Immunologic response to () in a dairy farm family

Brummund, Walter; Kurup, Viswanath P.; Resnick, Abe; Milson, Thomas J.; Fink, Jordan N.

doi:10.1016/0091-6749(88)90998-0

Cited by 17 publications

(3 citation statements)

References 15 publications

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“…The genus Faenia (26) comprises only one species on the Approved Lists (40), the thermophilic organism Faenia rectivirgula (formerly Micropolyspora rectivirgula [49] ; synonym, Micropolyspora faeni [l]), one of the causative agents of farmer's lung disease (3,25,28,43). A mesophilic species, "Faenia interjecta" (41), has not been validly published and was not available for our studies.…”

mentioning

confidence: 99%

Transfer of Faenia rectivirgula Kurup and Agre 1983 to the Genus Saccharopolyspora Lacey and Goodfellow 1975, Elevation of Saccharopolyspora hirsuta subsp. taberi Labeda 1987 to Species Level, and Emended Description of the Genus Saccharopolyspora

Korn-Wendisch

Kempf

Grund

et al. 1989

International Journal of Systematic Bacteriology

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mentioning

confidence: 99%

Transfer of Faenia rectivirgula Kurup and Agre 1983 to the Genus Saccharopolyspora Lacey and Goodfellow 1975, Elevation of Saccharopolyspora hirsuta subsp. taberi Labeda 1987 to Species Level, and Emended Description of the Genus Saccharopolyspora

Korn-Wendisch

Kempf

Grund

et al. 1989

International Journal of Systematic Bacteriology

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“…The heterogeneity of BAL CD4+/CD8+ ratios, with most T-cells being CD4+ in the majority of patients, may seem puzzling. Most earlier EAA studies, reviewed in [34], report a decreased CD4+/CD8+ ratio compared to PBLs, although ratios that were unchanged [35] or increased [36] have also been noted. The present patient group had a very acute disease, however, and in such conditions a BAL CD4+ predominance has previously been reported [37].…”

Section: Discussionmentioning

confidence: 99%

Lung and blood T-cell receptor repertoire in extrinsic allergic alveolitis

Wahlström¹,

Berlin²,

Lundgren³

et al. 1997

Eur Respir J

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Patients with extrinsic allergic alveolitis (EAA) have accumulations of T-lymphocytes in their lungs. CD8+ lung T-cells, in particular, have been implicated in the pathogenesis of EAA. The objective of the present study was to analyse the T-cell receptor (TCR) V alpha and V beta gene usage of CD4+ and CD8+ lung and peripheral blood lymphocytes (PBLs) before and after treatment. Twelve patients with clinical signs of extrinsic allergic alveolitis were studied at disease onset, and nine of the 12 were also studied after treatment and clinical recovery. Lung cells, obtained by bronchoalveolar lavage (BAL), and paired PBL samples were analysed by flow cytometry using a panel of anti-TCR V monoclonal antibodies. The changes in TCR V gene usage were most pronounced in BAL CD8+ cells, as compared to the BAL CD4+, PBL CD8+ and PBL CD4+ subsets. At disease onset, 10 of the 12 patients had lung restricted expansions of CD8+ T-cells using a particular V alpha or V beta gene segment, and 8 of the 12 patients had CD8+ T-cell expansions in PBL. For the patients in whom a follow-up was possible, a majority of the expansions in the lungs were normalized, whereas most of the expansions in PBL remained. An over-representation of human leucocyte antigen (HLA)-DR2 (15) was detected, particularly among patients with farmer's lung. An increased selected T-cell receptor V gene usage may follow specific interactions between T-cells and antigens. In extrinsic allergic alveolitis, we determined that such expansions occur most frequently in the lung CD8+ T-cells. Since most expansions of lung CD8+ T-cells normalized with clinical improvement, these are further implicated in the pathogenesis of extrinsic allergic alveolitis.

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“…Several reports have shown that antibody responses of patients with normal lungs and inflamed lungs were different, and more often influenced by the environment and age of individuals [13][14][15][16][17][18][19]. However, no data are available on specific immune responses in the respiratory tract of already inflamed lungs.…”

Section: Discussionmentioning

confidence: 99%

Immune responsiveness to inhaled antigens: local antibody production in the respiratory tract in health and lung diseases

Yoshizawa

Ohtani

Inoue

et al. 1995

Clinical and Experimental Immunology

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The pulmonary defence mechanism in summer type hypersensitivity pneumonitis induced by Trichosporon cutaneum was investigated. We have studied the antibody response to fungal antigens in sera and bronchoalveolar lavage (BAL) fluids from patients with summer type hypersensitivity pneumonitis, bird fancier's lung, interstitial pneumonia associated with collagen vascular disease (INT-PNE), and from normal volunteers. Antigens extracted from fungi frequently isolated from home environments were used in ELISA to detect IgG and IgA antibodies in sera and BAL fluids. The results of the present study show that antibody titre in the respiratory tract to a variety of fungi from home environments is modulated by ongoing pulmonary inflammation, and that antibody production against inhaled antigens is altered by pulmonary inflammation resulting from diverse pathogenesis. This study concludes that the preexisting pulmonary inflammatory disease alters antibody production in the respiratory tract in response to inhaled fungi, and that the type of alteration depends in part on the etiology of the preexisting disease.

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Immunologic response to () in a dairy farm family

Cited by 17 publications

References 15 publications

Transfer of Faenia rectivirgula Kurup and Agre 1983 to the Genus Saccharopolyspora Lacey and Goodfellow 1975, Elevation of Saccharopolyspora hirsuta subsp. taberi Labeda 1987 to Species Level, and Emended Description of the Genus Saccharopolyspora

Transfer of Faenia rectivirgula Kurup and Agre 1983 to the Genus Saccharopolyspora Lacey and Goodfellow 1975, Elevation of Saccharopolyspora hirsuta subsp. taberi Labeda 1987 to Species Level, and Emended Description of the Genus Saccharopolyspora

Lung and blood T-cell receptor repertoire in extrinsic allergic alveolitis

Immune responsiveness to inhaled antigens: local antibody production in the respiratory tract in health and lung diseases

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