Trained immunity is a concept in immunology in which innate immune cells, such as monocytes and macrophages, exhibit enhanced responsiveness and memory-like characteristics following initial contact with a pathogenic stimulus that may promote a more effective immune defense following subsequent contact with the same pathogen. Helicobacter pylori, a bacterium that colonizes the stomach lining, is etiologically associated with various gastrointestinal diseases, including gastritis, peptic ulcer, gastric adenocarcinoma, MALT lymphoma, and extra gastric disorders. It has been demonstrated that repeated exposure to H. pylori can induce trained immunity in the innate immune cells of the gastric mucosa, which become more responsive and better able to respond to subsequent H. pylori infections. However, interactions between H. pylori and trained immunity are intricate and produce both beneficial and detrimental effects. H. pylori infection is characterized histologically as the presence of both an acute and chronic inflammatory response called acute-on-chronic inflammation, or gastritis. The clinical outcomes of ongoing inflammation include intestinal metaplasia, gastric atrophy, and dysplasia. These same mechanisms may also reduce immunotolerance and trigger autoimmune pathologies in the host. This review focuses on the relationship between trained immunity and H. pylori and underscores the dynamic interplay between the immune system and the pathogen in the context of gastric colonization and inflammation.

UNASSIGNED: The effect of vitamin A on the manifestations of liver fibrosis is controversial and establishing the causes of its multidirectional influence is an urgent problem. In the work, the functional characteristics of the liver with Cu-induced fibrosis were determined after the restoration of vitamin A to the control level at the F0/F1 stage.
UNASSIGNED: In animals with liver fibrosis, classical indicators of physiology, functional activity of the liver, histological, and hematological characteristics were determined; the content of calcium and ROS was determined in bone marrow cells.
UNASSIGNED: It was shown that in the liver with Cu-induced fibrosis, the restoration of vitamin A content to control values after per os injections of a retinol acetate solution at a dose of 0.10 mg (300 IU)/100 g of body weight in the early stages of this pathology development (Fо/F1) was accompanied by: a decrease in the number of immunocompetent cells in the bloodstream to control values; normalization of the amount of calcium ions and ROS in bone marrow cells; restoration to the control level of activity of alkaline phosphatase; an increase in the number of binuclear hepatocytes; and restoration of the dynamics of body weight growth in experimental animals, even against the background of the ongoing action of the hepatotoxic factor.
UNASSIGNED: We came to the conclusion that the multidirectional action of vitamin A, which occurs in liver fibrosis, depends not only on the concentration of vitamin A in the liver but also on temporal characteristics of cellular and metabolic links involved in the adaptive response formation. It was suggested that knowledge of the initial temporal metabolic characteristics and the amount of vitamin A in the liver, taking into account the stages of fibrosis development, can be an effective way to restore the altered homeostatic parameters of the body.

BACKGROUND: It has been hypothesized that the origin of early-onset endometriosis could be from endometrial mesenchymal stem cells (eMSCs) in neonatal uterine blood (NUB). There is no information on the possible mechanistic basis linking an association between NUB/neonatal endometrium and development of early-onset endometriosis. In this study we performed a series of experiments to clarify the mechanistic link between NUB and/or neonatal endometrium and development of early-onset endometriosis.
METHODS: We retrospectively collected postmortem neonatal endometria (n = 15) and prospectively collected NUB (n = 18) of female babies for the analysis of different biological markers including eMSCs. Immunohistochemical analysis of neonatal endometria was performed to examine the expression patterns of ovarian steroid receptors (ER/PGR), decidualization (prolactin, IGFBP1), pre-decidualization (Glycodelin A, α-SMA), proliferation (Ki-67 index), vascularity (CD31 + cells), immunocompetent CD68+, CD45+, CD56 + cells and some putative markers of eMSCs. Cell transfer method and immunocytochemistry were used to investigate the eMSCs and/or endometrial cells in NUB.
RESULTS: Immunohistochemical analysis of postmortem neonatal endometria revealed variable staining response to ER/PGR, decidual markers, and substantial proliferative and angiogenic activity. A moderate to strong immunoexpression of Glycodelin-A was found in both neonatal and adult endometria. The tissue infiltration of CD56+, CD45 + and CD68 + immunocompetent cells was significantly low in neonatal endometria than that in adult endometria (p = 0.0003, p < 0.0001, p = 0.034, respectively). No eMSCs or even endometrial cells were detected in NUB. However, a variable expression of some phenotypes of eMSCs (CD90/CD105) was found in neonatal endometria.
CONCLUSIONS: Based on our serial experiments we did not find any supporting evidence for the role of NUB in early-onset endometriosis. Neonatal endometria showed variable expression of ovarian steroid receptors, decidualization, and a substantial amount of proliferative and angiogenic activity. As an alternative mechanism, a significantly less tissue accumulation of immunocompetent cells in neonatal endometria may explain the survival of ER + and PGR + cells should they make entry into the pelvis and consequent development of early endometriosis with the onset of ovarian function. Future study with large sample size and application of modified technological tools is warranted to test the NUB hypothesis and to clarify their biological or clinical significance.
BACKGROUND: not applicable.

