https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:38603 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 (PGF2_α) 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 ll1b, ll6 in the uterine horn of Cmu-inoculated mice (P < 0.01 to P < 0.001), suggesting that the changes in the Otr and Ptger4mRNA 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.]]> Wed 17 Nov 2021 15:27:35 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:36328 Wed 01 Apr 2020 08:53:27 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:40893 Streptococcus pneumoniae, non-typeable Haemophilus influenzae, Mycobacterium tuberculosis, Aspergillus fumigatus, etc., have the ability to elicit pro-oxidant pathways in the respiratory tract. Also, these pathogens are equipped with enzymatic and non-enzymatic mechanisms to neutralize host-associated oxidative molecules that facilitate the persistence of these pathogens in the lungs. We will discuss the CRD/pathogen-triggered oxidative stress in the lungs. We will also discuss the microbial mechanisms that may further increase oxidative stress in patients with CRDs that potentially results in the heightened inflammatory response in the lungs. Finally, we will discuss the current treatment strategies to limit the oxidative response-associated lung pathologies.]]> Fri 22 Jul 2022 10:38:45 AEST ]]>