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.

The Pathophysiology of Asthma

1997 ◽  
Vol 10 (3) ◽  
pp. 176-185
Author(s):  
Thomas G. Vondracek ◽  
Walter F. Stanaszek
Keyword(s):  
Airway Inflammation ◽  
T Lymphocyte ◽  
Inflammatory Cells ◽  
Predisposing Factor ◽  
Inflammatory Reactions ◽  
Acute Exacerbations ◽  
Infiltrating Cells ◽  
Mucosal Edema ◽  
Ige Mediated

Atopy predisposes an individual to the development of asthma, whereby specific triggers may repeatedly cause acute exacerbations and contribute to chronic inflammation. This IgE-mediated response to common allergens is the strongest predisposing factor for developing asthma. Airway inflammation involves release of immunological mediators via T lymphocyte dependent, and IgE dependent and independent mechanisms which attract inflammatory cells from the circulation. The role of the eicosanoids as pivotal mediators in promoting some of the changes in asthma has only recently been fully explored. Inflammatory reactions result when mediators and cytokines released from resident and infiltrating cells interact. This interaction also contributes to the bronchoconstriction, hypersecretion, and mucosal edema in the airways.

scholarly journals Airway Epithelium in Atopic and Nonatopic Asthma: Similarities and Differences

ISRN Allergy ◽  
2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Prathap Pillai ◽  
Chris J. Corrigan ◽  
Sun Ying
Keyword(s):  
Mast Cells ◽  
Airway Inflammation ◽  
Airway Epithelium ◽  
Inflammatory Cells ◽  
Inflammatory Disorder ◽  
Pathogenic Mechanisms ◽  
Similarities And Differences ◽  
Available Information

Asthma is an inflammatory disorder of the airways, and the airway epithelium has the central role in its pathogenesis. In general, the airway inflammation is characterised by the infiltration of the epithelium and submucosa by a range of inflammatory cells driven largely by Th-2 lymphocytes, eosinophils, and mast cells. The pathogenic mechanisms of nonatopic asthma in comparison to its atopic counterpart have always been a subject of debate. Although clinically are two distinct entities, more similarities than differences have been observed between the two in terms of immunopathogenesis, underlying IgE mechanisms, and so on. in a number of previous studies. More information has become available in recent years comparing the ultrastructure of the epithelium in these two types of asthma. A comparison of airway epithelium in atopic and nonatopic asthma is presented here from the available information in the literature. Similarities outnumber the differences, until we unravel the mystery surrounding these two important phenotypes of asthma in more detail.

scholarly journals HDAC2 attenuates airway inflammation by suppressing IL-17A production in HDM-challenged mice

2019 ◽  
Vol 316 (1) ◽  
pp. L269-L279 ◽  
Author(s):  
Tianwen Lai ◽  
Mindan Wu ◽  
Chao Zhang ◽  
Luanqing Che ◽  
Feng Xu ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Inflammatory Cytokines ◽  
Allergic Inflammation ◽  
Allergic Airway Inflammation ◽  
Inflammatory Cells ◽  
Protective Role ◽  
In Vivo Models

Histone deacetylase (HDAC)2 is expressed in airway epithelium and plays a pivotal role in inflammatory cells. However, the role of HDAC2 in allergic airway inflammation remains poorly understood. In the present study, we determined the role of HDAC2 in airway inflammation using in vivo models of house dust mite (HDM)-induced allergic inflammation and in vitro cultures of human bronchial epithelial (HBE) cells exposed to HDM, IL-17A, or both. We observed that HDM-challenged Hdac2+/− mice exhibited substantially enhanced infiltration of inflammatory cells. Higher levels of T helper 2 cytokines and IL-17A expression were found in lung tissues of HDM-challenged Hdac2+/− mice. Interestingly, IL-17A deletion or anti-IL-17A treatment reversed the enhanced airway inflammation induced by HDAC2 impairment. In vitro, HDM and IL-17A synergistically decreased HDAC2 expression in HBE cells. HDAC2 gene silencing further enhanced HDM- and/or IL-17A-induced inflammatory cytokines in HBE cells. HDAC2 overexpresion or blocking IL-17A gene expression restored the enhanced inflammatory cytokines. Collectively, these results support a protective role of HDAC2 in HDM-induced airway inflammation by suppressing IL-17A production and might suggest that activation of HDAC2 and/or inhibition of IL-17A production could prevent the development of allergic airway inflammation.

scholarly journals Expression and Role of the Calcium-Sensing Receptor in Rat Peripheral Blood Polymorphonuclear Neutrophils

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Tai-yu Zhai ◽  
Bao-hong Cui ◽  
Lei Zou ◽  
Jing-ya Zeng ◽  
Song Gao ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Peripheral Blood ◽  
Inflammatory Cells ◽  
Polymorphonuclear Neutrophils ◽  
Calcium Sensing Receptor ◽  
Inflammatory Reactions ◽  
Calcium Sensing ◽  
Pmn Functions ◽  
The Relationship

