Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirty male patients with sexually acquired reactive arthritis (SARA) have been studied at the time of their initial presentation and thereafter. Chlamydia trachomatis was isolated from the urethral exudate of 9 (36.0%) of the 25 patients from whom urethral specimens were taken, and elevated titres of IgM antibody of C. trachomatis were detected in 11 (36.6%) of the 30 initial sera. Thirteen (43.3%) of the patients has a positive urethral culture and/or elevated titre of IgM antibody, and it is therefore suggested that 43.3% of these patients suffered an acute chlamydial infection at or near the time of the onset of their joint disease. The demonstration of 4-fold or greater rises and/or falls in IgM antibody titre (8 patients) and IgG antibody titre (6 patients) in a group of 15 men studied throughout the course of their disease strongly supports this conclusion. A positive urethral culture and/or raised titre of IgM serum antibody was also detected in 25 (50%) of 50 men with uncomplicated nongonococcal urethritis (NGU), suggesting that the prevalence of chlamydial infections in the 2 conditions is similar. Titres of IgG serum antibody to C. trachomatis were, however, significantly higher in patients with SARA than in those with NGU or other rheumatic diseases, and in healthy controls. The geometric mean titres (GMT) of IgG serum antibody in patients with SARA, NGU, rheumatoid arthritis, ankylosing spondylitis, systemic lupus erythematosus, and in healthy controls were 1:47.5, 1:8.6, 1:2.2, 1;2.2, 1:3.5, and 1:1.4, respectively. These findings suggest that an exaggerated antibody response to acute infection by C. trachomatis may be an important factor in the development of SARA in some but not all patients.
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PMID:Evidence of Chlamydia trachomatis infection in sexually acquired reactive arthritis. 689 52

L7 is one of the ribosomal proteins frequently targeted by autoantibodies in rheumatic autoimmune diseases. A computer search revealed a region within the immunodominant epitope of L7 (peptide II) that is highly homologous to amino acid sequence 264-286 of the RNA polymerase major sigma factor of the eubacterium Chlamydia trachomatis. Anti-L7 autoantibodies affinity purified from the immunodominant epitope were able to recognize this sequence as they reacted with purified recombinant sigma factor. Immunofluorescence labeling experiments on C. trachomatis lysates revealed a punctate staining pattern of numerous spots when incubated with the affinity-purified anti-peptide II autoantibodies. Binding of autoantibodies to peptide II was inhibited by the homologous sigma peptide. This is the first demonstration of epitope mimicry between a human and a chlamydial protein on the level of B cells. Antibody screening revealed a significant correlation between the presence of anti-L7 autoantibodies and C. trachomatis infection in patients with systemic lupus erythematosus and mixed connective tissue disease. Our results suggest that molecular mimicry is involved in the initiation of anti-L7 autoantibody response and may represent a first glance into the immunopathology of Chlamydia with respect to systemic rheumatic diseases.
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PMID:Correlation between chlamydial infection and autoimmune response: molecular mimicry between RNA polymerase major sigma subunit from Chlamydia trachomatis and human L7. 984 29

A 40-year-old female was admitted with right chest pain. SLE was absent from her past history, although she complained of polyarthralgia in winter. Atypical pneumonia/pleuritis was suspected by chest X-ray film, showing a nodular shadow in the right lower field and moderate pleural effusion. Chlamydia pneumonia was diagnosed by elevated anti-C. psittsci antibody, while characteristics of pleural fluid revealed serositis accompanied by SLE because of the high titered anti-DNA antibody and the low titered complement. She was cured by clarithromycin and subsequent administration of prednisolone and cyclophosphamide.
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PMID:[A case of Chlamydia pneumonia and systemic lupus erythematosus (SLE) pleurisy]. 1021 98

Over the past two decades, a number of studies have failed to provide direct evidence of specific microbial chronic infection in primary biliary cirrhosis (PBC). However, a recent report suggests that there is a specific association of Chlamydia pneumoniae in patients with PBC and that C. pneumoniae or similar antigens might play a role in the pathogenesis of disease. To determine if Chlamydia infection is associated with PBC, we applied a combination of immunological and molecular approaches to investigate (a) the serological reactivity against two common Chlamydia human pathogens, C. pneumoniae and C. trachomatis, by immunoblotting, (b) the presence of Chlamydia in liver samples of patients with PBC and controls by PCR amplification of Chlamydia specific 16S rRNA and (c) the presence of Chlamydia proteins in liver samples of patients with PBC and controls by immunohistochemical staining. By immunoblotting, C. trachomatis and C. pneumoniae specific serological antibodies were found in 52/57 (91.2%) AMA positive PBC, 7/33 (21/2%) of AMA negative PBC, 1/25 (4%) PSC, 0/15 (0%) Sjorgen's syndrome and 0/20 (0%) systemic lupus erythematosus patients and 0/20 (0%) healthy volunteers at 1:200 sera dilution. PBC sera reacted to Chlamydia and E. coli lysates in western blots up to a maximum of 10(-4) dilution. However, PCR amplification of the Chlamydia specific 16S rRNA gene was negative in 25/25 PBC livers but positive in 1/4 PSC liver, 3/6 in other liver disease controls and 1/4 normal liver samples. While two commercially available specific monoclonal antibodies stained positive controls (Chlamydia infected HEp-2 cells) they failed to detect Chlamydia antigens in PBC livers. The detection of Chlamydia specific antibodies but not Chlamydia rRNA gene and Chlamydia antigens in PBC suggests that Chlamydia infection is not involved in PBC.
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PMID:Is there a relation between Chlamydia infection and primary biliary cirrhosis? 1476 55

