Chlamydia muridarum infection differentially alters smooth muscle function in mouse uterine horn and cervix.
- Publisher:
- American Physiological Society
- Publication Type:
- Journal Article
- Citation:
- American journal of physiology. Endocrinology and metabolism, 2020, 318, (6), pp. E981-E994
- Issue Date:
- 2020-06
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Full metadata record
Field | Value | Language |
---|---|---|
dc.contributor.author | Lee, JM | |
dc.contributor.author | Mayall, JR | |
dc.contributor.author | Chevalier, A | |
dc.contributor.author | McCarthy, H | |
dc.contributor.author | Van Helden, D | |
dc.contributor.author | Hansbro, PM | |
dc.contributor.author | Horvat, JC | |
dc.contributor.author | Jobling, P | |
dc.date.accessioned | 2020-11-08T05:54:38Z | |
dc.date.available | 2021-08-12T19:00:29Z | |
dc.date.issued | 2020-06 | |
dc.identifier.citation | American journal of physiology. Endocrinology and metabolism, 2020, 318, (6), pp. E981-E994 | |
dc.identifier.issn | 0193-1849 | |
dc.identifier.issn | 1522-1555 | |
dc.identifier.uri | http://hdl.handle.net/10453/143844 | |
dc.description.abstract | Chlamydia trachomatis infection is a primary cause of reproductive tract diseases including infertility. Previous studies showed that this infection alters physiological activities in mouse oviducts. Whether this occurs in the uterus and cervix has never been investigated. This study characterized the physiological activities of the uterine horn and the cervix in a Chlamydia muridarum (Cmu)-infected mouse model at three infection time points of 7, 14, and 21 days postinfection (dpi). Cmu infection significantly decreased contractile force of spontaneous contraction in the cervix (7 and 14 dpi; P < 0.001 and P < 0.05, respectively), but this effect was not observed in the uterine horn. The responses of the uterine horn and cervix to oxytocin were significantly altered by Cmu infection at 7 dpi (P < 0.0001), but such responses were attenuated at 14 and 21 dpi. Cmu infection increased contractile force to prostaglandin (PGF2α) by 53-83% in the uterine horn. This corresponded with the increased messenger ribonucleic acid (mRNA) expression of Ptgfr that encodes for its receptor. However, Cmu infection did not affect contractions of the uterine horn and cervix to PGE2 and histamine. The mRNA expression of Otr and Ptger4 was inversely correlated with the mRNA expression of Il1b, Il6 in the uterine horn of Cmu-inoculated mice (P < 0.01 to P < 0.001), suggesting that the changes in the Otr and Ptger4 mRNA expression might be linked to the changes in inflammatory cytokines. Lastly, this study also showed a novel physiological finding of the differential response to PGE2 in mouse uterine horn and cervix. | |
dc.format | Print-Electronic | |
dc.language | eng | |
dc.publisher | American Physiological Society | |
dc.relation | http://purl.org/au-research/grants/nhmrc/1059242 | |
dc.relation.ispartof | American journal of physiology. Endocrinology and metabolism | |
dc.relation.isbasedon | 10.1152/ajpendo.00513.2019 | |
dc.rights | info:eu-repo/semantics/embargoedAccess | |
dc.subject | 06 Biological Sciences, 11 Medical and Health Sciences | |
dc.subject.classification | Endocrinology & Metabolism | |
dc.subject.mesh | Muscle, Smooth | |
dc.subject.mesh | Myometrium | |
dc.subject.mesh | Uterus | |
dc.subject.mesh | Cervix Uteri | |
dc.subject.mesh | Oviducts | |
dc.subject.mesh | Animals | |
dc.subject.mesh | Mice | |
dc.subject.mesh | Chlamydia muridarum | |
dc.subject.mesh | Chlamydia Infections | |
dc.subject.mesh | Histamine | |
dc.subject.mesh | Oxytocics | |
dc.subject.mesh | Dinoprostone | |
dc.subject.mesh | Dinoprost | |
dc.subject.mesh | Receptors, Prostaglandin | |
dc.subject.mesh | Receptors, Oxytocin | |
dc.subject.mesh | RNA, Messenger | |
