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- Could periostin be a viable biomarker for IPF?
- Are acute exacerbations driven by cellular mechanisms?
- What are the outcomes of combined pulmonary fibrosis and emphysema in patients with IPF?
- How does the lung microbiome change during acute exacerbation?
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How does the lung microbiome change during acute exacerbation?
Acute exacerbations of idiopathic pulmonary fibrosis (AE-IPF) are events of clinically significant respiratory deterioration that occur due to unidentifiable cause(s).1 These events produce significant levels of morbidity and mortality for patients with IPF.2-5 The authors set out to understand whether AE-IPF produce changes in the lung microbiome that could provide insights into its mechanism and result in strategies to manage or mitigate its impact.
What They Did
In this pilot study, the authors collected bronchoalveolar lavage (BAL) samples from 20 patients who were hospitalized with AE-IPF and 15 patients with stable IPF who were matched based on age, sex, smoking history, and lung function.6 All patients tested negative for a range of standard infective agents. The authors probed the BAL samples for the presence of the bacterial 16S ribosomal RNA, an indicator of bacterial load.
What They Found
Patients with AE-IPF had 4-fold higher levels of 16S rRNA than patients with stable IPF (P=.012).6 The level of bacterial burden correlated independently with diagnosis of AE-IPF. While the dominant phyla stayed the same between groups, the relative amounts of each changed (Figure). Two potentially pathogenic species, Campylobacter sp and Stenotrophomonas sp, both proteobacteria, were found at higher levels in samples from AE-IPF than in controls.
What It Means
Changes in the microbial balance during AE-IPF support the idea that specific antibiotics may have a role in treating AE-IPF. Further, the increased levels of Campylobacter (which is best known as a GI pathogen) in the AE-IPF lung samples in this study suggest that AE-IPF may be linked to silent microaspiration and/or gastroesophageal reflux (GERD).6,7 Further studies should investigate the pathologic implications of these microbial shifts and work toward understanding whether targeted antibiotic use and prophylactic treatment of GERD may reduce the morbidity and mortality associated with AE-IPF.
Link to abstract: http://www.ncbi.nlm.nih.gov/pubmed/28143484
- Collard HR, Moore BB, Flaherty KR, et al. Acute exacerbations of idiopathic pulmonary fibrosis. Am J Respir Crit Care Med. 2007;176(7):636-643.
- Daniels CE, Yi ES, Ryu JH. Autopsy findings in 42 consecutive patients with idiopathic pulmonary fibrosis. Eur Respir J. 2008;32(1):170-174.
- Kim DS, Park JH, Park BK, Lee JS, Nicholson AG, Colby T. Acute exacerbation of idiopathic pulmonary fibrosis: frequency and clinical features. Eur Respir J. 2006;27(1):143-150.
- Kubo H, Nakayama K, Yanai M, et al. Anticoagulant therapy for idiopathic pulmonary fibrosis. Chest. 2005;128(3):1475-1482.
- Song JW, Hong SB, Lim CM, Koh Y, Kim DS. Acute exacerbation of idiopathic pulmonary fibrosis: Incidence, risk factors and outcome. Eur Respir J. 2011;37(2):356-363.
- Molyneaux PL, Cox MJ, Wells AU, et al. Changes in the respiratory microbiome during acute exacerbations of idiopathic pulmonary fibrosis. Respir Res. 2017;18(1):29.
- Raghu G, Collard HR, Egan JJ, et al. An official ATS/ERS/JRS/ALAT statement: idiopathic pulmonary fibrosis: evidence-based guidelines for diagnosis and management. Am J Respir Crit Care Med. 2011;183(6):788-824.