Recent<i>Chlamydia pneumoniae</i>infection is highly associated with active ankylosing spondylitis in a Chinese cohort

Feng, Xiugao; Xu, Xingyan; Ye, S; Lin, Yeong‐Jang; Chen, P; Zhang, X J; Lin, Guiying; Lin, Xiao

doi:10.3109/03009742.2011.560891

Cited by 11 publications

(18 citation statements)

References 15 publications

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“…Although bacterial infection such as Chlamydia could cause chronic arthritis [40], it is still premature to conclude that bacterial infection can cause AS [41]. Conversely, evidence suggests that AS disease activity became worse, following the different bacterial infections such as Salmonella, Yersinia, Campylobacter and Chlamydia [42][43][44][45][46]. Although molecular mimicry between the bacterial components and self-peptides was considered to play a role [47], our results may provide an alternative explanation, that the bacterial LPS could suppress IFN-g production in activated normal T cells.…”

Section: Discussionmentioning

confidence: 99%

Aberrant expression of microRNAs in T cells from patients with ankylosing spondylitis contributes to the immunopathogenesis

Lai

Chen

et al. 2013

Clinical and Experimental Immunology

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Summary Ankylosing spondylitis (AS) is a chronic inflammatory disorder characterized by dysregulated T cells. We hypothesized that the aberrant expression of microRNAs (miRNAs) in AS T cells involved in (TLR-4), a target of let-7i, in T cells from AS patients were decreased. In addition, the mRNA expression of interferon (IFN)-g was elevated in AS T cells. Lipopolysaccharide (LPS), a TLR-4 agonist, inhibited IFN-g secretion by anti-CD3+ anti-CD28 antibodiesstimulated normal T cells but not AS T cells. In the transfection studies, we found the increased expression of let-7i enhanced IFN-g production by anti-CD3 + anti-CD28 + lipopolysaccharide (LPS)-stimulated normal T cells. In contrast, the decreased expression of let-7i suppressed IFN-g production by anti-CD3 + anti-CD28 + LPS-stimulated AS T cells. In conclusion, we found that miR-16, miR-221 and let-7i were over-expressed in AS T cells, but only miR-221 and let-7i were associated with BASRI of lumbar spine. In the functional studies, the increased let-7i expression facilitated the T helper type 1 (IFN-g) immune response in T cells.

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Section: Discussionmentioning

confidence: 99%

Aberrant expression of microRNAs in T cells from patients with ankylosing spondylitis contributes to the immunopathogenesis

Lai

Chen

et al. 2013

Clinical and Experimental Immunology

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“…119 The role of environmental factors in AS pathogenesis and why many HLA-B27 -positive individuals never develop AS or other forms of spondyloarthritis are yet unsolved. 120, 121 …”

Section: Introductionmentioning

confidence: 99%

Genetics, Environment, and Gene-Environment Interactions in the Development of Systemic Rheumatic Diseases

Costenbader¹

2014

Rheumatic Disease Clinics of North America

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Understanding disease susceptibility factors and gene-environment interactions may offer valuable insights into the biological mechanisms for the etiology of rheumatic diseases. Defining the contributions of genetic and environmental factors to the pathogenesis of rheumatic diseases such as rheumatoid arthritis (RA), systemic lupus erythematosus (SLE) and ankylosing spondylitis (AS), may have important implications for understanding risk prediction, pathogenic mechanisms, cellular pathways, drug discovery, and prevention strategies. However, rheumatic diseases offer distinct challenges to researchers due to heterogeneity in disease phenotypes, low disease incidence, and geographic variation in both genetic and environmental factors. Emerging research areas, including epigenetics, metabolomics, and the microbiome, may provide additional links between genetic and environmental risk factors in rheumatic disease pathogenesis. This article reviews the methods used to establish genetic and environmental risk factors and to study gene-environment interactions in rheumatic diseases and provides specific examples of successes and challenges for identifying gene-environment interactions in RA, SLE, and AS. Finally, we describe how emerging research strategies may build upon previous discoveries as well as future challenges.

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“…On the other hand, the traditional mechanisms that explain the association of infection and autoimmunity include bystander activation, molecular mimicry, cryptic antigens, and epitope spreading; 21 it should be noted that the infection of some microorganisms can also increase the severity of the disease itself such as chlamydia infection for patients with ankylosing spondylitis. 22 We noted that some patients with SLE who suffered from arthritis/arthralgia had no evidence of JCV reactivation. There is a possibility the reactivation of JCV in patients with SLE may enhance the joint inflammation of SLE.…”

Section: Discussionmentioning

confidence: 80%

Increased prevalence of JC polyomavirus viruria was associated with arthritis/arthralgia in patients with systemic lupus erythematosus

et al. 2014

Lupus

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RecentChlamydia pneumoniaeinfection is highly associated with active ankylosing spondylitis in a Chinese cohort

Abstract: Recent Cp infections occur frequently in AS patients and Cp IgM antibody is correlated with active disease. These findings indicate that Cp infections may be a triggering factor for active AS.

Cited by 11 publications

References 15 publications

Aberrant expression of microRNAs in T cells from patients with ankylosing spondylitis contributes to the immunopathogenesis

Aberrant expression of microRNAs in T cells from patients with ankylosing spondylitis contributes to the immunopathogenesis

Genetics, Environment, and Gene-Environment Interactions in the Development of Systemic Rheumatic Diseases

Increased prevalence of JC polyomavirus viruria was associated with arthritis/arthralgia in patients with systemic lupus erythematosus

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