Chlamydia-infected macrophages are resistant to azithromycin treatment and are associated with chronic oviduct inflammation and hydrosalpinx development.
Animals
Azithromycin
/ pharmacology
Chlamydia Infections
/ genetics
Chlamydia muridarum
/ drug effects
Chronic Disease
Cytokines
/ metabolism
Drug Resistance, Bacterial
/ drug effects
Fallopian Tubes
/ drug effects
Female
Gene Expression Regulation
/ drug effects
Inflammation
/ pathology
Inflammation Mediators
/ metabolism
Macrophages
/ drug effects
Mice, Inbred BALB C
Oviducts
/ drug effects
Chlamydia
Antibiotic
infertility
macrophage
Journal
Immunology and cell biology
ISSN: 1440-1711
Titre abrégé: Immunol Cell Biol
Pays: United States
ID NLM: 8706300
Informations de publication
Date de publication:
11 2019
11 2019
Historique:
received:
16
05
2018
revised:
23
07
2019
accepted:
24
07
2019
pubmed:
28
7
2019
medline:
24
4
2020
entrez:
27
7
2019
Statut:
ppublish
Résumé
Chlamydia infection remains the leading sexually-transmitted bacterial infection worldwide, causing damaging sequelae such as tubal scarring, infertility and ectopic pregnancy. As infection is often asymptomatic, prevention via vaccination is the optimal strategy for disease control. Vaccination strategies aimed at preventing bacterial infection have shown some promise, although these strategies often fail to prevent damaging inflammatory pathology when Chlamydia is encountered. Using a murine model of Chlamydia muridarum genital infection, we employed two established independent models to compare immune responses underpinning pathologic development of genital Chlamydia infection. Model one uses antibiotic treatment during infection, with only early treatment preventing pathology. Model two uses a plasmid-cured variant strain of C. muridarum that does not cause pathologic outcomes like the plasmid-containing wild-type counterpart. Using these infection models, contrasted by the development of pathology, we identified an unexpected role for macrophages. We observed that mice showing signs of pathology had greater numbers of activated macrophages present in the oviducts. This may have been due to early differences in macrophage activation and proinflammatory signaling leading to persistent or enhanced infection. These results provide valuable insight into the cellular mechanisms driving pathology in Chlamydia infection and contribute to the design and development of more effective vaccine strategies for protection against the deleterious sequelae of Chlamydia infection of the female reproductive tract.
Substances chimiques
Cytokines
0
Inflammation Mediators
0
Azithromycin
83905-01-5
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
865-876Informations de copyright
© 2019 Australian and New Zealand Society for Immunology Inc.
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