Atherosclerosis is a chronic inflammatory disease of the arteries associated with various risk factors that promote lipid abnormalities (i.e., dyslipidemia), development and progression of atherosclerotic lesions, plaque rupture, and vascular thrombosis. Experimental evidence from biochemical and clinical studies support the idea that arterial thrombosis is an autoimmune process resulting from 'autoantibody'-mediated pro-atherogenic mechanisms now seen in systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS). In addition, it has been shown that persistent infections of Chlamydia pneumoniae (C. pneumoniae), Porphyromonas gingivalis (P. gingivalis), and Helicobacter pylori (H. pylori) cause immune responses (infectious immunity) in their hosts that promote atherogenesis. In this article, we review recent progress in our understanding of immune- and infection-mediated atherosclerosis.
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PMID:Preventing autoimmune and infection triggered atherosclerosis for an enduring healthful lifestyle. 1819 Aug 81

Major developments have taken place to further our understanding of the relationship between genetics and the environment in the pathogenesis of rheumatic disorders. The association between HLA markers and human disease is becoming clearer. For instance, HLA-DRW4 frequently occurs in patients with rheumatoid disease, and penicillamine and gold toxicity are seen most often in patients with HLA-DRW2 or DRW3. Antisera to B alloantigens help define the genetic differences between systemic lupus erythematosus and rheumatoid arthritis. As yet, the most dramatic link is that between HLA-B27 and primary ankylosing spondylitis. This same antigen is related, to varying degrees, with other members of the seronegative spondylarthritides and there is strong evidence that this association is related to HLA-B27, itself, rather than an associated disease gene. Nevertheless, some data refute a single gene theory. We are just beginning to learn more about interactions between different genes on the sixth chromosome and genes on other chromosomes.The sex ratio of the spondylarthritides is now better defined. Sacroiliitis may have a comparable sex distribution although females have more peripheral joint disease and males have greater spinal involvement. Unfortunately, the explanation for these differences remains elusive.The specific infective agents related to the development of rheumatic disorders are becoming clarified. Chlamydia, Salmonella, Yersinia and Shigella flexneri types 1b and 2a are arthritogenic, while Shigella sonnei appears not to cause disease. Although the Reiter syndrome is now considered a chronic disease, the reason for remissions and relapses remains unclear.
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PMID:The relationship between genetics and environment in the pathogenesis of rheumatic diseases. 1874 70

Autoimmune diseases have several etiologies. Acute Chlamydia pneumoniae (C. pneumoniae) infection may be involved in the pathogenesis of several autoimmune diseases. In this study, 82 patients with several autoimmune diseases and 70 controls were enrolled, and acute C. pneumoniae infection has been evaluated by monitoring the levels of IgM antibody. Chlamydia pneumoniae IgM positive results were observed in 29% (P < 0.05) of the patients with several autoimmune diseases and in 10% of the controls. Chlamydia pneumoniae IgM positive cases were more frequent among the patients with rheumatoid arthritis (RA; 30%, P < 0.05), systemic lupus erythematosus (SLE; 28.0%, P < 0.05), dermatomyositis/polymyositis (23%, NS), myeloperoxidase-antineutrophil cytoplasmic autoantibody (MPO-ANCA)-associated vasculitis (33%, NS), adult onset of Still's disease (29%, NS) and giant cell arteritis/Takayasu arteritis (50%, NS) than among the controls. This positive frequency was statistically significant in RA and SLE. These results suggest that acute C. pneumoniae infection is probably involved in the pathogenesis of autoimmune diseases.
Lupus 2009 Feb
PMID:Acute Chlamydia pneumoniae infection in the pathogenesis of autoimmune diseases. 1976 92