The understanding of the synbiotics´ impact on the host is incomplete. To improve the knowledge, we study the effect of Lacto-Immuno-Vital synbiotic preparation in chickens on local and systemic immune response by evaluation of immunocompetent cells in the peripheral blood and jejunal mucosa. Hematological method was used for determination of white blood cell count, and flow cytometry for measurement the functions of phagocytes and subpopulation of lymphocytes (CD3, CD4, CD8, IgM, and IgA). Cell Qest programme (Germany) was used for analysing of data obtained from flow cytometer and GraphPad Prism version 4.0 for comparison by paired t test between control and experimental groups. The experiment was conducted in a commercial broiler chicken fattening farm, the birds were handled and sacrificed in a humane manner. A flock of 64,400 one-day-old Hybrid ROSS 308 chickens were included in the 42-d experiment. The chickens were randomly divided into 2 equal groups, experimental and control, and each group of chickens was housed in a different hall while maintaining the same conditions. The chickens in the experimental group (Lactovital) received 500 g of Lacto-Immuno-Vital (Hajduvet Kft., Hungary) in 1,000 L of drinking water. Lacto-Immuno-Vital was administered daily from the first day (D1) to D7 of the experiment. From D 7 to D 22 it was given in a pulsed manner (every third day) at a dose of 300 g in 1,000 L of drinking water. Control group received only the standard diet. For immune analyses 6 randomly chosen chickens from experimental and control group were taken from the halls. The sampling days were set at D 8 and D 22 of the experiment. Samples of peripheral blood were collected from vena subclavia. The chickens were euthanized and whole jejunum was taken during necropsy into Hanks ice solution (pH 7.2-7.3). Administration of Lacto-Immuno-Vital in drinking water of nonstressed broilers during fattening period in commercial production increased phagocytic activity and phagocytic index. The number of IgA+ and CD8+ cells in lamina propria of intestine was decreased in chickens fed diet supplemented with Lacto-Immuno-Vital in drinking water. We suggest that increased phagocytic activity and decreased number of immunocompetent cells in mucosa of intestine was caused by improved systemic and local immune system function.

Research on lipid peroxidation in food degradation, oil and fat nutrition, and age-related diseases has gained significant international attention for the view of improvement of societal health and longevity. In order to promote basic studies on these topics, a chemiluminescence detection-high performance liquid chromatography instrument using a high-sensitivity single photon counter as a detector was developed. This instrument enabled us to selectively detect and quantify lipid hydroperoxides, a primary product of lipid peroxidation reactions, as hydroperoxide groups at the lipid class level. Furthermore, an analytical method using liquid chromatography-tandem mass spectrometry has been established to discriminate the position and stereoisomerization of hydroperoxide groups in lipid hydroperoxides. Using these two methods, the reaction mechanisms of lipid peroxidation in food and in the body have been confirmed.

UNASSIGNED: This study aimed to investigate the inflammatory-immune cells in the peripheral blood of women with polycystic ovary syndrome (PCOS) and assessed the potential correlation between inflammatory-immune cells and infertility in PCOS women.
UNASSIGNED: In this case-control study, the profiles of lymphocyte subsets were analyzed by flow cytometry. White blood cells (WBC), neutrophils (Neu), lymphocytes, Ferriman-Gallwey (F-G) score, testosterone, prolactin, follicle-stimulating hormone, luteinizing hormone, fasting blood glucose, and fasting plasma insulin were measured, together with body mass index. Association between inflammatory-immune cells and PCOS was evaluated. Moreover, inflammatory-immune cells of the PCOS women with infertility were evaluated, and the relative operating characteristic (ROC) curve and cutoff values were calculated.
UNASSIGNED: The number of WBC, Neu, and lymphocytes was higher in PCOS women than controls (P<0.05). The percentages of total T lymphocytes, CD4+T, and NK were significantly increased in the PCOS group (P<0.001). The CD4/CD8 ratio was obviously elevated for increasing CD4+T (P<0.05). Consequently, T%, CD4+T%, and NK% were found to be the independent risk factors of PCOS by ROC curve and multivariate logistic regression analysis. Furthermore, only NK% was significantly higher in PCOS women with infertility than those who had PCOS without infertility (P<0.001). To diagnose infertility in PCOS, the cutoff value of NK% was calculated as 16.43%.
UNASSIGNED: These findings suggest that the pathogenesis of PCOS is related to immune cells including T, CD4+T, and NK cells. NK cells are likely to be a potential predictive factor for PCOS women with infertility.

