Interleukin-1 Genotype in Periodontitis, Abstract This paper presents the current knowledge concerning the role of polymorphisms of IL1A and IL1B genes in periodontitis. Attention has been paid to the role of IL-1 in the pathogenesis of the disease, and to the significance of a genetic test, investigating the presence of composite two polymorphisms of IL-1 gene, as a risk factor for severe periodontitis. The significance of this test for prevention of periodontitis and its therapy has been discussed. IL-1 polymorphisms have been presented and described according to the reference single nucleotide polymorphism (SNP) identification number (rsID), established to eradicate the redundancy of reported polymorphisms in the SNP database processed by the National Center for Biotechnology Information. The prevalence of these genotypes in different populations and ethnic groups and its effect on periodontal health have been discussed. The presented data show inconsistent results. It seems that at least two polymorphisms, rs1800587 and rs1143634, are associated with periodontal inflammation. Therefore, they can be regarded as candidate genes involved in further periodontitis risk assessment. It seems that geographical and ethnical factors can play a great role, as the prevalence of specific polymorphisms varies greatly depending on the population studied. Professor Włodzimierz Ptak (1928–2019)

Induction of Chronic Subclinical Systemic Inflammation in Sprague–Dawley Rats Stimulated by Intermittent Bolus Injection of Lipopolysaccharide Abstract Chronic subclinical systemic inflammation has a key role in stimulating several chronic conditions associated with cardiovascular diseases, cancer, rheumatoid arthritis, diabetes, and neurodegenerative diseases. Hence, developing in vivo models of chronic subclinical systemic inflammation are essential to the study of the pathophysiology and to measure the immunomodulatory agents involved. Male Sprague–Dawley rats were subjected to intraperitoneal, intermittent injection with saline, or lipopolysaccharide (LPS) (0.5, 1, 2 mg/kg) thrice a week for 30 days. Hematological, biochemical, and inflammatory mediators were measured at different timepoints and at the end of the study. The hearts, lungs, kidneys, and livers were harvested for histological evaluation. Significant elevation in peripheral blood leukocyte includes neutrophils, monocytes, and lymphocytes, as well as the neutrophils-to-lymphocyte ratio. The pro-inflammatory mediator levels [C-reactive protein, tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-1β, and IL-8] along with the biochemical profile (alkaline phosphatase, aspartate aminotransferase, alanine aminotransferase, gamma-glutamyl transferase, creatine kinase, creatinine, and urea) were increased significantly (P < 0.05) and increased the expression of monocyte chemoattractant protein-1 and TNF-β. The histopathological changes of heart, lung, kidney, and liver tissues revealed degeneration, cellular infiltration of leukocyte in the inflammatory foci and interstitial space, edema, early signs of fibrosis, apoptosis, and necrosis. In conclusion, these results indicate that intermittent exposure to LPS produces chronic subclinical systemic inflammation in multiple organs leading to chronic conditions and supports this model to be a useful preclinical tool for developing immunotherapeutic agents that could prevent, or reduce, chronic inflammatory diseases associated with, or without, bacterial translocation.

Peripheral Blood B and T Cell Profiles in Children with Active Juvenile Idiopathic Arthritis Abstract Juvenile idiopathic arthritis (JIA) is one of the most common autoimmune diseases in children. Our study aimed to evaluate the peripheral blood B and T lymphocyte subpopulations in children with JIA. This case–control study included 20 children with JIA as well as 20 healthy children with matching age and sex as a control group. All patients included in the study were in activity as determined by visual analog scale. In addition to complete clinical evaluation, basic investigations, peripheral blood B and T lymphocyte subpopulations were done to all participants by flow cytometry. JIA patients displayed a significant decrease in IgM memory B lymphocytes, switched memory B lymphocytes, and total memory B lymphocytes when compared to the healthy controls. The percentages of naïve B lymphocytes were significantly increased in JIA patients than in controls. Total T lymphocytes, CD8+CD28null cells, and CD4+CD28null cells were significantly increased in JIA patients as compared to controls. In conclusion; JIA patients have an alteration in both B and T lymphocytes with the predisposition of memory cells which may have a role in sustaining the JIA disease activity.

