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Results for “Chlamydia Infections”

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PubMed1991

[Erythema nodosum in Chlamydia pneumoniae infection].

Chlamydia pneumonia is now recognized as a species of the Chlamydia genus distinct from C psittaci and C trachomatis species. It is a common cause of pneumonia and other acute respiratory tract infections. We describe a patient with erythema nodosum secondary to infection with C pneumoniae. Since this agent usually causes a mild illness, with no distinct clinical findings, we recommend adding serological tests for C pneumoniae to other relevant laboratory investigations in patients with erythema nodosum.

Adolescent↗
PubMed2001

Recognition of the 60 kilodalton cysteine-rich outer membrane protein OMP2 by CD4(+) T cells from humans infected with Chlamydia trachomatis.

T cell-mediated immunity is important in the control of chlamydia infection but chlamydia-specific T cells are also implicated in the inflammation and tissue damage which characterize chlamydia associated diseases. To investigate target antigens of the T cell-mediated immune response to chlamydia infection, Chlamydia trachomatis-specific CD4+ T cell clones were isolated from a patient with chlamydia-induced reactive arthritis. T cell immunoblotting indicated that an antigen of approximately 60 kilodaltons molecular mass was recognized, and recombinant 60 kilodalton cysteine-rich outer membrane 2 (OMP2) proved to be stimulatory. By using deletion constructs and synthetic peptides an epitope presented by HLA-DRB1*0401 was defined and proved to contain the nonamer peptide within the OMP2 sequence predicted to have the greatest binding affinity for DRB1*0401 The sequence of the epitope is conserved in all C. trachomatis strains but not in C. pneumoniae. Investigation of patients with acute urethritis and additional patients with sexually acquired reactive arthritis showed that OMP2-reactive T cells were readily detectable in peripheral blood and synovial fluid. Thus OMP2 is a target antigen of the T cell-mediated immune response to CT infection.

Antigens, Bacterial↗
PubMed2005

Do the characteristics of sexual health centre clients predict chlamydia infection sufficiently strongly to allow selective screening?

OBJECTIVES: This study aimed to estimate chlamydia prevalence and risk factors for infection and to assess the performance of chlamydia-selective screening criteria among clients attending a large sexually transmitted infection (STI) clinic. METHODS: Computerised records for all attendances between 1 July 2002 and 30 June 2003 were analysed. Chlamydia prevalence and risk factors for infection were determined for all new clients. The sensitivity and specificity of risk factors for chlamydia were assessed. RESULTS: 2642 male and 2084 female new clients were tested for chlamydia with a prevalence of 7.3% (95% CI: 6.3%, 8.4%) among men and 3.9% (95% CI: 3.1%, 4.9%) among women. Screening heterosexual men based on a positive contact or symptoms of non-specific urethritis or any two of age <25 years, 4+ partners last 12 months, inconsistent condom use or not presenting for an asymptomatic screen detected 88% of infections by screening 62%. Screening women based on a positive contact or injecting drug use or any two of age <25 years, 2+ partners last 12 months or inconsistent condom use would detect 86% of infections by screening 57%. CONCLUSIONS: Selective screening could be used to more efficiently identify heterosexual men and women at risk of chlamydia.

Adult↗
PubMed2002

Upregulation of extracellular matrix metalloproteinase inducer (EMMPRIN) and gelatinases in human atherosclerosis infected with Chlamydia pneumoniae: the potential role of Chlamydia pneumoniae infection in the progression of atherosclerosis.

Chlamydia pneumoniae infection implicated as an important etiologic factor of atherosclerosis, especially in coronary artery disease (CAD), was found in vitro to be associated with the induction of matrix metalloproteinases (MMPs). An extracellular matrix metalloproteinase inducer (EMMPRIN)/ membrane-type 1 matrix metalloproteinase (MT1-MMP) system which induces and activates MMPs, is suggested to be functional and were upregulated in the failing myocardium. However, the upstream regulation of MMPs by C. pneumoniae within atheroma itself remains unclear. We evaluated the seroepidemiologic study of C. pneumoniae infection in CAD patients (n= 391) and controls (n=97) and performed histopathological and in vitro analysis in atherosclerotic vascular tissues obtained from patients with seropositive to C. pneumoniae (n=20), by using immunochemistry for C. pneumoniae, EMMPRIN/MT1-MMP, MMP-2, and MMP-9. The seropositive rates of both anti-C. pneumoniae IgG and IgA were 56.7% in CAD group and 43.3% in control group (P=0.033). Seropositive rate was increased in subgroups of CAD patients without conventional coronary risk factors compared to those with conventional risk factors. Immunoreactivities of EMMPRIN, MT1-MMP, MMP-2, and MMP-9 were increased in the atheromatous plaque itself, predominantly in immunoreactive macrophages/mononuclear cells to C. pneumoniae. Furthermore, Western blot analysis showed that EMMPRIN and MMP-2 were detected more prominently in atherosclerotic tissues infected with C. pneumoniae compared to control tissues. Zymographic analysis revealed that activities of MMP-2 and MMP-9 were more increased in atherosclerotic tissues infected with C. pneumoniae compared to control tissues. The present study demonstrated upstream regulation of MMPs can be induced by C. pneumoniae within atheromatous plaque itself. These findings help to understand the potential role of C. pneumoniae in the progression of atherosclerosis.

Aged↗
PubMed2000

Degradation of transcription factor RFX5 during the inhibition of both constitutive and interferon gamma-inducible major histocompatibility complex class I expression in chlamydia-infected cells.

We have previously shown that the obligate intracellular pathogen chlamydia can suppress interferon (IFN)-gamma-inducible major histocompatibility complex (MHC) class II expression in infected cells by degrading upstream stimulation factor (USF)-1. We now report that chlamydia can also inhibit both constitutive and IFN-gamma-inducible MHC class I expression in the infected cells. The inhibition of MHC class I molecule expression correlates well with degradation of RFX5, an essential downstream transcription factor required for both the constitutive and IFN-gamma-inducible MHC class I expression. We further demonstrate that a lactacystin-sensitive proteasome-like activity identified in chlamydia-infected cell cytosolic fraction can degrade both USF-1 and RFX5. This proteasome-like activity is dependent on chlamydial but not host protein synthesis. Host preexisting proteasomes may not be required for the unique proteasome-like activity. These observations suggest that chlamydia-secreted factors may directly participate in the proteasome-like activity. Efforts to identify the chlamydial factors are underway. These findings provide novel information on the molecular mechanisms of chlamydial evasion of host immune recognition.

Bacterial Proteins↗