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Using a Bacterial Pathogen to Probe for Cellular and Organismic-level Host Responses
Published on: February 22, 2019
Chlamydia pneumoniae replicates in Kupffer cells in mouse model of liver infection
Antonella Marangoni1, Manuela Donati, Francesca Cavrini
1Sezione di Microbiologia DMCSS, University of Bologna, Policlinico S.Orsola, 9 Via Massarenti, Bologna 40138, Italy.
Aim:
To develop an animal model of liver infection with Chlamydia pneumoniae (C. pneumoniae) in intraperitoneally infected mice for studying the presence of chlamydiae in Kupffer cells and hepatocytes.
Methods:
A total of 80 BALB/c mice were inoculated intraperitoneally with C. pneumoniae and sacrificed at various time points after infection. Chlamydiae were looked for in liver homogenates as well as in Kupffer cells and hepatocytes separated by liver perfusion with collagenase. C. pneumoniae was detected by both isolation in LLC-MK2 cells and fluorescence in situ hybridization (FISH). The releasing of TNFA-alpha by C. pneumoniae in vitro stimulated Kupffer cells was studied by enzyme-linked immunosorbent assay.
Results:
C. pneumoniae isolation from liver homogenates reached a plateau on d 7 after infection when 6 of 10 animals were positive, then decreased, and became negative by d 20. C. pneumoniae isolation from separated Kupffer cells reached a plateau on d 7 when 5 of 10 animals were positive, and became negative by d 20. The detection of C. pneumoniae in separated Kupffer cells by FISH, confirmed the results obtained by culture. Isolated hepatocytes were always negative. Stimulation of Kupffer cells by alive C. pneumoniae elicited high TNF-alpha levels.
Conclusion:
A productive infection by C. pneumoniae may take place in Kupffer cells and C. pneumoniae induces a local pro-inflammatory activity. C. pneumoniae is therefore, able to act as antigenic stimulus when localized in the liver. One could speculate that C. pneumoniae infection, involving cells of the innate immunity such as Kupffer cells, could also trigger pathological immune reactions involving the liver, as observed in human patients with primary biliary cirrhosis.
Insights
This study developed a mouse model for liver infection by Chlamydia pneumoniae, finding it primarily infects Kupffer cells and triggers inflammation. This model aids research into chlamydial liver pathogenesis and immune responses.
Area of Science:
- Immunology
- Hepatology
- Microbiology
Background:
- Chlamydia pneumoniae (C. pneumoniae) is a pathogen with implications for various diseases.
- The role of C. pneumoniae in liver infections and its interaction with liver-resident immune cells remains incompletely understood.
- Establishing reliable animal models is crucial for investigating C. pneumoniae pathogenesis in the liver.
Purpose of the Study:
- To create and validate an animal model for studying liver infection by C. pneumoniae.
- To investigate the presence and localization of C. pneumoniae within Kupffer cells and hepatocytes in infected mice.
- To assess the inflammatory response induced by C. pneumoniae in the liver microenvironment.
Main Methods:
- BALB/c mice were infected intraperitoneally with C. pneumoniae.
- Liver homogenates, Kupffer cells, and hepatocytes were analyzed for C. pneumoniae presence using culture and fluorescence in situ hybridization (FISH).
- Tumor Necrosis Factor-alpha (TNF-α) release from stimulated Kupffer cells was quantified via ELISA.
Main Results:
- C. pneumoniae was successfully isolated from liver homogenates and Kupffer cells, peaking around day 7 post-infection and clearing by day 20.
- FISH analysis confirmed the presence of C. pneumoniae within Kupffer cells, while hepatocytes remained negative.
- In vitro stimulation of Kupffer cells with live C. pneumoniae resulted in elevated TNF-α levels, indicating a pro-inflammatory response.
Conclusions:
- Kupffer cells support productive C. pneumoniae infection in the liver.
- C. pneumoniae infection in the liver induces a local pro-inflammatory response mediated by Kupffer cells.
- This model provides a platform for exploring C. pneumoniae as an antigenic stimulus in the liver and its potential role in triggering immune-mediated liver pathologies.
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