Preparation of graphene oxide-stabilized Pickering emulsion adjuvant for Pgp3 recombinant vaccine and enhanced immunoprotection against infection.

Background: Traditional emulsion adjuvants are limited in clinical application because of their surfactant dependence. Graphene oxide (GO) has unique amphiphilic properties and therefore has potential to be used as a surfactant substitute to stabilize Pickering emulsions.

Methods: In this study, GO-stabilized Pickering emulsion (GPE) was prepared and used as an adjuvant to facilitate an enhanced immune response to the () Pgp3 recombinant vaccine.

Novel use of graphene oxide quantum dots in a pickering emulsion as a Chlamydia trachomatis vaccine adjuvant.

Graphene oxide quantum dots (GOQDs), which are graphene-based nanoparticles, are potential surfactant substitutes for stabilizing Pickering emulsions, due to their high surface area, biodegradability, and reasonable biocompatibility. In the present study, GOQDs stabilized Pickering emulsion (GQPE) was prepared by simple sonication and then used as an adjuvant to enhance immune responses to the Chlamydia trachomatis Pgp3 recombinant vaccine. Immunization of mice showed that GQPE robustly activates adaptive immunity by efficiently stimulating IgG, sIgA, IFN-γ, IL-4, and TNF-α production.

Pgp3 protein of Chlamydia trachomatis inhibits apoptosis via HO-1 upregulation mediated by PI3K/Akt activation.

As an obligate intracellular pathogen, Chlamydia trachomatis assumes various strategies to inhibit host cells apoptosis, thereby providing a suitable intracellular environment to ensure completion of the development cycle. In the current study, we revealed that Pgp3 protein, one of eight plasmid proteins of C. trachomatis that has been illustrated as the key virulence factor, increased HO-1 expression to suppress apoptosis, and downregulation of HO-1 with siRNA-HO-1 failed to exert anti-apoptosis activity of Pgp3 protein.

Chitosan particle stabilized Pickering emulsion/interleukin-12 adjuvant system for Pgp3 subunit vaccine elicits immune protection against genital chlamydial infection in mice.

Considering the shortcomings in current chlamydia infection control strategies, a major challenge in curtailing infection is the implementation of an effective vaccine. The immune response induced by plasmid encoded Pgp3 was insufficient against infection, which requires adjuvant applications to achieve the robust immune response induced by Pgp3. There is increasing promising in developing adjuvant systems relying on the delivery potential of Pickering emulsions and the immunomodulatory effects of interleukin (IL)-12.

Alterations of Vaginal Microbiota in Women With Infertility and Infection.

() is the most common etiological agent of bacterial sexually transmitted infections (STIs) worldwide and causes serious health sequelae such as cervicitis, pelvic inflammatory disease, and even infertility if ascending from the lower to the upper female genital tract. Previous studies have revealed the pivotal role of vaginal microbiota in susceptibility to STIs. However, alterations in the vaginal microbiota in women who are infertile and infected with remain unknown.

Chlamydia trachomatis Pgp3 protein regulates oxidative stress via activation of the Nrf2/NQO1 signal pathway.

Aim: Chlamydia trachomatis has evolved various strategies to alleviate oxidative stress of host cells to maintain their intracellular survival. However, the exact mechanism of anti-oxidative stress of C. trachomatis is still unclear.

Plasmid Protein pORF5 Up-Regulates ZFAS1 to Promote Host Cell Survival via MAPK/p38 Pathway.

Long non-coding RNAs (lncRNAs) have been demonstrated to play essential roles in many diseases. However, few studies have shown that lncRNAs take part in the pathogenesis of (). Here, we used a lncRNA microarray to detect the global lncRNA expression profiles in HeLa cells transfected with pORF5 plasmid protein, an important virulence factor for .

Chlamydia trachomatis plasmid-encoded protein pORF5 activates unfolded protein response to induce autophagy via MAPK/ERK signaling pathway.

Chlamydia trachomatis (C. trachomatis) is an obligate intracellular organism that depends on nutrients from the host cell for their replication and proliferation. Therefore, the interaction between this pathogen and host induces sustained endoplasmic reticulum (ER) stress in the infected cells.

Antiapoptotic activity of Chlamydia trachomatis Pgp3 protein involves activation of the ERK1/2 pathway mediated by upregulation of DJ-1 protein.

Chlamydia trachomatis has evolved strategies to prevent host cell apoptosis to evade the host immune defense. However, the precise mechanisms of antiapoptotic activity of C. trachomatis still need to be clarified.