Alterations In Immune Parameters Research Articles

Alterations in Immune Parameters ADP, ANA, IL-1, IL-6, IL-8, STAT-4, and TNF Alpha in Patients with Rheumatoid Arthritis and Osteoarthritis

Background: Rheumatoid arthritis (RA) and osteoarthritis (OA) are chronic joint diseases with distinct pathophysiological mechanisms, but both involve alterations in immune parameters. This research investigates the alterations in several immune parameters, specifically adiponectin (ADP), antinuclear antibodies (ANA), interleukin-1 (IL-1), interleukin-6 (IL-6), interleukin-8 (IL-8), signal transducer and activator of transcription 4 (STAT-4), and tumor necrosis factor-alpha (TNF Alpha), in patients with rheumatoid arthritis (RA) and osteoarthritis (OA). Also, the current study aims to identify the changes occurring in the physiological and immune parameters of people suffering from rheumatic diseases, as Evaluation of Immunological Inflammatory biomarkers levels ADP, ANA, IL1, IL6, IL8, STAT-4 and TNF-α. Material & Methods: A cross-sectional laboratory-based study with 90 patient’s participant was conducted. Using ELISA kits and laboratory tests, various biomarkers (Immunological Inflammatory biomarkers levels ADP, ANA, IL1, IL6, IL8, STAT-4 and TNF-α were measured among rheumatoid arthritis and Osteoarthritis patients. Results: The findings revealed elevated levels of IL-1, IL-6, IL-8, STAT-4, and TNF Alpha in RA patients, reflecting a heightened inflammatory state. In contrast, OA patients exhibited a more moderate increase in these parameters, suggesting differing immune activation pathways. ADP and ANA levels showed distinct variations between the two patient groups, indicating their potential roles in the pathogenesis and progression of RA and OA. Conclusion: These results contribute to a better understanding of the immune mechanisms underlying RA and OA, highlighting the importance of targeted therapeutic strategies to manage these conditions effectively. Further research is recommended to explore the clinical implications of these findings and develop personalized treatment approaches.

Interrelations of immunological parameters, nutrition, and healthcare-associated infections: Prospective study in elderly in-patients

Healthcare-associated infections [HAI] are common in elderly individuals and may be related to both nutritional deficiencies and immunosenescence. Here, we assessed whether overall malnutrition and/or specific nutrient deficiencies were associated with HAI via alterations in immune parameters. Prospective observational cohort study in patients aged ≥ 70 years admitted to the geriatric rehabilitation unit of a teaching hospital in France between July 2006 and November 2008. Clinical and laboratory parameters reflecting nutritional status and immune function were collected at baseline. Flow cytometry was used to assess blood lymphocyte subsets including the naive CD4 T-cell count, naive and memory CD8 T-cell counts, effector CD8 T-cell count, and CD4/CD8 ratio. Patients were monitored for HAI for 3 months or until discharge from the geriatric unit or death. Of 252 consecutive in-patients aged ≥ 70 years [mean age, 85 ± 6.2 years], 181 [72%] met French National Authority for Health criteria for malnutrition and 97 [38%] experienced one or more HAI. Patients who subsequently experienced HAI had significantly lower baseline values for energy intake [odds ratio (OR), 0.76; 95% confidence interval (95%CI), 0.59-0.99], serum albumin [OR, 0.43; 95%CI, 0.32-0.58], serum zinc [OR, 0.77; 95%CI, 0.62-0.97], selenium [OR, 0.76; 95%CI, 0.61-0.95], and vitamin C [OR, 0.71; 95%CI, 0.54-0.93]. Associations linking these five variables to HAI were not significantly changed by adjusting for flow cytometry T-cell subset values. Our results suggest a direct effect of nutritional parameters on HAI rather than an indirect effect mediated by immune parameters.

