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Use of the EpiAirway Model for Characterizing Long-term Host-pathogen Interactions
Published on: September 2, 2011
Modelling persistent Mycoplasma pneumoniae infection of human airway epithelium
Oliver A Prince1, Thomas M Krunkosky2, Edward S Sheppard1
1Department of Microbiology, University of Georgia, Athens, GA, USA.
Abstract:
Mycoplasma pneumoniae is a human respiratory tract pathogen causing acute and chronic airway disease states that can include long-term carriage and extrapulmonary spread. The mechanisms of persistence and migration beyond the conducting airways, however, remain poorly understood. We previously described an acute exposure model using normal human bronchial epithelium (NHBE) in air-liquid interface culture, showing that M. pneumoniae gliding motility is essential for initial colonisation and subsequent spread, including localisation to epithelial cell junctions. We extended those observations here, characterizing M. pneumoniae infection of NHBE for up to 4 weeks. Colonisation of the apical surface was followed by pericellular invasion of the basolateral compartment and migration across the underlying transwell membrane. Despite fluctuations in transepithelial electrical resistance and increased NHBE cell desquamation, barrier function remained largely intact. Desquamation was accompanied by epithelial remodelling that included cytoskeletal reorganisation and development of deep furrows in the epithelium. Finally, M. pneumoniae strains S1 and M129 differed with respect to invasion and histopathology, consistent with contrasting virulence in experimentally infected mice. In summary, this study reports pericellular invasion, NHBE cytoskeletal reorganisation, and tissue remodelling with persistent infection in a human airway epithelium model, providing clear insight into the likely route for extrapulmonary spread.
Insights
Mycoplasma pneumoniae invades human airway tissue, spreading beyond initial infection sites. This study reveals how the pathogen remodels epithelial cells, offering insights into respiratory disease persistence and extrapulmonary spread.
Area of Science:
- Microbiology
- Pathogenesis
- Epithelial Biology
Background:
- Mycoplasma pneumoniae causes respiratory illness, with poorly understood mechanisms of long-term persistence and spread.
- Previous work showed gliding motility is crucial for M. pneumoniae colonization and spread in airway epithelium.
Purpose of the Study:
- To characterize the long-term infection dynamics of M. pneumoniae in normal human bronchial epithelium (NHBE).
- To investigate the pathogen's invasion, migration, and host tissue response over 4 weeks.
Main Methods:
- Utilized an air-liquid interface culture model of NHBE infected with M. pneumoniae for up to 4 weeks.
- Monitored pathogen colonization, invasion of basolateral compartments, and transwell migration.
- Assessed epithelial barrier function (transepithelial electrical resistance) and histopathology, including cell desquamation and epithelial remodeling.
Main Results:
- M. pneumoniae colonized the apical surface, then invaded the basolateral compartment and migrated across the transwell membrane.
- Despite barrier function fluctuations and cell shedding, the epithelial barrier remained largely intact.
- Observed epithelial remodeling, cytoskeletal reorganization, and deep furrow formation.
- Different M. pneumoniae strains (S1 and M129) exhibited distinct invasion patterns and histopathology.
Conclusions:
- This study demonstrates pericellular invasion and persistent infection of human airway epithelium by M. pneumoniae.
- Reveals pathogen-induced epithelial remodeling and cytoskeletal reorganization.
- Provides insights into potential routes for M. pneumoniae extrapulmonary spread.
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