Potential Role of Bacterial Infection in Autoimmune Diseases: A New Aspect of Molecular Mimicry

Alam, Jehan; Kim, Yong Chul; Choi, Youngok

doi:10.4110/in.2014.14.1.7

Cited by 33 publications

(25 citation statements)

References 37 publications

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“…Thus, it is likely that both species share highly conserved antigens, capable of inducing a similar immune response in patients with sarcoidosis [34]. A second possible mechanism is an auto-antigen-like reaction invoked by Atopobium antigens, as described for rheumatoid arthritis (RA) [35].…”

Section: Discussionmentioning

confidence: 99%

Atopobium and Fusobacterium as novel candidates for sarcoidosis-associated microbiota

et al. 2017

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Sarcoidosis is a granulomatous disease that mainly affects the lung. A role of microbial factors in disease pathogenesis is assumed, but has not been investigated systematically in a large cohort.This cross-sectional study compared the lung microbiota of 71 patients with sarcoidosis, 15 patients with idiopathic pulmonary fibrosis (non-infectious controls) and 10 healthy controls (HCs). Next-generation sequencing of 16S DNA was used on bronchoalveolar lavage samples to characterise the microbial composition, which was analysed for diversity and indicator species. Host genotypes for 13 known sarcoidosis risk variants were determined and correlated with microbial parameters.The microbial composition differed significantly between sarcoidosis and HC samples (redundancy analysis ANOVA, p=0.025) and between radiographic Scadding types. spp. was detected in 68% of sarcoidosis samples, but not in HC samples. spp. was significantly more abundant in sarcoidosis samples compared with those from HCs. Mycobacteria were found in two of 71 sarcoidosis samples. Host-genotype analysis revealed an association of the rs2076530 () risk allele with a decrease in bacterial burden (p=0.002).Our results indicate Scadding type-dependent microbiota in sarcoidosis BAL samples. spp. and spp. were identified as sarcoidosis-associated bacteria, which may enable new insights into the pathogenesis and treatment of the disease.

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Section: Discussionmentioning

confidence: 99%

Atopobium and Fusobacterium as novel candidates for sarcoidosis-associated microbiota

et al. 2017

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“…Many studies have implied a role for PAMPs in the etiology of chronic inflammation and autoimmune disease (65, 66), an association that is believed to stem from molecular mimicry between pathogen-derived antigenic determinants and evolutionarily conserved motifs in eukaryotes. In this context, it is notable that CL, an ancient prokaryotic phospholipid, has been retained by the mitochondria, an organelle that is considered to have evolved from eubacterial ancestors (67).…”

Section: Discussionmentioning

confidence: 99%

Dichotomous roles for externalized cardiolipin in extracellular signaling: Promotion of phagocytosis and attenuation of innate immunity

et al. 2015

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Among the distinct molecular signatures present in the mitochondrion is the tetra-acylated anionic phospholipid cardiolipin, a lipid also present in primordial, single-cell bacterial ancestors of mitochondria and multiple bacterial species today. Cardiolipin is normally localized to the inner mitochondrial membrane; however, when cardiolipin becomes externalized to the surface of dysregulated mitochondria, it promotes inflammasome activation and stimulates the elimination of damaged or nonfunctional mitochondria by mitophagy. Given the immunogenicity of mitochondrial and bacterial membranes that are released during sterile and pathogen-induced trauma, we hypothesized that cardiolipins might function as “eat me” signals for professional phagocytes. In experiments with macrophage cell lines and primary macrophages, we found that membranes with mitochondrial or bacterial cardiolipins on their surface were engulfed through phagocytosis, which depended on the scavenger receptor CD36. Distinct from this process, the copresentation of cardiolipin with the Toll-like receptor 4 (TLR4) agonist lipopolysaccharide dampened TLR4-stimulated production of cytokines. These data suggest that externalized, extracellular cardiolipins play a dual role in host-host and host-pathogen interactions by promoting phagocytosis and attenuating inflammatory immune responses.

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“…Molecular mimicry is an attractive mechanism for triggering autoimmunity that could explain these findings [64]. The wide distribution of the highly conserved stress proteins or enzymes among the members of the normal flora and common infectious microorganisms raises a new question on how cross-reactive autoantibodies are not produced during the immune response to these bacteria in most healthy people.…”

Section: The Potential Role Of Bacteria In Juvenile Idiopathic Arthritismentioning

confidence: 98%

The Etiology of Juvenile Idiopathic Arthritis

Rigante

Bosco

Esposito

2014

Clinic Rev Allerg Immunol

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Over the years, the commonly used term to describe juvenile idiopathic arthritis (JIA) has changed. By definition, JIA includes all types of arthritis with no apparent cause, lasting more than 6 weeks, in patients aged less than 16 years at onset. JIA pathogenesis is still poorly understood: the interaction between environmental factors and multiple genes has been proposed as the most relevant working mechanism to the development of JIA. The concept that various microbes that colonize or infect not only the mucosal surfaces, like the oral cavity, but also the airways and gut might trigger autoimmune processes, resulting in chronic arthritides, and JIA was first drafted at the outset of last century. JIA development might be initiated and sustained by the exposure to environmental factors, including infectious agents which affect people at a young age, depending on the underlying genetic predisposition to synovial inflammation. Many data from patients with JIA suggest a scenario in which different external antigens incite multiple antigen-specific pathways, cytotoxic T cell responses, activation of classical complement cascade, and production of proinflammatory cytokines. In this review, emphasis is paid not only to the potential role of parvovirus B19 and Epstein-Barr virus in primis but also to the general involvement of different bacteria as Salmonella spp., Shigella spp., Campylobacter spp., Mycoplasma pneumoniae, Chlamydophila pneumoniae, Bartonella henselae, and Streptococcus pyogenes for the development of immune-mediated arthritides during childhood. No unequivocal evidence favoring or refuting these associations has been clearly proved, and today, the strict definition of JIA etiology remains unknown. The infection can represent a random event in a susceptible individual, or it can be a necessary factor in JIA development, always in combination with a peculiar genetic background. Further studies are needed in order to address the unsolved questions concerning this issue.

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Potential Role of Bacterial Infection in Autoimmune Diseases: A New Aspect of Molecular Mimicry

Cited by 33 publications

References 37 publications

Atopobium and Fusobacterium as novel candidates for sarcoidosis-associated microbiota

Atopobium and Fusobacterium as novel candidates for sarcoidosis-associated microbiota

Dichotomous roles for externalized cardiolipin in extracellular signaling: Promotion of phagocytosis and attenuation of innate immunity

The Etiology of Juvenile Idiopathic Arthritis

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