Role of microbiome in the pathogenesis and progression of chronic pulmonary aspergillosis using a clone library analysis of 16S rRNA gene

Role of microbiome in the pathogenesis and progression of chronic pulmonary aspergillosis using a clone library analysis of 16S rRNA gene - Role of microbiome in the pathogenesis and progression of chronic pulmonary aspergillosis using a clone library analysis of 16S rRNA gene

Status

Recruiting

Phases

Unknown

Study type

Observational

Source

JPRN

Registry ID

JPRN-UMIN000034100

Enrollment

Registered

2018-09-11

Start date

2018-11-20

Completion date

Unknown

Last updated

2026-06-29

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

chronic pulmonary aspergillosis

Interventions

None listed

Eligibility

Sex/Gender

All

Inclusion criteria

Inclusion criteria: Patients with suspected chronic pulmonary aspergillosis and do not conflict with the exclusion criteria are registered. We use the criteria of the Guidelines for Management of Deep-seated Mycoses in Japan were revised in February 2014 to diagnosis chronic pulmonary aspergillosis. Patients who are positive for serum anti-Aspergillus sedimentation antibody, Aspergillus GM antigen, B-D glucan or histopathological findings are defined clinical diagnosis. Patients who are positive for culture tests are defined confirmed diagnosis.

Exclusion criteria

Exclusion criteria: The following patients are excluded. 1. Patients who do not agree with this study 2. Patients for whom bronchoscopy is difficult to preform because of comorbidity and who do not agree with bronchoscopy 3. Patients who received antibiotic therapy within 3 days before bronchoscopy. (Excluding small-volume long-term therapy of macrolide drugs)

Design outcomes

Primary

Measure	Time frame
The relationship between microbiome and chest CT findings of patients with chronic pulmonary aspergillosis.	—

Secondary

Measure	Time frame
We evaluate the following problems at the start of the test and 24 to 28 weeks and 48 to 52 weeks after this trial started. 1) Clinical manifestations, laboratory findings 2) Microbiological evaluation: Transition of causative bacteria with sputum 3) Cytokines, oxidative stress markers in BALF (including TNF-a, NOS, HO-1, IL-4, IL-6, IL-8, IL-13 and others). 4) The time-dependent change of the CT findings 5) The statistically significant differences in the differentiation ability according to the macrophages phenotypes (proportion of macrophages phenotype), and the CT findings.	—

Measure

Time frame

We evaluate the following problems at the start of the test and 24 to 28 weeks and 48 to 52 weeks after this trial started. 1) Clinical manifestations, laboratory findings 2) Microbiological evaluation: Transition of causative bacteria with sputum 3) Cytokines, oxidative stress markers in BALF (including TNF-a, NOS, HO-1, IL-4, IL-6, IL-8, IL-13 and others). 4) The time-dependent change of the CT findings 5) The statistically significant differences in the differentiation ability according to the macrophages phenotypes (proportion of macrophages phenotype), and the CT findings.

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Countries

Japan

Contacts

Public ContactHiroaki Ikegami

University of Occupational and Environmental Health, Japan Department of Respiratory Medicine

ikgamihiroaki@med.uoeh-u.ac.jp093-691-7453

Outcome results