Welcome to the Autoimmunity 2021 Congress Calendar

Background and Aims

Human microbiome colonizes our digestive tract, skin and epithelial surfaces. Within such parts as the neural or adipose tissues, microbes may also occur. They define our health and disease, being often the fundamental game-changers. During the early years, some microbial strains get rooted in the digestive tract without repulsion by our immune system, becoming members of the normal flora. Whatever the roles of our microbial strains, beneficial, commensal, opportunistic or pathogenic ones, the emissions of metabolites or structural components or toxins may provoke an immune response or other reactions by the host.

Methods

Selective plate cultures, or PMEU (Portable Microbe Enrichment Unit) broths were used for the expression surface components or metabolites. They were characterized by immunoassays, microscopy and nucleic magnetic resonance (NMR).

Results

Several commensal or opportunistic strains may contribute to the aetiology of various diseases, such as Sarcina sp. (carcinogenic acetaldehyde), Ruminococcus sp. (lowering the cortisol levels) and Morganella sp. (initiate IBS). Toxins of Gram-positive bacilli or staphylococci initiate a stroke. Such facultative as Salmonella or obligate anaerobes as Propionibacterium may contribute to the diseases of the musculoskeletal system. Hybrid peptides of Salmonella and anaerobic Pectinatus sp. caused hair loss and skin tumour in rats.

Conclusions

Gut microbes can contribute to many neurological disorders, such as Horton’s neuralgia, Alzheimer’s or lower back pains, or autoimmune reactions such as type 1 diabetes, tumours, or vascular problems. The distorted Bacteriological Intestinal Balance (BIB) induces chronic fatigue, IBS and other physiological conditions difficult to diagnose without proper microbiological characterization.

Background and Aims

Many forms of immune dysregulation, which lead to inflammaging and senescence, have been demonstrated in Lupus patients and in aging populations, and the discovery of the microbiome and its association with human health and pathology has led it to become a main suspect as a contributor to the pathogenesis of immunosenescence in both populations. Similar alterations in the microbiome (i.e dysbiosis) demonstrated in both Lupus patients and elders, may help explain the significant overlap in clinical manifestations seen in these groups.

Methods

We performed a literature review, utilizing Pubmed search engine for studies evaluating the microbiome in elderly populations and in Lupus patients (both murine and human models), between the years 2010-2019. The key words: microbiome, dysbiosis, lupus, elderly, aging and inflammaging yielded over 300 articles, of which 67 were used for preparation of this paper. We compared the similarities between the populations.

Results

We have found that the similar processes of immune dysregulation, in both aging populations and Lupus patients, extend to the microbiome, in the form of dysbiosis. Some of these similarities include loss of microbiota biodiversity, increased representation of microbes that are associated with inflammation and disease (i.e Proteobacteria, Bacteroidetes), a relative decrease in protective microbes (i.e Firmicutes) as well as compromise to the intestinal barrier, leading to leakage of proinflammatory microbial components in both groups.

Conclusions

We conclude that several alterations in the composition and function of the microbiome are demonstrated in both lupus patients and aging individuals. Immunosenescence may also be a contributing mechanism in SLE.

Background and Aims

The mechanistic basis of HLA interaction in Rheumatoid Arthritis (RA) etiology and pathogenesis is unknown; accordingly our aim was to test associations between HLA alleles, the main genetic factor in RA, with environmental and individual factors in RA patients and in their first degree relatives (FDR).

Methods

90 patients with RA, 46 FDR, and 50 healthy controls (HC) were selected from the Tatarstan’s cohort and tested by NGS for HLA locus variability (HLA-A/B/C/DQ and DRB1) and gut microbiota (16S rRNA). HSV1/2 infection/reactivation was explored (PCR, serology and blister report), and questionnaires were used for environmental and individual factors.

Results

Protective HLA class II allele usage was reduced in RA (HLA-DRB1*0701 and HLA-DQB1*0302) and the ratio (r) between HLA-DRB1 susceptible alleles (shared epitope [SE] and *0901) and protective alleles (*0701 and *1301/2) evolves from HC (r=0.5) à FDR (r=1.1) à RA (r=5.1). In both FDR and RA patients, the driver/risk factor HLA-DRB1-SE influences (i) gut microbiota with an impact on the balance between pro/anti-inflammatory flora; (ii) HSV1/2 reactivation events (blister in FDR and viremia in RA); and (iii) oral infection reports in the previous year. In RA patients, systemic HSV1/2 reactivation was associated with higher disease activity (DAS28). No associations were retrieved with smoking, alcohol consumption, education level, pregnancy, and obesity in this cohort.

Conclusions

HLA-DRB1 allele usage in FDR and RA influences interaction with microbiota (microbiome, HSV1/2 reactivation and oral infections) and such association in RA may be suspected to amplify the disease risk and/or activity.

Funding: “Russian Science Foundation” (№ 17-15-01099)

Background and Aims

The relationship between autoimmune diseases and infections is an interesting and complex issue. Infections may be trigger factors of the onset or exacerbation of autoimmune diseases and could also modulate the disease’s clinical presentation. The seroprevalence for parvovirus B19 and Epstein-Barr virus is reported with different results.

Methods

We evaluated the seroprevalence for PVB19 and EBV in 280 pregnant women with autoimmune diseases and in 207 healthy pregnant women. Among women with autoimmune diseases 89 were affected by Antiphospholipid Syndrome, defined as APS group.

Results

The prevalence of IgG positive for EBV (EBNA and VCA) and PV B19 resulted higher in autoimmune diseases group and in APS group in comparison with that of control group. The prevalence of positive PV B19 IgG in the autoimmune diseases group was greater than in the control group (63.6% and 52.6%, respectively; p-value 0.058) but was statistically significantly higher only in the APS group than in the control group (76.7% and 52.6%, respectively, with a p-value 0.004).

Conclusions

Our results support the hypothesis that PV B19 is an important environmental factor involved in the onset of autoimmune diseases, particularly in women affected by APS.