scholarly journals Role of Mast Cells in Antigen-Induced Airway Inflammation and Bronchial Hyperresponsiveness in Rats

2001 ◽  
Vol 85 (3) ◽  
pp. 250-259 ◽  
Author(s):  
Naoki Kawada ◽  
Hiroyuki Tanaka ◽  
Toshiaki Takizawa ◽  
Takatoshi Yamada ◽  
Yoshimasa Takahashi ◽  
...  
Keyword(s):  
Mast Cells ◽  
Airway Inflammation ◽  
Bronchial Hyperresponsiveness

Childhood Asthma: Update

1992 ◽  
Vol 13 (11) ◽  
pp. 403-412
Author(s):  
Gail G. Shapiro
Keyword(s):  
Smooth Muscle ◽  
Mast Cells ◽  
Airway Inflammation ◽  
Immunoglobulin E ◽  
Bronchial Hyperresponsiveness ◽  
Basement Membrane Thickening ◽  
Infiltrating Cells ◽  
Lung Biopsies ◽  
Airways Reactivity ◽  
Mast Cell Mediator Release

Definition and Pathophysiology Asthma is a reversible airways disease characterized by both smooth muscle hyperreactivity and airway inflammation. During the 1970s and early 1980s the focus was on smooth muscle constriction, and it was believed that better bronchodilators would greatly diminish our difficulties in controlling this condition. This, unfortunately, was not the case. The emphasis of therapy today has turned to airway inflammation. Lung biopsies from patients who have asthma show destruction of respiratory epithelium, basement membrane thickening, and inflammatory cellular infiltrate. Among the infiltrating cells are eosinophils, macrophages, and neutrophils that are called to the site of inflammation by the chemotactic products released by activated mast cells. Upon their arrival, these cells release their own products of inflammation, which amplify this immunologic response. A variety of neuropeptides also play a role, some serving to stabilize and others to destabilize the airway. One result of this airway inflammation is airways reactivity, also known as bronchial hyperresponsiveness. A common example of this scenario is the child who has allergic asthma and encounters a problematic allergen. This child has immunoglobulin E (IgE) to this allergen bound to mast cells in his or her airway. Upon exposure to the allergen, the binding of IgE and antigen triggers mast cell mediator release within minutes.

scholarly journals The murine CCR3 receptor regulates both the role of eosinophils and mast cells in allergen-induced airway inflammation and hyperresponsiveness

2002 ◽  
Vol 99 (3) ◽  
pp. 1479-1484 ◽  
Author(s):  
A. A. Humbles ◽  
B. Lu ◽  
D. S. Friend ◽  
S. Okinaga ◽  
J. Lora ◽  
...  
Keyword(s):  
Mast Cells ◽  
Airway Inflammation

IL-33 induces Th17-mediated airway inflammation via mast cells in ovalbumin-challenged mice

2012 ◽  
Vol 302 (4) ◽  
pp. L429-L440 ◽  
Author(s):  
Kyung-Ah Cho ◽  
Jee Won Suh ◽  
Jung Ho Sohn ◽  
Jung Won Park ◽  
Hyejin Lee ◽  
...  
Keyword(s):  
Mast Cells ◽  
Airway Inflammation ◽  
Allergic Asthma ◽  
Th2 Cytokine ◽  
Cytokine Levels ◽  
Th17 Differentiation ◽  
Deficient Mice ◽  
Important Cytokine

Allergic asthma is characterized by infiltration of eosinophils, elevated Th2 cytokine levels, airway hyperresponsiveness, and IgE. In addition to eosinophils, mast cells, and basophils, a variety of cytokines are also involved in the development of allergic asthma. The pivotal role of eosinophils in the progression of the disease has been a subject of controversy. To determine the role of eosinophils in the progression of airway inflammation, we sensitized and challenged BALB/c wild-type (WT) mice and eosinophil-deficient ΔdblGATA mice with ovalbumin (OVA) and analyzed different aspects of inflammation. We observed increased eosinophil levels and a Th2-dominant response in OVA-challenged WT mice. In contrast, eosinophil-deficient ΔdblGATA mice displayed an increased proportion of mast cells and a Th17-biased response following OVA inhalation. Notably, the levels of IL-33, an important cytokine responsible for Th2 immune deviation, were not different between WT and eosinophil-deficient mice. We also demonstrated that mast cells induced Th17-differentiation via IL-33/ST2 stimulation in vitro. These results indicate that eosinophils are not essential for the development of allergic asthma and that mast cells can skew the immune reaction predominantly toward Th17 responses via IL-33 stimulation.