Modulatory Effect of the Euro-Lupus Low-Dose Intravenous Cyclophosphamide Regimen on Circulating Immune Cells in Systemic Lupus Erythematosus Abstract A Euro-Lupus regimen of low-dose intravenous cyclophosphamide (CFA) is commonly used to treat severe organ manifestations of systemic lupus erythematosus (SLE), particularly lupus nephritis (LN). There are no data on the distributions and dynamics of immune cell populations in patients with various treatment outcomes. The circulating immune cells of 11 female SLE patients were assessed before and after Euro-Lupus regimen (cumulative dose of 3000 mg CFA) by flow cytometry together with those of 16 healthy women. A subanalysis was performed in LN patients who achieved complete remission (CR; n = 3), partial remission (PR; n = 4), and no response (NR; n = 2). In SLE, the Euro-Lupus regimen decreased the percentage and absolute count of B cells; increased the percentage of CD8+ T cells, T regulatory cells, neutrophils, and monocyte subsets; and activated T and NK cells compared to healthy controls (P < 0.050). Patients with LN achieving CR had significantly lower proportions of CD27+ B memory cells compared to poor responders (PR/NR, P = 0.035). The post-treatment percentages and absolute numbers of B cells, T cells, NK cells, monocytes, and neutrophils showed high inter-individual variability with no association with treatment outcome. Our pilot study revealed the dynamics of changes in immune cell populations in SLE patients during a Euro-Lupus regimen, mainly the lowering of B cells. In LN patients who achieved CR, a lower proportion of CD27+ B memory cells was evident compared to poor responders (PR/NR). Further studies on usefulness of monitoring immune cells for treatment response prediction on larger cohorts are needed.

Mitochondrial Heat Shock Response Induced by Ectromelia Virus is Accompanied by Reduced Apoptotic Potential in Murine L929 Fibroblasts Abstract Poxviruses utilize multiple strategies to prevent activation of extrinsic and intrinsic apoptotic pathways for successful replication. Mitochondrial heat shock proteins (mtHsps), especially Hsp60 and its cofactor Hsp10, are engaged in apoptosis regulation; however, until now, the influence of poxviruses on mtHsps has never been studied. We used highly infectious Moscow strain of ectromelia virus (ECTV) to investigate the mitochondrial heat shock response and apoptotic potential in permissive L929 fibroblasts. Our results show that ECTV-infected cells exhibit mostly mitochondrial localization of Hsp60 and Hsp10, and show overexpression of both proteins during later stages of infection. ECTV infection has only moderate effect on the electron transport chain subunit expression. Moreover, increase of mtHsp amounts is accompanied by lack of apoptosis, and confirmed by reduced level of pro-apoptotic Bax protein and elevated levels of anti-apoptotic Bcl-2 and Bcl-xL proteins. Taken together, we show a positive relationship between increased levels of Hsp60 and Hsp10 and decreased apoptotic potential of L929 fibroblasts, and further hypothesize that Hsp60 and/or its cofactor play important roles in maintaining protein homeostasis in mitochondria for promotion of cell survival allowing efficient replication of ECTV.

Gut Microbiota in Neurological Disorders Abstract The incidence of neurological disorders such as multiple sclerosis (MS), Alzheimer’s disease (AD) and Parkinson’s disease (PD) is increasing throughout the world, but their pathogenesis remains unclear and successful treatment remains elusive. Bidirectional communications between the central nervous system and gut microbiota may play some role in the pathogenesis of the above disorders. Up to a thousand bacterial species reside in human intestine; they colonize the gut shortly after birth and remain for life. Numerous studies point to the role of microbiota composition in the development, course and treatment of MS, AD and PD.

Retinoids as an Immunity-modulator in Dermatology Disorders Abstract The skin is the largest epithelial surface protecting the body from invading microbes. Vitamin A plays vital roles in the host defence of the skin, including promoting epithelial cell integrity, proliferation, and differentiation and even mediating immune responses. Furthermore, vitamin A derivatives, retinoid drugs, are widely used to treat skin diseases, such as acne and psoriasis. However, the immunoregulatory mechanisms of retinoids in dermatology have not been systematically described. In this paper, we discuss the immunological functions of retinoids during disease treatment, especially in skin disorders caused by exogenous infections.

Correction to: Significance and Role of Pattern Recognition Receptors in Malignancy The authors would like to correct the following error.

90th Birthday of Prof. Czesław Radzikowski