What question did this study set out to answer?

To review the host-pathogen interface driving cystic fibrosis lung disease, focusing on neutrophil-mediated innate immunity and bacterial adaptive evasion mechanisms.

May 28, 2019Clinical Microbiology ReviewsOpen Access

Cystic Fibrosis and Pseudomonas aeruginosa: the Host-Microbe Interface

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Authors

SMSankalp MalhotraArizona Heart Hospital DHDon HayesCincinnati Children's Hospital Medical Center DWDaniel J. WozniakThe Ohio State University

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Implication

Review demonstrates how Pseudomonas aeruginosa evades neutrophil effectors and drives chronic lung decline in cystic fibrosis, highlighting critical targets within host-microbe interfaces.

Key Points

To review the host-pathogen interface driving cystic fibrosis lung disease, focusing on neutrophil-mediated innate immunity and bacterial adaptive evasion mechanisms.
Synthesized evidence on early cystic fibrosis airway pathophysiology and the dual contribution of host hyperinflammation versus bacterial factors.
Assessed neutrophil-derived immune effectors, including reactive oxygen species and antimicrobial peptides like LL-37, during chronic infection.
Examined Pseudomonas aeruginosa virulence factors, adaptive mutations, and the anatomical colocalization of host and pathogen factors in the lung.
Neutrophil-derived effectors such as reactive oxygen species and LL-37 fail to clear chronic infection and contribute significantly to airway tissue destruction.
Pseudomonas aeruginosa effectively resists innate immunity and antibiotics through adaptive mutations and virulence factors, including antioxidants and exopolysaccharides.
Heterogeneous microenvironments and anatomical niches in the lung govern distinct spatial interactions between host immune effectors and persisting bacterial populations.

Cite This Study

Malhotra et al. (2019) studied this question.

synapsesocial.com/papers/69d841dea2a48916bbbefa68 https://doi.org/10.1128/cmr.00138-18

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Implication

Review demonstrates how Pseudomonas aeruginosa evades neutrophil effectors and drives chronic lung decline in cystic fibrosis, highlighting critical targets within host-microbe interfaces.

Cystic Fibrosis and Pseudomonas aeruginosa: the Host-Microbe Interface

Discussion

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Implication

Key Points

Cite This Study

Cystic Fibrosis and Pseudomonas aeruginosa: the Host-Microbe Interface

Discussion

Member takes

Implication

Key Points

Cite This Study

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