Systemic sclerosis (SSc) is a connective tissue disease that is characterized by widespread skin and internal organ fibrosis vasculopathy and immune response abnormalities, including T, B, natural killer (NK), and natural killer T (NKT) cell involvement. The aim of the study was to investigate the immune cell profile in patients with systemic sclerosis in relation to the disease activity, severity, and antibody presence and their relation to the type of immunosuppressive treatment. Cytometric examination identified following cell lines: B cells (Breg, B memory, B mature) and plasmablasts, T cell, T double positive-Tdp, T double negative-Tdn, NK, and NKT cell and monocytes. The disease severity and activity were assessed based on the Medsger and the EULAR Scleroderma Trials and Research Group (EUSTAR) 2017 scales respectively. In the study, SSc patients were characterized by higher total lymphocyte count parallel to increased frequency of Ts and Th cells. In SSc patients, increment of Tdp and reduction of Tdn as well as NK and NKT cells were observed. Additionally in SSc patients the reduction of B memory was noted. Head to head comparison between cyclophosphamide (CYC) and mycophenolate mofetil (MMF) treatment showed a reduction of CD19+ cells, but increment of plasmablasts in CYC treated patients.

暂无摘要。

BACKGROUND: An impaired leukocytes function is the factor causing the susceptibility of patients with diabetes mellitus to infections. The outmost importance for the understanding of the immunological processes involved in diabetes pathogenesis is to give the characteritics of the immunological profile and changes therein, during the course of desease. Long-used in folk medicine to treat diabetes Galega officinalis L. has been chosen for the correction of the immune system dysfunction.
METHODS: The experiments were conducted on male Wistar rats. Fractionation of bone marrow cells suspension was performed in a three-layer ficoll-sodium amidotrizoate density gradient. The lymphocytic-granulocytic cells proliferative activity was studied using enzyme immunoassay with 5-bromo-2\'-deoxyuridine (BrdU). For staining of bone marrow preparations May-Gruenwald-Romanowsky-Giemsa (Pappenheim) method was used. To evaluate the content of cationic proteins and myeloperoxidase in neutrophilic leukocytes cytochemical studies were performed. Content of tumor necrosis factor alpha was carried out by immuno-enzymatic analysis. Lymphocytes apoptosis was examined by fluorescent analysis using annexin V.
RESULTS: Diabetes mellitus development was accompanied with violation of neutrophils and lymphocytes proliferation, increased activity of myeloperoxidase and enhanced apoptosis process. Administration of Galega officinalis extract under the condition of diabetes promotes the restoration of neutrophils bone marrow pool and the reduction of lymphoblasts number and causes inhibition of the lymphocytes apoptosis process.
CONCLUSIONS: Investigated medicine has a pronounced immunocorrective effect under the conditions of diabetes mellitus and can become the basis for creating a new generation of antidiabetic drugs.

BACKGROUND: Cigarette smoke, the principal risk factor for chronic obstructive pulmonary disease (COPD), negatively influences the effectiveness of the immune system\'s response to a pathogen. The antibiotic ceftaroline exerts immune-modulatory effects in bronchial epithelial cells exposed to cigarette smoke.
OBJECTIVE: The present study aims to assess the effects of ceftaroline on TLR2 and TLR4 expression, LPS binding and TNF-α and human beta defensin (HBD2) release in an undifferentiated and PMA-differentiated human monocyte cell line (THP-1) exposed or not to cigarette smoke extracts (CSE). TLR2, TLR4, and LPS binding were assessed by flow cytometry, TNF-α and HBD2 release were evaluated by ELISA.
RESULTS: The constitutive expression of TLR2 and TLR4 and LPS binding were higher in differentiated compared to undifferentiated THP-1 cells. In undifferentiated THP-1 cells, CSE increased TLR2 and TLR4 protein levels, LPS binding and TNF-α release and reduced HBD2 release and ceftaroline counteracted all these effects. In differentiated THP-1, CSE did not significantly affect TLR2 and TLR4 expression and LPS binding but reduced HBD2 release and increased TNF-α release. Ceftaroline counteracted the effects of CSE on HBD2 release in differentiated THP-1.
CONCLUSIONS: Ceftaroline counteracts the effect of CSE in immune cells by increasing the effectiveness of the innate immune system. This effect may also assist in reducing pathogen activity and recurrent exacerbations in COPD patients.