Psittacosis is a zoonosis caused by Chlamydia psittaci,a Gram-negative intracellular bacterium.This condition is caused by the ingestion of contaminated fecal matter and nasal secretions from infected birds.The severi...Psittacosis is a zoonosis caused by Chlamydia psittaci,a Gram-negative intracellular bacterium.This condition is caused by the ingestion of contaminated fecal matter and nasal secretions from infected birds.The severity of human psittacosis varies from mildflu-like symptoms to life-threatening severe pneumonia.[1]Given that C.psittaci is not a part of the traditional microbiological diagnosis’human psittacosis is often underreported,misdiagnosed,and inadequately diagnosed.In this study,the clinical data of C.psittaci pneumonia patients were retrospectively analyzed.展开更多
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 cytok...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. trachomatis triggers this production, and which protein（s） stimulate inflammatory cytokines remains unknown. In the present study, the C. trachomatis pORF5 protein induced tumor necrosis factor alpha （TNF-a）, interleukin-1 beta （IL-1β） and interleukin-8 （IL-8） in dose and time-dependent manners in the THP-1 human monocyte cell line. We found that intracellular p38/mitogen-activated protein kinase （MAPK） and extracellular signal-regulated kinase （ERK）/MAPK signaling pathways were required for the induction of TNF- a, IL-1β and IL-8. Blockade of toll-like receptor 2 （TLR2） signaling reduced induction levels of TNF-a, IL-8 and IL-1β. We concluded that the C. trachomatis pORF5 protein might contribute to the inflammatory processes associated with chlamydial infections.展开更多
To validate the immune protective efficacy of pORF5 DNA vaccine and to analyze potential mechanisms related to this protection. In this study, pORF5 DNA vaccine was constructed and evaluated for its protective immunit...To validate the immune protective efficacy of pORF5 DNA vaccine and to analyze potential mechanisms related to this protection. In this study, pORF5 DNA vaccine was constructed and evaluated for its protective immunity in a mouse model of genital chlamydial infection. Groups of BALB/c mice were immunized intranasally with pORF5 DNA vaccine. Humoral and cell mediated immune responses were evaluated. The clearance ability of chlamydial challenge from the genital tract and the chlamy- dia-induced upper genital tract gross pathology and histopathological characterization were also de- tected. The results showed that the total and the IgG2a anti-pORF5 antibody levels in serum were sig- nificantly elevated after pcDNA3.1-pORF5 vaccination, as were the total antibody and IgA levels in vaginal fluids. pcDNA3.1-pORF5 induced a significantly high level of Th1 response as measured by robust gamma interferon (IFN-γ). Minimal IL-4 was produced by immune T cells in response to the re-stimulation with pORF5 protein or the inactive elementary body in vitro. pcDNA3.1-pORF5-vacci- nated mice displayed significantly reduced bacterial shedding upon a chlamydial challenge and an accelerated resolution of infection. 100% of pcDNA3.1-pORF5 vaccinated mice successfully resolved the infection by day 24. pcDNA3.1-pORF5-immunized mice also exhibited protection against patho- logical consequences of chlamydial infection. The stimulated index was significantly higher than that of mice immunized with pcDNA3.1 and PBS (P<0.05). Together, these results demonstrated that immu- nization with pORF5 DNA vaccine is a promising approach for eliciting a protective immunity against a genital chlamydial challenge.展开更多
文摘Psittacosis is a zoonosis caused by Chlamydia psittaci,a Gram-negative intracellular bacterium.This condition is caused by the ingestion of contaminated fecal matter and nasal secretions from infected birds.The severity of human psittacosis varies from mildflu-like symptoms to life-threatening severe pneumonia.[1]Given that C.psittaci is not a part of the traditional microbiological diagnosis’human psittacosis is often underreported,misdiagnosed,and inadequately diagnosed.In this study,the clinical data of C.psittaci pneumonia patients were retrospectively analyzed.
基金supported by the National Natural Science Foundation of China(30970165,81102230)Team Project for the Technology Innovation of Higher Education of Hunan Province,China,2010
文摘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. trachomatis triggers this production, and which protein（s） stimulate inflammatory cytokines remains unknown. In the present study, the C. trachomatis pORF5 protein induced tumor necrosis factor alpha （TNF-a）, interleukin-1 beta （IL-1β） and interleukin-8 （IL-8） in dose and time-dependent manners in the THP-1 human monocyte cell line. We found that intracellular p38/mitogen-activated protein kinase （MAPK） and extracellular signal-regulated kinase （ERK）/MAPK signaling pathways were required for the induction of TNF- a, IL-1β and IL-8. Blockade of toll-like receptor 2 （TLR2） signaling reduced induction levels of TNF-a, IL-8 and IL-1β. We concluded that the C. trachomatis pORF5 protein might contribute to the inflammatory processes associated with chlamydial infections.
基金the National High-Tech Research and Development Program of China (Grant No. 2004AA2Z3530)the Hunan Province "Eleventh Five-Year Plan" Impor-tant Special Program (Grant No. 2006SK1001)the National Institutes of Health, USA (Grant No.1 R01 AI47997-01)
文摘To validate the immune protective efficacy of pORF5 DNA vaccine and to analyze potential mechanisms related to this protection. In this study, pORF5 DNA vaccine was constructed and evaluated for its protective immunity in a mouse model of genital chlamydial infection. Groups of BALB/c mice were immunized intranasally with pORF5 DNA vaccine. Humoral and cell mediated immune responses were evaluated. The clearance ability of chlamydial challenge from the genital tract and the chlamy- dia-induced upper genital tract gross pathology and histopathological characterization were also de- tected. The results showed that the total and the IgG2a anti-pORF5 antibody levels in serum were sig- nificantly elevated after pcDNA3.1-pORF5 vaccination, as were the total antibody and IgA levels in vaginal fluids. pcDNA3.1-pORF5 induced a significantly high level of Th1 response as measured by robust gamma interferon (IFN-γ). Minimal IL-4 was produced by immune T cells in response to the re-stimulation with pORF5 protein or the inactive elementary body in vitro. pcDNA3.1-pORF5-vacci- nated mice displayed significantly reduced bacterial shedding upon a chlamydial challenge and an accelerated resolution of infection. 100% of pcDNA3.1-pORF5 vaccinated mice successfully resolved the infection by day 24. pcDNA3.1-pORF5-immunized mice also exhibited protection against patho- logical consequences of chlamydial infection. The stimulated index was significantly higher than that of mice immunized with pcDNA3.1 and PBS (P<0.05). Together, these results demonstrated that immu- nization with pORF5 DNA vaccine is a promising approach for eliciting a protective immunity against a genital chlamydial challenge.