The calcium-sensing receptors (CaSRs) play an important role in many tissues and organs that are involved in inflammatory reactions. Peripheral blood polymorphonuclear neutrophils (PMNs) are important inflammatory cells. However, the expression and functions of CaSR in peripheral blood PMNs are still not reported. In this study, we collected rat peripheral blood PMNs to observe the relationship between CaSR and PMNs. From the results, we found first that the CaSR protein was expressed in PMNs, and it increased after PMNs were activated with fMLP. In addition, CaSR activator cincalcet promoted the expression of CaSR and P-p65 (NF-κB signaling pathway protein) and Bcl-xl (antiapoptosis protein), and it increased the secretion of interleukin-6 (IL-6) and myeloperoxidase (MPO); meanwhile, it decreased proapoptosis protein Bax expression and the production of IL-10 and reactive oxygen species (ROS). At the same time, cincalcet also decreased the PMN apoptosis rate analyzed by flow cytometry. However, CaSR inhibitor NPS-2143 and NF-κB signaling pathway inhibitor PDTC reverse the results cited earlier. All of these results indicated that CaSR can regulate PMN functions and status to play a role in inflammation, which is probably through the NF-κB signaling pathway.

Airway response to emotional stimuli in asthma: the role of the cholinergic pathway

2010 ◽  
Vol 108 (6) ◽  
pp. 1542-1549 ◽  
Author(s):  
Thomas Ritz ◽  
Antje Kullowatz ◽  
Michael D. Goldman ◽  
Hans-Jürgen Smith ◽  
Frank Kanniess ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Ipratropium Bromide ◽  
Airway Hyperreactivity ◽  
Respiratory Resistance ◽  
Placebo Condition ◽  
Double Blind ◽  
Physiological Basis ◽  
Airway Pathology ◽  
Cholinergic Pathway

In asthma, airways constrict in response to emotion and stress, but underlying mechanisms, potential extrathoracic contributions, and associations with airway pathophysiology have not been elucidated. We therefore investigated the role of the cholinergic pathway in emotion-induced airway responses in patients with asthma and the association of these responses with airway pathophysiology. Patients with asthma ( n = 54) and healthy participants ( n = 25) received either 40 μg ipratropium bromide or a placebo in a double-blind double-dummy cross-over design in two laboratory sessions with experimental emotion induction. Stimuli were preevaluated films and pictures of pleasant, unpleasant, and neutral quality. Respiratory resistance and reactance at 5 and 20 Hz were measured continuously before and during presentations, together with respiration by impedance plethysmography and end-tidal Pco2 by capnometry. In addition, measures of airway inflammation (fraction of exhaled nitric oxide), airway hyperreactivity (methacholine challenge), and reversibility of obstruction were obtained. Respiratory resistance at 5 and 20 Hz increased during unpleasant stimuli in asthma patients. This response was blocked by ipratropium bromide and was not substantially associated with asthma severity, airway inflammation, hyperreactivity and reversibility, or pattern of ventilation and Pco2. Under the placebo condition, changes in resistance during unpleasant films were positively correlated with patients’ reports of psychological asthma triggers. In conclusion, airway constriction to unpleasant stimuli in asthma depends on an intact cholinergic pathway, is largely due to the central airways, and is not substantially associated with other indicators of airway pathology. Its link to the perceived psychological triggers in patients’ daily lives suggests a physiological basis for emotion-induced asthma.

scholarly journals Immunoglobulin E–dependent Active Fatal Anaphylaxis in Mast Cell–deficient Mice

1998 ◽  
Vol 188 (9) ◽  
pp. 1587-1592 ◽  
Author(s):  
Il Hwan Choi ◽  
Young Min Shin ◽  
Jae Seung Park ◽  
Moo Sam Lee ◽  
Eue Hyeog Han ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Immunoglobulin E ◽  
Platelet Activating Factor ◽  
Serum Levels ◽  
Effector Cells ◽  
Plasma Histamine Level ◽  
Central Effector ◽  
Fatal Anaphylaxis

Mast cells have long been believed to be the central effector cells in the development of immunoglobulin (Ig)E-dependent anaphylaxis. In this study, we investigated the role of mast cells in IgE-dependent hapten-induced active fatal anaphylaxis using mast cell–deficient WBB6F1- W/Wv (W/Wv) and congenic normal (+/+) mice. Although a 5-min delay in shock signs and death were observed in W/Wv mice, 100% fatal reactions to penicillin V (Pen V) occurred in both +/+ and W/Wv mice. Administration of monoclonal anti–IL-4 antibody completely prevented the fatal reactions, and the effect of anti–IL-4 was associated with its suppressive activity on Pen V–specific serum levels of IgE, but not IgG. The platelet-activating factor (PAF) antagonist, BN 50739, completely prevented the fatal reactions in both strains of mice. Our kinetic study revealed, in contrast to no elevation of plasma histamine level in W/Wv mice, high levels of PAF in the circulation after challenge in both +/+ and W/Wv mice, albeit to a lesser degree in the latter case. These data indicate that cells other than mast cells are sufficient to induce an IgE-dependent active fatal anaphylaxis by elaborating PAF, which is the critical mediator for fatal murine anaphylaxis.

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
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