Protection promoted by pGP3 or pGP4 against Chlamydia muridarum is mediated by CD4(+) cells in C57BL/6N mice.

Urogenital tract infection with Chlamydia trachomatis is a leading cause of sexually transmitted infections. There is currently no commercially available vaccine against C. trachomatis.

Anti-chlamydial effect of plant peptides.

Even in asymptomatic cases of Chlamydia trachomatis infection, the aim of the antibiotic strategy is eradication of the pathogen so as to avoid the severe late sequelae, such as pelvic inflammatory disease, ectopic pregnancy, and tubal infertility. Although first-line antimicrobial agents have been demonstrated to be predominantly successful in the treatment of C. trachomatis infection, treatment failures have been observed in some cases.

Expression of Chlamydia muridarum plasmid genes and immunogenicity of pGP3 and pGP4 in different mouse strains.

Chlamydia muridarum carries a cryptic plasmid (pMoPn) of 7.5kb, which encodes seven genes. Our aims were to describe the transcriptional pattern of the pMoPn genes in C.

Chlamydophila pneumoniae re-infection triggers the production of IL-17A and IL-17E, important regulators of airway inflammation.

Objective: Investigation of the effects of interleukin (IL)-17 cytokines in Chlamydophila pneumoniae-infected mice.

Methods: Mice were infected with C. pneumoniae once or three times and the expression of IL-17 cytokines was followed by RT qPCR from day 1 to day 28 after infection and re-infection.

Chlamydophila pneumoniae induces production of the defensin-like MIG/CXCL9, which has in vitro antichlamydial activity.

CXC chemokines that lack the ELR motif, including the monokine induced by IFN-γ (MIG/CXCL9), the IFN-induced protein of 10 kDa (IP-10/CXCL10), and the IFN-inducible T-cell α-chemoattractant (I-TAC/CXCL11), have been shown to mediate the generation of type 1 immune responses and to possess defensin-like bactericidal effects. This study revealed that the infection of mice with Chlamydophila pneumoniae via the intranasal route resulted in the local expression of MIG/CXCL9, IP-10/CXCL10, and I-TAC/CXCL11. The expression of IP-10/CXCL10 and I-TAC/CXCL11 mRNA peaked on day 4.