ariga ◽  
T. Goloubkova ◽  
R. Curi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mouse Model ◽  
Immune Cells ◽  
Endotoxin Tolerance ◽  
And Oxidative Stress

scholarly journals Immune cells and oxidative stress in the endotoxin tolerance mouse model

2010 ◽  
Vol 43 (1) ◽  
Author(s):  
E.S. Melo ◽  
H.V. Barbeiro ◽  
S. Ariga ◽  
T. Goloubkova ◽  
R. Curi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mouse Model ◽  
Immune Cells ◽  
Endotoxin Tolerance ◽  
And Oxidative Stress

Regenerating myofibers in tibialis anterior muscles of young ‘MDX’ mice

1987 ◽  
Vol 45 ◽  
pp. 726-727
Author(s):  
H. D. Geissinge ◽  
L.D. Rhodes
Keyword(s):  
Muscular Dystrophy ◽  
Mouse Model ◽  
Tibialis Anterior ◽  
Physiological Activity ◽  
Mdx Mice ◽  
Mode Of Inheritance

A recently discovered mouse model (‘mdx’) for muscular dystrophy in man may be of considerable interest, since the disease in ‘mdx’ mice is inherited by the same mode of inheritance (X-linked) as the human Duchenne (DMD) muscular dystrophy. Unlike DMD, which results in a situation in which the continual muscle destruction cannot keep up with abortive regenerative attempts of the musculature, and the sufferers of the disease die early, the disease in ‘mdx’ mice appears to be transient, and the mice do not die as a result of it. In fact, it has been reported that the severely damaged Tibialis anterior (TA) muscles of ‘mdx’ mice seem to display exceptionally good regenerative powers at 4-6 weeks, so much so, that these muscles are able to regenerate spontaneously up to their previous levels of physiological activity.

Mouse model of gastric infection with cytotoxin-expressing strain of Helicobacter pylori in studying of pathogenesis of chronic gastric ulcer

1998 ◽  
Vol 13 (11-s4) ◽  
pp. S178-S184 ◽  
Author(s):  
PETER KONTUREK ◽  
TOMASZ BRZOZOWSKI ◽  
STANISLAW KONTUREK ◽  
ELZBIETA KARCZEWSKA ◽  
ROBERT PAJDO ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Ulcer ◽  
Mouse Model ◽  
Chronic Gastric Ulcer
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