<i>Aspergillus</i>in chronic lung disease: Modeling what goes on in the airways

Takazono, Takahiro; Sheppard, Donald C.

doi:10.1093/mmy/myw117

Cited by 27 publications

(22 citation statements)

References 81 publications

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“…Then, many animal models have been developed, particularly using A. fumigatus , the classical causative agent of allergic bronchopulmonary aspergillosiss. 54 Animals that underwent Aspergillus sensitization and challenge develop high levels of IgE, eosinophilia and lung inflammation. 54 …”

Section: Introductionmentioning

confidence: 99%

“… 54 Animals that underwent Aspergillus sensitization and challenge develop high levels of IgE, eosinophilia and lung inflammation. 54 …”

Section: Introductionmentioning

confidence: 99%

“…One of the most commonly repeated protocols was animal sensitization with two IP injections spaced by 7–14 days and the challenge is performed 1 week later with the culprit allergen. 51 – 54 …”

Section: Introductionmentioning

confidence: 99%

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Animal models of asthma: utility and limitations

Aun

Bonamichi-Santos

Arantes-Costa

et al. 2017

JAA

186

137

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Clinical studies in asthma are not able to clear up all aspects of disease pathophysiology. Animal models have been developed to better understand these mechanisms and to evaluate both safety and efficacy of therapies before starting clinical trials. Several species of animals have been used in experimental models of asthma, such as Drosophila, rats, guinea pigs, cats, dogs, pigs, primates and equines. However, the most common species studied in the last two decades is mice, particularly BALB/c. Animal models of asthma try to mimic the pathophysiology of human disease. They classically include two phases: sensitization and challenge. Sensitization is traditionally performed by intraperitoneal and subcutaneous routes, but intranasal instillation of allergens has been increasingly used because human asthma is induced by inhalation of allergens. Challenges with allergens are performed through aerosol, intranasal or intratracheal instillation. However, few studies have compared different routes of sensitization and challenge. The causative allergen is another important issue in developing a good animal model. Despite being more traditional and leading to intense inflammation, ovalbumin has been replaced by aeroallergens, such as house dust mites, to use the allergens that cause human disease. Finally, researchers should define outcomes to be evaluated, such as serum-specific antibodies, airway hyperresponsiveness, inflammation and remodeling. The present review analyzes the animal models of asthma, assessing differences between species, allergens and routes of allergen administration.

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Section: Introductionmentioning

confidence: 99%

“… 54 Animals that underwent Aspergillus sensitization and challenge develop high levels of IgE, eosinophilia and lung inflammation. 54 …”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Animal models of asthma: utility and limitations

Aun

Bonamichi-Santos

Arantes-Costa

et al. 2017

JAA

186

137

View full text Add to dashboard Cite

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“…Under certain conditions, such as immunosuppression, or in the presence of underlying pulmonary diseases such as allergic asthma, cystic fibrosis (CF), and chronic obstructive pulmonary disease (COPD), A . fumigatus can persist in airways and become infectious 3 . However, conidia inhaled by healthy people with functional immune systems and normal airway function are rapidly cleared.…”

Section: Introductionmentioning

confidence: 99%

Human Bronchial Epithelial Cells Inhibit Aspergillus fumigatus Germination of Extracellular Conidia via FleA Recognition

Richard

Marti

Varrot

et al. 2018

Sci Rep

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Aspergillus fumigatus is an environmental filamentous fungus that may act as an opportunistic pathogen causing a variety of diseases, including asthma or allergic bronchopulmonary aspergillosis, and infection, ranging from asymptomatic colonization to invasive pulmonary form, especially in immunocompromised patients. This fungus is characterized by different morphotypes including conidia which are the infective propagules able to germinate into hyphae. Due to their small size (2–3 µm), conidia released in the air can reach the lower respiratory tract. The objective of this study was to characterize the interactions between conidia and bronchial epithelial cells. To this end, we studied the role of bronchial epithelial cells, i.e., the BEAS-2B cell line and human primary cells, in conidial germination of a laboratory strain and three clinical strains of A. fumigatus. Microscopic observations and galactomannan measurements demonstrated that contact between epithelial cells and conidia leads to the inhibition of conidia germination. We demonstrated that this fungistatic process is not associated with the release of any soluble components nor internalization by the epithelial cells. We highlight that this antifungal process involves the phosphoinositide 3-kinase pathway on the host cellular side and the lectin FleA on the fungal side. Collectively, our results show that bronchial epithelial cells attenuate fungal virulence by inhibiting germination of extracellular conidia, thus preventing the morphological change from conidia to filaments, which is responsible for tissue invasion.

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“…These chronic infections may include chronic pulmonary aspergillosis, Aspergillus bronchitis, fungal asthma, and allergic bronchopulmonary aspergillosis (APBA) (34).…”

Section: Aspergillus Fumigatusmentioning

confidence: 99%