Editorial: Microbial and Environmental Factors in Autoimmune and Inflammatory Diseases

Arleevskaya, Marina I; Manukyan, Gayane; Inoüe, Ryo; Aminov, Rustam

doi:10.3389/fimmu.2017.00243

Cited by 22 publications

(23 citation statements)

References 2 publications

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“…The interplay of various genetic, hormonal, immunological, and environmental factors constitutes the mosaic of autoimmunity [45]. Viral infections play a substantial role in the development of several autoimmune diseases in individuals with underlying immune dysregulation [46]. Follow up data from survivors of viral outbreaks like influenza, Zika, Ebola, and Chikungunya have shown development of autoimmune phenomenon within weeks to months after recovery.…”

Section: Sars-cov-2 Infection and Autoimmunitymentioning

confidence: 99%

Autoimmune and rheumatic musculoskeletal diseases as a consequence of SARS-CoV-2 infection and its treatment

et al. 2020

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The coronavirus disease-2019 (COVID-19) pandemic is likely to pose new challenges to the rheumatology community in the near and distant future. Some of the challenges, like the severity of COVID-19 among patients on immunosuppressive agents, are predictable and are being evaluated with great care and effort across the globe. A few others, such as atypical manifestations of COVID-19 mimicking rheumatic musculoskeletal diseases (RMDs) are being reported. Like in many other viral infections, severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection can potentially lead to an array of rheumatological and autoimmune manifestations by molecular mimicry (cross-reacting epitope between the virus and the host), bystander killing (virus-specific CD8 + T cells migrating to the target tissues and exerting cytotoxicity), epitope spreading, viral persistence (polyclonal activation due to the constant presence of viral antigens driving immune-mediated injury) and formation of neutrophil extracellular traps. In addition, the myriad of antiviral drugs presently being tried in the treatment of COVID-19 can result in several rheumatic musculoskeletal adverse effects. In this review, we have addressed the possible spectrum and mechanisms of various autoimmune and rheumatic musculoskeletal manifestations that can be precipitated by COVID-19 infection, its therapy, and the preventive strategies to contain the infection. Keywords Coronavirus disease-2019 (COVID-19) • Rheumatic musculoskeletal diseases (RMDs) • Autoimmunity • Rheumatology Abbreviations AAV Anti-neutrophil cytoplasmic antibodyassociated vasculitis ACE2 Angiotensin-converting enzyme 2 ANA Antinuclear antibodies AIDS Acquired immunodeficiency syndrome APCs Antigen-presenting cells APS Antiphospholipid antibody syndrome ARDS Acute respiratory distress syndrome CAHA Coronavirus-associated hemostatic lung abnormality CART Chimeric antigen receptor T cell CCL2 Chemokine (C-C motif) ligand 2 CK Creatine kinase COVID-19 Coronavirus disease-2019 CSF Cerebrospinal fluid CRS Cytokine release syndrome CXCL8 C-X-C motif chemokine ligand 8 DADA-2 Deficiency of adenosine deaminase-2 DIC Disseminated intravascular coagulation Rheumatology INTERNATIONAL Sanket Shah and Debashish Danda have contributed equally as first authors.

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Section: Sars-cov-2 Infection and Autoimmunitymentioning

confidence: 99%

Autoimmune and rheumatic musculoskeletal diseases as a consequence of SARS-CoV-2 infection and its treatment

et al. 2020

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“…Besides, it is clear that the genetic component could not been changed substantially during the relatively short period of human evolution to explain the recent and dramatic rise of autoimmune diseases in human populations ( 150 ). Thus, the role of environmental factors in the onset of autoimmune diseases becomes increasingly recognized ( 151 ).…”

Section: Can Hgt Play a Role In Autoimmune Disease?mentioning

confidence: 99%

Potential Effects of Horizontal Gene Exchange in the Human Gut

Tenbusch²,

2017

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Many essential functions of the human body are dependent on the symbiotic microbiota, which is present at especially high numbers and diversity in the gut. This intricate host–microbe relationship is a result of the long-term coevolution between the two. While the inheritance of mutational changes in the host evolution is almost exclusively vertical, the main mechanism of bacterial evolution is horizontal gene exchange. The gut conditions, with stable temperature, continuous food supply, constant physicochemical conditions, extremely high concentration of microbial cells and phages, and plenty of opportunities for conjugation on the surfaces of food particles and host tissues, represent one of the most favorable ecological niches for horizontal gene exchange. Thus, the gut microbial system genetically is very dynamic and capable of rapid response, at the genetic level, to selection, for example, by antibiotics. There are many other factors to which the microbiota may dynamically respond including lifestyle, therapy, diet, refined food, food additives, consumption of pre- and probiotics, and many others. The impact of the changing selective pressures on gut microbiota, however, is poorly understood. Presumably, the gut microbiome responds to these changes by genetic restructuring of gut populations, driven mainly via horizontal gene exchange. Thus, our main goal is to reveal the role played by horizontal gene exchange in the changing landscape of the gastrointestinal microbiome and potential effect of these changes on human health in general and autoimmune diseases in particular.

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“…It is a widely accepted view that pathogenesis of many autoimmune diseases is largely driven by inappropriate or inadequate immune responses toward bacterial agents (50, 51). Similarly, a number of Gram-positive and Gram-negative bacteria are recognized as being linked to aPL production.…”

Section: Bacteriamentioning

confidence: 99%

Environmental Triggers of Autoreactive Responses: Induction of Antiphospholipid Antibody Formation

2019

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Antiphospholipid antibodies (aPLs) comprise a diverse family of autoantibodies targeted against proteins with the affinity toward negatively charged phospholipids or protein-phospholipid complexes. Their clinical significance, including prothrombotic potential of anti-cardiolipin antibodies (aCLs), anti-β2-glycoprotein I antibodies (aβ2-GPIs), and lupus anti-coagulant (LA), is well-established. However, the ontogeny of these pathogenic aPLs remains less clear. While transient appearance of aPLs could be induced by various environmental factors, in genetically predisposed individuals these factors may eventually lead to the development of the antiphospholipid syndrome (APS). Since the first description of APS, it has been found that a wide variety of microbial and viral agents influence aPLs production and contribute to clinical manifestations of APS. Many theories attempted to explain the pathogenic potential of different environmental factors as well as a phenomenon termed molecular mimicry between β2-GPI molecule and infection-relevant structures. In this review, we summarize and critically assess the pathogenic and non-pathogenic formation of aPLs and its contribution to the development of APS.

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Editorial: Microbial and Environmental Factors in Autoimmune and Inflammatory Diseases

Cited by 22 publications

References 2 publications

Autoimmune and rheumatic musculoskeletal diseases as a consequence of SARS-CoV-2 infection and its treatment

Autoimmune and rheumatic musculoskeletal diseases as a consequence of SARS-CoV-2 infection and its treatment

Potential Effects of Horizontal Gene Exchange in the Human Gut

Environmental Triggers of Autoreactive Responses: Induction of Antiphospholipid Antibody Formation

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