MiR-184 targeting FOXO1 regulates host-cell oxidative stress induced by via the Wnt/β-catenin signaling pathway.

is a human pathogen that causes atypical pneumonia after zoonotic transmission. We confirmed that infection induces oxidative stress in human bronchial epithelial (HBEs) cells and explored how this is regulated through miR-184 and the Wnt/β-catenin signaling pathway. miR-184 mimic, miR-184 inhibitor, FOXO1 siRNA, or negative control sequence was transfected into HBE cells cultured in serum-free medium using Lipofectamine 2000.

Protective Immunity against Lung Infection Induced by a DNA Plasmid Vaccine Carrying Gene Inhibits Dissemination in BALB/c Mice.

(), a zoonotic pathogen, poses a potential threat to public health security and the development of animal husbandry. Vaccine-based preventative measures for infectious diseases have a promising landscape. DNA vaccines, with many advantages, have become one of the dominant candidate strategies in preventing and controlling the chlamydial infection.

Efficacy of Pgp3 vaccination for urogenital tract infection depends on its native conformation.

Urogenital tract infections with have frequently been detected among patients diagnosed with sexually transmitted infections, and such infections lead to inflammatory complications. Currently, no licensed chlamydial vaccine is available in clinical practice. We previously reported that immunization with recombinant plasmid-encoded virulence factor Pgp3 provided cross-serovar protection against genital tract infection.

Fluorescent Biosensor Based on Hairpin DNA Stabilized Copper Nanoclusters for Chlamydia trachomatis Detection.

Chlamydia trachomatis (C. trachomatis) is a kind of intracellular parasitic microorganism, which can causes many diseases such as trachoma. In this strategy, a specific hairpin DNA with the probe loop as specific regions to recognize C.

The roles of microRNAs played in lung diseases via regulating cell apoptosis.

MicroRNAs (miRNAs) are a type of endogenous non-coding short-chain RNA, which plays a crucial role in the regulation of many essential cellular functions, including cellular migration, proliferation, invasion, autophagy, oxidative stress, apoptosis, and differentiation. The lung can be damaged by pathogenic microorganisms, as well as physical or chemical factors. Research has confirmed that miRNAs and lung cell apoptosis can affect the development and progression of several lung diseases.

The role of an enzymatically inactive CPAF mutant vaccination in Chlamydia muridarum genital tract infection.

Chlamydia trachomatis urogenital tract infection causes pelvic inflammatory disease and infertility, increases the risk of co-infection with HPV and HIV. Chlamydial vaccination is considered the most promising approach to prevent and control its infection. Among various chlamydial vaccine candidates, chlamydial protease-like activity factor (CPAF) have been reported to provide robust protective immunity against genital chlamydial infection in mice with reduced vaginal shedding and oviduct pathology.

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.

Chlamydia trachomatis glycogen synthase promotes MAPK-mediated proinflammatory cytokine production via TLR2/TLR4 in THP-1 cells.

Aims: To investigate the roles and mechanisms of C. trachomatis glycogen synthase (GlgA) in regulating the inflammatory response in THP-1 cells.

Main Methods: In this work, after THP-1 cells were stimulated with GlgA, transcript and protein expression levels were measured by qRT-PCR and ELISA, respectively.

[Role of tumor necrosis factor-α in infection in the urogenital tract of mice].

Objective: To explore the role of tumor necrosis factor-α (TNF-α) in immune response to urogenital chlamydial infection and urogenital pathology in mice.

Methods: Fifteen female wild-type (WT) C57BL/6J mice and 15 TNF-α receptor knockout (TNF-αR KO) mice were inoculated intravaginally with 1×10 inclusion forming units (IFUs) of live . At 56 days after the first inoculation, 8 mice from each group were subjected to a second inoculation at the same dose.

Identification of HeLa cell proteins that interact with Chlamydia trachomatis glycogen synthase using yeast two‑hybrid assays.

Chlamydia trachomatis (C. trachomatis) is the leading cause of bacterial sexually transmitted diseases and infectious diseases that cause blindness. The pathophysiology of chlamydial infections is poorly understood, but secreted proteins have emerged as key virulence factors.

Vaccination with MIP or Pgp3 induces cross-serovar protection against chlamydial genital tract infection in mice.

Previously we reported that recombinant Chlamydia muridarum macrophage infectivity potentiator (MIP) provided partial protection against C. muridarum genital tract infection in mice. On the other hand, Chlamydia trachomatis plasmid encoded Pgp3could induce the protection against C.

Deficiency of LIGHT signaling pathway exacerbates Chlamydia psittaci respiratory tract infection in mice.

LIGHT, a costimulatory member of the immunoglobulin superfamily (Ig SF), can greatly impact T cell activation. The role of the LIGHT signaling pathway in chlamydial infection was evaluated in mice following respiratory tract infection with Chlamydia psittaci. Compared with wild type (WT) mice, LIGHT knockout (KO) mice showed significant reduction of body weight, much lower survival rate, higher bacterial burden, prolonged infection time courses and more severe pathological changes in lung tissue.

[Role of LIGHT signal pathway in Chlamydia muridarum urogenital infection in mice].

Objective: To study the role of lymphotoxin-like inducible protein that competes with glycoprotein D for herpesvirus entry on T cells (LIGHT) in the development of protective immunity and pathology during Chlamydia Muridarum urogenital infection in mice.

Methods: C57BL/6J wild type (wt) and mice deficient in LIGHT (LIGHT KO) were inoculated intravaginally with 1 x 10(4) IFUs of live C. muridarum organisms.

[Sports injuries and illnesses during the 2008 Olympic Games and 2013 China National Games in Shenyang Division].

Objective: To retrospectively analyse the medical imaging examination results of the injuries and illnesses during the 2008 Olympic Games and 2013 China National Games in Shenyang Divison.

Methods: Collected and analyzed the health information and medical imaging examination results from Shengjing Hospital of China Medical University during the two games.

Results: There was 9 cases of sports injuries in the 2008 Olympic Games, mainly for knee, ankle ligament injury and muscle sprain, 36 cases of sports injuries in the 2013 China National Games, mainly for head traumas (9 cases), knee injuries (7 cases), ankle injuries (7 cases), shoulder injures (4 cases).

Identification of Plasmid-Free Chlamydia muridarum Organisms Using a Pgp3 Detection-Based Immunofluorescence Assay.

Chlamydia possesses a conserved 7.5 kb plasmid that is known to play an important role in chlamydial pathogenesis, since some chlamydial organisms lacking the plasmid are attenuated. The chlamydial transformation system developed recently required the use of plasmid-free organisms.

Contribution of interleukin-12 p35 (IL-12p35) and IL-12p40 to protective immunity and pathology in mice infected with Chlamydia muridarum.

The p35 molecule is unique to interleukin-12 (IL-12), while p40 is shared by both IL-12 and IL-23. IL-12 promotes Th1 T cell responses, while IL-23 promotes Th17 T cell responses. The roles of IL-12p35- and IL-12p40-mediated responses in chlamydial infection were compared in mice following an intravaginal infection with Chlamydia muridarum.

PORF5 plasmid protein of Chlamydia trachomatis induces MAPK-mediated pro-inflammatory cytokines via TLR2 activation in THP-1 cells.

Infection with Chlamydia trachomatis induces inflammatory pathologies in the urogenital tract that can lead to infertility and ectopic pregnancy. Pathogenesis of infection has been mostly attributed to excessive cytokine production. However, precise mechanisms on how C.