Allergic bronchopulmonary aspergillosis in cystic fibrosis

Laufer, Peter; Fink, Jordan N.; Bruns, W; Unger, George F.; Kalbfleisch, John H.; Greenberger, Paul A.; Patterson, Roy

doi:10.1016/0091-6749(84)90482-2

Cited by 223 publications

(117 citation statements)

References 10 publications

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“…In that study, antibodies (precipitins) were found in more than 50% of the patients with CF but without ABPA. (25) In our pilot study, all serological test results we re negative. In a longitudinal study involving 118 patients with CF, it was reported that 42% of the patients without ABPA presented skin test reactivity to A. fumigatus antigen, 42% presented antibodies (precipitins), 54% presented IgE positivity to A. fumigatus, and 23% had IgE levels > 500 IU/mL.…”

Section: Discussionmentioning

confidence: 99%

Prevalência de aspergilose broncopulmonar alérgica em pacientes com fibrose cística na Bahia, Brasil

et al. 2008

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Section: Discussionmentioning

confidence: 99%

Prevalência de aspergilose broncopulmonar alérgica em pacientes com fibrose cística na Bahia, Brasil

et al. 2008

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“…This opportunistic fungal pathogen is generally found in homes particularly in the farming population (Kauffman et al, 1995). ABPA is prevalent among patients with cystic fibrosis (Laufer et al, 1984) and is characterized by elevated levels of serum IgE and eosinophils indicating a Th2 response (Kauffman et al, 1995). Indeed, in a murine model of ABPA, Th2 cytokines, particularly IL4 and IL5, were detected in cell cultures from the lungs (Kurup et al, 1992;Kurup et al, 1994a) and BAL (Grunig et al, 1997) of Af sensitized mice and administration of antibodies to IL4 and IL5 abrogated the IgE and eosinophilia in these animals (Kurup et al, 1994b).…”

Section: Introductionmentioning

confidence: 99%

Second‐Hand Smoke Increases Bronchial Hyperreactivity and Eosinophilia in a Murine Model of Allergic Aspergillosis

Seymour

Schelegle

Pinkerton

et al. 2003

Journal of Immunology Research

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Involuntary inhalation of tobacco smoke has been shown to aggravate the allergic response. Antibodies to fungal antigens such as Aspergillus fumigatus (Af) cause an allergic lung disease in humans. This study was carried out to determine the effect of environmental tobacco smoke (ETS) on a murine model of allergic bronchopulmonary aspergillosis (ABPA). BALB/c mice were exposed to aged and diluted sidestream cigarette smoke to simulate 'second-hand smoke'. The concentration was consistent with that achieved in enclosed public areas or households where multiple people smoke. During exposure, mice were sensitized to Af antigen intranasally. Mice that were sensitized to Af antigen and exposed to ETS developed significantly greater airway hyperreactivity than did mice similarly sensitized to Af but housed in ambient air. The effective concentration of aerosolized acetylcholine needed to double pulmonary flow resistance was significantly lower in Af þ ETS mice compared to the Af þ AIR mice. Immunological data that supports this exacerbation of airway hyperresponsiveness being mediated by an enhanced type 1 hypersensitivity response include: eosinophilia in peripheral blood and lung sections. All Af sensitized mice produced elevated levels of IL4, IL5 and IL10 but no IFN-g indicating a polarized Th2 response. Thus, ETS can cause exacerbation of asthma in ABPA as demonstrated by functional airway hyperresponsiveness and elevated levels of blood eosinophilia.

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“…5 Another inflammatory phenotype that is quite peculiar to CF patients is a hyper-IgE syndrome known as allergic bronchopulmonary aspergillosis (ABPA), a syndrome characterized by an IgE antibody response specific for Aspergillus fumigatus (Af), a total serum IgE level of greater than 5000 ng/ ml and clinical signs of allergic airway hyperreactivity. ABPA is quite common in CF patients (10-15% affected) 6,7 and very rare outside of CF. One report has indicated that even among those individuals who have ABPA without overt CF, approximately 50% will have one identifiable CFTR mutation.…”

mentioning

confidence: 99%

Enhanced IgE allergic response to Aspergillus fumigatus in CFTR−/− mice

Müller

Braag

Herlihy

et al. 2006

Laboratory Investigation

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To gain insight into aberrant cytokine regulation in cystic fibrosis (CF), we compared the phenotypic manifestations of allergen challenge in gut-corrected CFTR-deficient mice with background-matched C57Bl6 (B6) mice. Aspergillus fumigatus (Af) antigen was used to mimic allergic bronchopulmonary aspergillosis, a peculiar hyper-IgE syndrome with a high prevalence in CF patients. CFTRÀ/À, C57BL/6 and FVB/NJ mice were sensitized with Af antigen by serial intraperitoneal injections. Control mice were mock sensitized with PBS. Challenges were performed by inhalation of Af antigen aerosol. After Af antigen challenge, histologic analysis showed goblet cell hyperplasia and lymphocytic infiltration in both strains. However, total serum IgE levels were markedly elevated in CF mice. Sensitized CF mice showed a five-fold greater IgE response to sensitization as compared with B6-and FVB-sensitized controls. Additional littermate controls to fully normalize for B6-FVB admixture in the strain background confirmed the role of CFTR mutation in the hyper-IgE syndrome. Cytokine mRNA levels of IL-5 and GM-CSF in the bronchoalveolar lavage (BAL) fluid, and BAL cell differentials indicated that CFTR mutation caused a shift from an IL-5-predominant to an IL-4-predominant cytokine profile. This system models a very specific type of airway inflammation in CF and could provide insights into pathogenesis and treatment of the disease.

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Allergic bronchopulmonary aspergillosis in cystic fibrosis

Cited by 223 publications

References 10 publications

Prevalência de aspergilose broncopulmonar alérgica em pacientes com fibrose cística na Bahia, Brasil

Prevalência de aspergilose broncopulmonar alérgica em pacientes com fibrose cística na Bahia, Brasil

Second‐Hand Smoke Increases Bronchial Hyperreactivity and Eosinophilia in a Murine Model of Allergic Aspergillosis

Enhanced IgE allergic response to Aspergillus fumigatus in CFTR−/− mice

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