Allergy and the lung

Abstract

SummaryAmong the 'allergic' conditions involving the lung, asthma is the more frequent and the most extensively investigated, although asthma itself may be caused by different disorders. The triggering event in allergic subjects is the reaction allergen-specific immunoglobulin E (IgE) that activates mast cells and initiates a complex and redundant inflammatory process, where cells, cytokines and adhesion molecules are involved at different stages. In fact, mucosal eosinophilic inflammation is one of the distinctive features of asthma and the particular T helper type 2 (Th2) phenotype of allergic patients favours it. In general, the clinical severity of asthma correlates well with the degree of inflammation. None the less, other phenomena such as non-specific bronchial hyperresponsiveness and remodelling intervene in the pathophysiology of allergic asthma. These phenomena are only partially inflammation-related. In particular, the remodelling of the bronchial wall seems to start very early in life and also seems to be a distinctive histological feature of the asthmatic bronchus. The recent introduction of biological treatments (monoclonal antibodies) has allowed elucidation of some of the pathogenic features of allergic asthma.

Natural Killer Cells Accumulate in Lung‐Draining Lymph Nodes and Regulate Airway Eosinophilia in a Murine Model of Asthma

“…Mucosal eosinophilic inflammation is one of the distinctive features of asthma, and the particular T helper type 2 (Th2) phenotype of allergic patients favours it. In general, the clinical severity of asthma correlates well with the degree of inflammation [1]. Numerous studies suggest a key role for the innate immune system in asthma development [2].…”

Inhibitory effect of phytoglycoprotein (24kDa) on allergy-related factors in compound 48/80-induced mast cells in vivo and in vitro

“…IL-4 (one of the Th2 cytokines) promotes B cell differentiation to plasma cells that secrete antigen-specific IgE, and also contributes to the proliferation of mast cells [23]. It has been shown that IgE binds to receptors on the surface of mast cells and stimulates the release of various mediators that promote human immediate hypersensitivity disease, mucus secretion, and increased vascular permeability [24]. It has been reported that compound 48/80 is well known as a potential agent for histamine release from mast cells, with a subsequent depletion of tissue histamine [25].…”

The Effect of Particle Deposition on Immunological Response as Measured by Cytokine Production

“…Studies have shown that exposure to particulate matter, in both human and mouse alveolar epithelial cells, in vitro, can induce expression of a variety of inflammatory cytokines (Barrett et al, 1998;Bonvallot et al, 2001;Aust et al, 2002;Adamson et al, 2004;Singal and Finkelstein, 2005a). There have been great strides in elucidating the mechanism by which particulate matter and allergenic materials promote the transcription of proinflammatory genes in alveolar epithelial cells, as well as other cells related to, or in proximity of, the respiratory tract (Glaab et al, 2005;Keinan et al, 2005;Laumbach et al, 2005;Singal and Finkelstein, 2005a;Barnes, 2008;Boverhof et al, 2008;Ciprandi and Passalacqua, 2008;Lewis et al, 2008;Matsuda et al, 2008;Pantano et al, 2008;Passalacqua and Ciprandi, 2008;Siddiqui et al, 2008;Verstraelen et al, 2008;Desai and Brightling, 2009;Ferguson et al, 2009;Hammad et al, 2009;Prefontaine et al, 2009;Qian et al, 2009;Volckens et al, 2009;Woodruff et al, 2009;Bhattacharyya et al, 2010;Burgess et al, 2010;Cao et al, 2010;Corps et al, 2010;Lambrecht and Hammad, 2010;Olin et al, 2010;Raja et al, 2010;Trivedi and Caughey, 2010;Chu and Chiang, 2011;Chustz et al, 2011;Fuchimoto et al, 2011;…”

“…Nonasthmatic respiratory allergy symptoms may manifest following induction of similar cytokine signaling profiles as with allergic asthma and present with an influx of eosinophils (antigen-specific or not) in the lower respiratory tract Siddiqui et al, 2008). The main profiles on which research is focused are the distinction between the T-helper cell type 1 (Th 1 ) and T-helper cell type 2 (Th 2 ) cytokines (Dearman and Kimber, 1999;Herrick et al, 2000Herrick et al, , 2003Tang et al, 2001;Dearman et al, 2002;Kuperman et al, 2002;Plitnick et al, 2002b;Dearman et al, 2003a,b;Duramad et al, 2004;Eisenbarth et al, 2004;Bisset and Schmid-Grendelmeier, 2005;Piggott et al, 2005;Tsiligianni et al, 2005;Holsapple et al, 2006;Selgrade et al, 2006;Farraj et al, 2007;Barrera et al, 2008;Ciprandi and Passalacqua, 2008;Matsuda et al, 2008;Passalacqua and Ciprandi, 2008;Turato et al, 2008;Zindler et al, 2008;Harada et al, 2009;Holgate and Davies, 2009;Hollams et al, 2009;Prefontaine et al, 2009;Woodruff et al, 2009;Hardy et al, 2010;Lambrecht and Hammad, 2010;Chu and Chiang, 2011;Fuchimoto et al, 2011;Hacha et al, 2012;Krishnaswamy et al, 2012;Makino et al, 2012;…”