dc.subject.mesh | Histamine Agonists | |
dc.subject.mesh | Interleukin-6 | |
dc.subject.mesh | Cytokines | |
dc.subject.mesh | Gene Expression Regulation | |
dc.subject.mesh | Uterine Contraction | |
dc.subject.mesh | Muscle Contraction | |
dc.subject.mesh | Female | |
dc.subject.mesh | Interleukin-1beta | |
dc.subject.mesh | Receptors, Prostaglandin E, EP4 Subtype | |
dc.subject.mesh | Reproductive Tract Infections | |
dc.subject.mesh | Animals | |
dc.subject.mesh | Cervix Uteri | |
dc.subject.mesh | Chlamydia Infections | |
dc.subject.mesh | Chlamydia muridarum | |
dc.subject.mesh | Cytokines | |
dc.subject.mesh | Dinoprost | |
dc.subject.mesh | Dinoprostone | |
dc.subject.mesh | Female | |
dc.subject.mesh | Gene Expression Regulation | |
dc.subject.mesh | Histamine | |
dc.subject.mesh | Histamine Agonists | |
dc.subject.mesh | Interleukin-1beta | |
dc.subject.mesh | Interleukin-6 | |
dc.subject.mesh | Mice | |
dc.subject.mesh | Muscle Contraction | |
dc.subject.mesh | Muscle, Smooth | |
dc.subject.mesh | Myometrium | |
dc.subject.mesh | Oviducts | |
dc.subject.mesh | Oxytocics | |
dc.subject.mesh | RNA, Messenger | |
dc.subject.mesh | Receptors, Oxytocin | |
dc.subject.mesh | Receptors, Prostaglandin | |
dc.subject.mesh | Receptors, Prostaglandin E, EP4 Subtype | |
dc.subject.mesh | Reproductive Tract Infections | |
dc.subject.mesh | Uterine Contraction | |
dc.subject.mesh | Uterus | |
dc.title | Chlamydia muridarum infection differentially alters smooth muscle function in mouse uterine horn and cervix. | |
dc.type | Journal Article | |
utslib.citation.volume | 318 | |
utslib.location.activity | United States | |
utslib.for | 06 Biological Sciences | |
utslib.for | 11 Medical and Health Sciences | |
pubs.organisational-group | /University of Technology Sydney/Faculty of Science | |
pubs.organisational-group | /University of Technology Sydney/Faculty of Science/School of Life Sciences | |
pubs.organisational-group | /University of Technology Sydney | |
utslib.copyright.status | open_access | * |
dc.date.updated | 2020-11-08T05:54:30Z | |
pubs.issue | 6 | |
pubs.publication-status | Published | |
pubs.volume | 318 | |
utslib.citation.issue | 6 |
Abstract:
Chlamydia trachomatis infection is a primary cause of reproductive tract diseases including infertility. Previous studies showed that this infection alters physiological activities in mouse oviducts. Whether this occurs in the uterus and cervix has never been investigated. This study characterized the physiological activities of the uterine horn and the cervix in a Chlamydia muridarum (Cmu)-infected mouse model at three infection time points of 7, 14, and 21 days postinfection (dpi). Cmu infection significantly decreased contractile force of spontaneous contraction in the cervix (7 and 14 dpi; P < 0.001 and P < 0.05, respectively), but this effect was not observed in the uterine horn. The responses of the uterine horn and cervix to oxytocin were significantly altered by Cmu infection at 7 dpi (P < 0.0001), but such responses were attenuated at 14 and 21 dpi. Cmu infection increased contractile force to prostaglandin (PGF2α) by 53-83% in the uterine horn. This corresponded with the increased messenger ribonucleic acid (mRNA) expression of Ptgfr that encodes for its receptor. However, Cmu infection did not affect contractions of the uterine horn and cervix to PGE2 and histamine. The mRNA expression of Otr and Ptger4 was inversely correlated with the mRNA expression of Il1b, Il6 in the uterine horn of Cmu-inoculated mice (P < 0.01 to P < 0.001), suggesting that the changes in the Otr and Ptger4 mRNA expression might be linked to the changes in inflammatory cytokines. Lastly, this study also showed a novel physiological finding of the differential response to PGE2 in mouse uterine horn and cervix.
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