Histamine as a Modulator of Airway Hyperreactivity L'histamine comme médiateur de l'hyperreactivité des voies aériennes

1987 ◽  
Vol 65 (3) ◽  
pp. 434-434
Author(s):  
John F. Burka
Keyword(s):  
Mast Cells ◽  
Airway Inflammation ◽  
Complex Disease ◽  
Muscle Tone ◽  
Platelet Activating Factor ◽  
Inflammatory Cells ◽  
Airway Hyperreactivity ◽  
Systematic Analysis ◽  
Inflammatory Reactions

Histamine has long been known as a bronchoconstrictor agonist, but its role in asthma and airway inflammation is not as clear. Histamine release occurs in response to allergic challenge of mast cells. However, it is now known that mast cells are heterogeneous in responsiveness and sensitivity to antiallergic agents. Other cells, such as alveolar macrophages, neutrophils, eosinophils, and lymphocytes, can also be activated during allergic and inflammatory reactions. Damage to the airway epithelium would reduce the release of an epithelium-derived relaxant factor and thus increase airway smooth muscle tone. Released mediators, including eicosanoids, platelet-activating factor (PAF), complement fragments, and neurotransmitters, also contribute to inflammation in the airways and the interaction of all these mediators complicates the interpretation of the role of individual mediators. Not only can individual mediators affect the biological activity of other mediators, but their synthesis and release can be modulated as well.The present symposium was organized to examine the putative role of histamine in airway hyperreactivity and how it might interact with other mediators. Papers were presented on the role of mast cells and epithelial cells in allergic bronchoconstriction. The interaction of mast cells with other inflammatory cells was also reviewed. Further information was presented on the biological characteristics of epithelium-derived relaxant factor. Other papers reviewed the interaction of mediators on bronchoconstrictor activity and in inflammation-induced changes in microvascular permeability. The speakers emphasized that asthma and other forms of airway inflammation are complex disease entities and that a systematic analysis of interactions between the cells and mediators in the airways is necessary to understand the aetiology of these diseases and to develop improved therapeutic regimens.This symposium was supported by the Pharmacological Society of Canada, the Canadian Histamine Association, the Upjohn Company of Canada, and Merck Frosst Canada Inc.

scholarly journals Human FcγRIIA induces anaphylactic and allergic reactions

Blood ◽  
2012 ◽  
Vol 119 (11) ◽  
pp. 2533-2544 ◽  
Author(s):  
Friederike Jönsson ◽  
David A. Mancardi ◽  
Wei Zhao ◽  
Yoshihiro Kita ◽  
Bruno Iannascoli ◽  
...  
Keyword(s):  
Mast Cells ◽  
Transgenic Mice ◽  
Airway Inflammation ◽  
Allergic Reactions ◽  
Systemic Anaphylaxis ◽  
Human Mast Cells ◽  
Ige Receptors ◽  
Igg Receptors

AbstractIgE and IgE receptors (FcϵRI) are well-known inducers of allergy. We recently found in mice that active systemic anaphylaxis depends on IgG and IgG receptors (FcγRIIIA and FcγRIV) expressed by neutrophils, rather than on IgE and FcϵRI expressed by mast cells and basophils. In humans, neutrophils, mast cells, basophils, and eosinophils do not express FcγRIIIA or FcγRIV, but FcγRIIA. We therefore investigated the possible role of FcγRIIA in allergy by generating novel FcγRIIA-transgenic mice, in which various models of allergic reactions induced by IgG could be studied. In mice, FcγRIIA was sufficient to trigger active and passive anaphylaxis, and airway inflammation in vivo. Blocking FcγRIIA in vivo abolished these reactions. We identified mast cells to be responsible for FcγRIIA-dependent passive cutaneous anaphylaxis, and monocytes/macrophages and neutrophils to be responsible for FcγRIIA-dependent passive systemic anaphylaxis. Supporting these findings, human mast cells, monocytes and neutrophils produced anaphylactogenic mediators after FcγRIIA engagement. IgG and FcγRIIA may therefore contribute to allergic and anaphylactic reactions in humans.

Sign in / Sign up

Export Citation Format

Share Document