Chlamydia trachomatis (CT) is the most common bacterial cause of sexually transmitted disease. It has been associated with arthritis and it is a risk factor for human papillomavirus (HPV)-induced lesions. There are few studies on the frequency of CT infection among systemic lupus erythematosus (SLE) patients. The aim of this study was to determine the prevalence of endocervical CT infection among SLE patients and evaluate whether or not CT infection is a risk factor for HPV-induced lesions. A cross-sectional study included a group of patients who fulfilled the American College Rheumatology criteria for a definite diagnosis of SLE and a control group of non-SLE female individuals from Bahia, Brazil. Polymerase chain reaction was used on endocervical swab specimens to test for CT; a gynecological examination including a cervical cytology and biopsy was done for the identification of HPV lesions. A total of 105 SLE patients were studied, and the control group was composed of 104 age-matched apparently normal women. The prevalence of CT endocervical infection was 3.0 % [confidence interval (CI) 95 % = 0.6-8.0 %] in the SLE group and 5.0 % (95 % CI = 2.0-11.0 %) in the control group; the prevalence ratio was 0.60 (95 % CI = 0.1-2.5). The prevalence of vulvar condyloma was higher among SLE patients (11.0 vs. 1.0 %, p < 0.001), as were the prevalences of low-grade lesion (12.0 vs. 1.0 %, p < 0.001) and cervical intraepithelial neoplasia 1 (9.0 vs. 1.0 %, p = 0.02). There was no association between the presence of HPV lesions and CT infections. However, the small number of patients with CT prevents a definite conclusion from being drawn. The prevalence of endocervical CT infection in women with SLE is low and similar to that of the normal population. This suggests that this infection has no role in the pathogenesis of SLE or the development of HPV-induced lesions.
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PMID:Prevalence of Chlamydia trachomatis endocervical infection in systemic lupus erythematosus patients and evaluation of the risk for HPV-induced lesions. 2248 38

A case of a genetically HLA-B27 patient fully investigated by molecular analyses, following a holistic vision and an anamnestic assessment of multi-site ecosystems is repeated. VDRL, Lupus anti-coagulant (LAC) and Widal-Wright (WWR), resulted positive. The antibodies (IgG/IgA anti-Ct) against chronic Chlamydia trachomatis inflammation were positive. In the context of all the enzymatic activities in reference range, the AMS and the ALP enzymatic activities showed an increasing trend and a time course augment depending respectively. Cultures, parasitological, digestibility tests and molecular analyses were then performed to investigate the different human ecosystems. Parasitological research and digestibility test were performed, resulting a latent chronic bowel inflammation, including certain enteroinvasive pathogens, such as, Salmonella, Shigella, Yersinia and Campylobacter (Enteric Pathogens Group, EPG) and Escherichia Coli pathogens (Escherichia Coli Pathogens Group, ECPG). The Salmonella typhi-DNA resulted positive, while 90% of the total microbic charge (TMC) was represented by C. freundi in culture analyses. Interpreting the VDRL positive test as early triggering of autoimmune disease, a few acute phase proteins as a pauci-symptomatic chronic phlogistic process, the amylase and alkaline phosphatase alterations as tissue markers of early intestinal inflammation, the Widal's reaction positivity together with the precocious clinical and faecal manifestations, this study suggests the prime triggering role of these atypical pathogens to cause a chronic low grade autoimmune response against the tissue/organ susceptible target, causing inflammaging phenomenon in young patient with chronic latent infection by Salmonella typhi, leading to Reiter's syndrome, in HLA-B27 positive patient.
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PMID:Can latent synergism of intestinal pathogens be responsible for inflammaging process causing Reiter's syndrome in a young patient HLA-B27 infected by atypical pathogens? A holistic view and clinical biochemical reinterpretation. 2324 Nov 24

Myalgic encephalomyelitis (ME, also called Chronic Fatigue Syndrome), a common disease with chronic fatigability, cognitive dysfunction and myalgia of unknown etiology, often starts with an infection. The chaperonin human heat shock protein 60 (HSP60) occurs in mitochondria and in bacteria, is highly conserved, antigenic and a major autoantigen. The anti-HSP60 humoral (IgG and IgM) immune response was studied in 69 ME patients and 76 blood donors (BD) (the Training set) with recombinant human and E coli HSP60, and 136 30-mer overlapping and targeted peptides from HSP60 of humans, Chlamydia, Mycoplasma and 26 other species in a multiplex suspension array. Peptides from HSP60 helix I had a chaperonin-like activity, but these and other HSP60 peptides also bound IgG and IgM with an ME preference, theoretically indicating a competition between HSP60 function and antibody binding. A HSP60-based panel of 25 antigens was selected. When evaluated with 61 other ME and 399 non-ME samples (331 BD, 20 Multiple Sclerosis and 48 Systemic Lupus Erythematosus patients), a peptide from Chlamydia pneumoniae HSP60 detected IgM in 15 of 61 (24%) of ME, and in 1 of 399 non-ME at a high cutoff (p<0.0001). IgM to specific cross-reactive epitopes of human and microbial HSP60 occurs in a subset of ME, compatible with infection-induced autoimmunity.
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PMID:Epitopes of microbial and human heat shock protein 60 and their recognition in myalgic encephalomyelitis. 2431 70


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