Protein content in bronchoalveolar lavage fluid of patients with asthma and control subjects

Vyve, T. Van; Chanez, Pascal; Bernard, Alfred; Bousquet, Jean; Godard, Pierre; Lauwerijs, R; Sibille, Yves

doi:10.1016/s0091-6749(95)70153-2

Cited by 122 publications

(108 citation statements)

References 38 publications

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“…All this evidence suggest that CC16 plays a protective role in the lung, and it is possible that low activity variants of CC16 may be associated with inflammatory lung disorders such as asthma. This view gains support from the observation that asthmatic individuals demonstrate significantly decreased levels of CC16 protein in their bronchoalveolar lavage fluid (BALF) (Van Vyve et al 1995) and serum when compared to normal controls (Shijubo et al 1999). …”

Section: Introductionmentioning

confidence: 98%

Association of an intragenic microsatellite marker in the CC16 gene with asthma in the Indian population

Sharma

Ghosh

2004

J Hum Genet

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The gene for Clara cell secretory protein (CC16) is an ideal candidate for investigating genetic predisposition to asthma because of its role in the airway as an antiinflammatory molecule, differences in its levels between asthmatics and healthy controls, and its genetic location (11q13). We investigated the association of an SNP (A38G) and an intragenic repeat polymorphism in the CC16 gene with asthma and its associated traits, such as total serum IgE levels, in a case control as well as in a family based study design. A significant association was observed for the microsatellite repeat at the level of alleles and genotypes with asthma (P<0.05) in both the study designs. However, no association was observed for the A38G SNP with asthma. When haplotypes were constructed for these two loci and compared, the haplotype A_18 was found at higher frequency in patients (OR=1.59, 95%CI=1.08, 2.33, P=0.016). Also, in the family based design, a biased transmission was observed for haplotypes from parents to affected offspring (P=0.003). Individually, haplotype A_18 showed preferential transmission (82.6%) to affected offspring (P=0.001), thereby confirming the case-control results. In summary, this is the first study identifying the CC16 gene to be associated with asthma in the Indian population.

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Section: Introductionmentioning

confidence: 98%

Association of an intragenic microsatellite marker in the CC16 gene with asthma in the Indian population

Sharma

Ghosh

2004

J Hum Genet

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“…Mucosal immunity mechanisms remain poorly explored in respiratory diseases. Our group found diminished concentrations of SC in the BAL of asthmatics compared with normal controls [8], which could be related to the imbalance between Th1 and Th2 subpopulations of T-lymphocytes in asthmatics [34,35], resulting in the downregulation of IFN-γ release.…”

Section: Discussionmentioning

confidence: 62%

“…Moreover, pIgA and SC transcytosis have also been demonstrated by immunoelectron microscopy of bronchial mucosa [7]. In human pathology, decreased SC levels have been described in the bronchoalveolar lavage (BAL) fluid of asthmatic patients compared with normal controls [8]. Furthermore, a prospective study in children suggested a relationship between transient salivary IgA deficiency during the first year of life and the later development of bronchial hyperreactivity [9].…”

mentioning

confidence: 99%

Secretory component production by human bronchial epithelial cells is upregulated by interferon gamma

Godding

Sibille²,

Massion³

et al. 1998

Eur Respir J

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The respiratory tract in humans represents a large mucosal area exposed to the environment. The secretory immune system is the first, noninflammatory line of defence, protecting the respiratory tract from viral and bacterial infections. Secretory immunoglobulin A (S-IgA) is the major immunoglobulin present in human airway secretions [1]. The humoral secretory immune response depends on interactions between the B-cell system for the production of J-chain-containing polymeric IgA (pIgA) and the mucosal epithelium for the epithelial expression of secretory component (SC), respectively. SC is the soluble extracellular domain of the polymeric Ig receptor (pIgR) present on the basolateral surface of most epithelial cells. The pIgA antibodies produced by plasma cells are transported into mucosal secretions by transcytosis through epithelial cells [2,3]. The pIgR at the basolateral pole of the epithelium, with or without bound pIgA, is constitutively endocytosed and transported by vesicles to the apical pole, where pIgR vesicles fuse with the apical membrane. A proteolytic cleavage then occurs between the extracellular and membrane domains of the pIgR, resulting in the release of SC or S-IgA, a complex of mostly dimeric IgA (dIgA), J-chain and SC [4,5]. Immunohistology and immunofluorescence studies have demonstrated the presence of SC in bronchial epithelial cells and of IgA-containing plasma cells in the bronchial mucosa [6]. Moreover, pIgA and SC transcytosis have also been demonstrated by immunoelectron microscopy of bronchial mucosa [7]. In human pathology, decreased SC levels have been described in the bronchoalveolar lavage (BAL) fluid of asthmatic patients compared with normal controls [8]. Furthermore, a prospective study in children suggested a relationship between transient salivary IgA deficiency during the first year of life and the later development of bronchial hyperreactivity [9].The production of SC by cultured human tracheal epithelial cells has been demonstrated to be influenced by cell polarization [10]. The influence of cell polarization on SC production was further stressed by studies using neoplastic colonic cells, demonstrating an enhancing effect of polarization on their in vitro SC production [11]. It is concluded that human bronchial epithelial cells produce secretory component and transcytose dimeric immunoglobulin A in vitro. These processes were apically polarized and upregulated by interferon-γ. Among the cell lines studied, only CALU-3 expressed secretory component-messenger ribonucleic acid and produced detectable secretory component.

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“…Van Vyve first reported that UGB was decreased in BAL fluid of asthma patients [16], while Wang suggested that UGB might be involved directly or indirectly in the pathogenesis of bronchial asthma by showing elevated levels of neutrophil in BAL of UGB knock out (KO) mouse [17]. Furthermore, Hung showed that the increased allergic reaction in a UGB KO mice could be attenuated by administration of recombinant UGB, suggesting the possible therapeutic use of UGB in allergy.…”

Section: Discussionmentioning

confidence: 99%

“…There are reports that the level of UGB in the bronchioalveolar lavage (BAL) fluid is decreased in bronchial asthma [16], the representative allergic disease of the lower airway, suggesting that UGB may act as modulator of allergic inflammation in the lung. However, studies of UGB in the nose are lacking.…”

Section: Introductionmentioning

confidence: 99%

Expression of uteroglobin in a murine model of allergic rhinitis

Won

Quan

Rhee

et al. 2007

Acta Oto-Laryngologica

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Protein content in bronchoalveolar lavage fluid of patients with asthma and control subjects

Cited by 122 publications

References 38 publications

Association of an intragenic microsatellite marker in the CC16 gene with asthma in the Indian population

Association of an intragenic microsatellite marker in the CC16 gene with asthma in the Indian population

Secretory component production by human bronchial epithelial cells is upregulated by interferon gamma

Expression of uteroglobin in a murine model of allergic rhinitis

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