Airway mucosa

Allergic rhinitis A highly prevalent, allergen-induced, upper airway inflammatory disease characterized by chronic hyperreactive airway mucosa with periods of acute exacerbations. 

Bronchial epithelial cells participate in inflammation by releasing eicosanoids, peptidases, matrix proteins, cytokines, and nitric oxide. Epithelial shedding results in heightened airway responsiveness, altered permeability of the airway mucosa, depletion of epithelial-derived relaxant factors, and loss of enzymes responsible for degrading inflammatory neuropeptides. 

Park, H.-S., Hwange, S-C, Nahm, D-H, andYim, H., Immunohistochemical characterization of the cellular infiltrate in airway mucosa of toluene diisocyanate (TDI)- induced asthma comparison with allergic asthma, J. Korean Med. Sci., 13, 1998. 

Atopic dermatitis has been proposed to be the cutaneous manifestation of IgE-mediated hypersensitive reaction to allergenic substances [29]. Conceptually, antagonizing IgE emerges as a logical therapeutic option. Systemic treatment with omalizumab, however, appears to be less efficacious in the skin than in the airway mucosa [23]. It is possible that small molecule Syk inhibitors may offer a more suitable mode to reach and prevent activation of sensitized dermal mast cells and dendritic cells. 

Greiff L, Andersson M, Svensson J, Wollmer P, Lundin S, Persson CGA (2002) Absorption across nasal airway mucosa in house dust mite perennial allergic rhinitis. Clin Physiol Funct Imaging 22 55-57. 

Huh JC, Strickland DH, Jahnsen FL, Turner DJ, Thomas JA, Napoli S, Tobagus I, Stumbles PA, Sly PD, Holt PG Bidirectional interactions between antigen-bearing respiratory tract dendritic cells (DCs) and T cells precede the late phase reaction in experimental asthma DC activation occurs in the airway mucosa but not in the lung parenchyma. J Exp Med 2003 198 19-30. 

Bronchial biopsies of subjects with occupational asthma induced by TDI revealed pathologic features such as increased number of inflammatory cells in the airway mucosa and thickening of subepithelial collagen. ... 

Airflow obstruction in asthma is due to bronchoconstriction resulting from contraction of bronchial smooth muscle, inflammation of the bronchial wall, and increased mucous secretion. Asthmatic attacks may be related to recent exposure to allergens, inhaled irritants leading to bronchial hyperactivity and inflammation of the airway mucosa. The symptoms of asthma may be effectively treated by several drugs, but none of the agents provide a cure for this obstructive lung disease. 

Chronic bronchitis is characterized by increased mucus production and hypertrophy of the mucus glands in the airway mucosa. It is defined as the presence of a chronic or recurrent cough with sputum production on most days, for at least three months of the year, during at least two consecutive years. Patients have hypoxia and retain excess CCh-they are sometimes referred to as blue bloaters. 

Pulmonary Dyspnea, necrosis of large airway mucosa with sloughing, chemical pneumonitis, pulmonary edema, ARDS, respiratory failure. 

B.B., Crit. Rev. Immunol. 24, 297-320, 2004 Fiset, P.O., Cameron, L., and Hamid, Q., Local isotype switching to IgE in airway mucosa, J. Allergy Clin. Immunol. 116, 233-236, 2005 Min, I.M. and Seising, E., Antibody class switch recombination roles for switch seqences and mismatch repair proteins, Adv. Immunol. 87, 297-328, 2005 Apian, P.D., Causes of oncogenic chromosomal translocation. Trends Genet. 22, 46-55, 2006. 

Churg A, Stevens B. 1993. Absence of amosite asbestos in airway mucosa of non-smoking long term workers with occupational exposure to asbestos. Br J Ind Med 50(4) 355-359. 

Macs are ubiquitous throughout the respiratory tract, and discrete populations can be discerned in the airway mucosa, the lung parenchyma ( interstitial macrophages IMs), the luminal surface of the alveoli (pulmonary alveolar macrophages PAMs) and the conducting airways, and in the vascular bed ( intravascular macrophages IVMs). The latter represent a stable marginated population, intimately associated with the endothelial basement membrane they are most common in ruminants (Winkler, 1989) but also occur in humans. 

Additionally, it is clear that a consistent feature of diseases such as asthma is the recruitment of monocytes into the alveolar spaces and the airway mucosa (Beasley etal., 1989 Poston etal., 1992). Monocytes are potent APCs for reactivation of primed T cells, and these cells additionally secrete cytokines such as GM-CSF and IL-1. 

Microvascular endothelial cells play a key role in coordinating the inflammatory response of the airway mucosa. Increased endothelial permeability and adhesion of leukocytes to the luminal surface of the endothelium are characteristic features of inflammation. By governing the... 

Asthma is a respiratory illness characterized by variable and reversible airflow obstruction. Over 100 years ago. Osier, in his influential Textbook of Medicine (Osier, 1892), concluded that airway wall edema, bronchoconstriaion and mucus plugging are responsible for the airflow obstruction in asthma. Since that time, edema of the airway mucosa has been assumed to be one of the central features of asthma, but comparatively few studies have addressed the issue directly. Therefore, there is litde information about the onset, duration, magnitude, location, mechanism, consequences and management of mucosal edema in asthma. 

The airways receive their blood supply from the systemic circulation via laryngeal, tracheal and bronchial arteries. In the trachea and large bronchi of humans and other large mammals, branches of arterioles deep in the airway wall supply the airway mucosa. In some peripheral airways, mucosal vessels may be supplied by the pulmonary circulation through vascular anastomoses. The airway mucosa has a rich blood supply, with a p>articularly extensive vascular network located immediately beneath the epithelium. Mucosal capillaries are tributaries of an extensive system of venules. In humans, a superficial plexus of venules connects with another plexus of venules located deeper in the mucosa. 

These observations demonstrate how rapidly edema can form in the human airway mucosa, but it is unknown how the changes relate to those found in asthmatics exposed to inhaled allergens. For example, there is a report that allergens applied directly to the airway mucosa increase the amounts of protein and inflammatory cells in BAL fluid more than do inhaled allergens (Calhoun etal., 1993). 

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