P190 Interrelations between immunological parameters, nutrition, and health care-associated infections : prospective study in elderly in-patients

summary Background & aims: Healthcare-associated infections [HAI] are common in elderly individuals and may be related to both nutritional deficiencies and immunosenescence. Here, we assessed whether overall malnutrition and/or specific nutrient deficiencies were associated with HAI via alterations in immune parameters. Methods: Prospective observational cohort study in patients aged � 70 years admitted to the geriatric rehabilitation unit of a teaching hospital in France between July 2006 and November 2008. Clinical and laboratory parameters reflecting nutritional status and immune function were collected at baseline. Flow cytometry was used to assess blood lymphocyte subsets including the naive CD4 T-cell count, naive and memory CD8 T-cell counts, effector CD8 T-cell count, and CD4/CD8 ratio. Patients were monitored for HAI for 3 months or until discharge from the geriatric unit or death. Results: Of 252 consecutive in-patients aged � 70 years [mean age, 85 � 6.2 years], 181 [72%] met French National Authority for Health criteria for malnutrition and 97 [38%] experienced one or more HAI. Patients who subsequently experienced HAI had significantly lower baseline values for energy intake [odds ratio (OR), 0.76; 95% confidence interval (95%CI), 0.59e0.99], serum albumin [OR, 0.43; 95%CI, 0.32 e0.58], serum zinc [OR, 0.77; 95%CI, 0.62e0.97], selenium [OR, 0.76; 95%CI, 0.61e0.95], and vitamin C [OR, 0.71; 95%CI, 0.54e0.93]. Associations linking these five variables to HAI were not significantly changed by adjusting for flow cytometry T-cell subset values. Conclusion: Our results suggest a direct effect of nutritional parameters on HAI rather than an indirect effect mediated by immune parameters.

Effect of oxidative stress on immunological parameters in type 2 diabetes mellitus in the Azerbaijan Republic

AimThe study of lipid peroxidation (LPO) state and antioxidant protection (AOP) in blood plasma of patients with diabetes mellitus and the consequent changes of some immunological data depending on the severity of the pathological process. MethodsAll patients (n=76), depending on the level of glycemia and disease duration were divided into 3 groups at the stages of compensation, subcompensation and decompensation. The level of glycated hemoglobin (Hb1Ac) was determined as the biochemical marker. Parameters of the LPO intensity – malondialdehyde and dien conjugates, antioxidant system parameters – SOD, GSH and ceruloplasmin, immune parameters – IgA, M, G, CIC and phagocytic activity were determined in all groups of patients including the control group. ResultsAmounts of MDA and DC increased at all stages of the disease. In contrast, decreases in antioxidant system parameters – SOD, GSH and ceruloplasmin were observed. The oxidative stress increase resulted in the decline of phagocytic activity in the three groups by 23%, 29% and 52%, respectively. Amounts of T-lymphocytes were also decreased by 9.8%, 28% and 32%. But CIC were observed to increase. ConclusionIntensification of the oxidative stress and the decrease in the antioxidant system protective function stimulate alterations in immune system parameters – amounts of immunoglobulins and immune complexes increased and phagocytic activity decreased. It suggests that the level of the oxidative stress effect on the alterations in immune parameters directly depends on the stage of the disease.

Effect of 17β‐estradiol on the immunocompetence of japanese sea bass (Lateolabrax Japonicus)

Environmental contaminants can interfere with hormonal regulation in both vertebrates and invertebrates, and these contaminants may disrupt the endocrine system of human and other organisms. Evidence is growing that contaminants may be partly responsible for the observed increase of disease in marine organisms by adversely affecting their immunity. Fish are commonly used as sentinel organisms in vertebrate immunotoxicology; however, to date, studies have been undertaken only on a single size group of fish (juvenile/adult) and for acute exposure. In the present study, Lateolabrax japonicus fingerlings and juveniles were exposed to two sublethal concentrations (200 and 2,000 ng/L) of 17beta-estradiol (E2) for 30 d under laboratory conditions, and alterations in immune parameters comprising differential leukocyte count, respiratory burst, myeloperoxidase, immunoglobulin levels, serum lysozyme, and bactericidal activity were investigated to establish whether estrogen produced immunomodulation and to understand the effects of long-term exposure on these immune parameters in fish fingerlings and juveniles. The results revealed a significant elevation of respiratory burst activity, myeloperoxidase, immunoglobulin levels, and differential leukocyte counts of the fish exposed to estrogen compared to the control. The remaining parameters were significantly reduced in the experimental groups when compared to the control. The results indicated that sublethal E(2) exposure induced immunomodulation in both fingerling and juvenile L. japonicus, and the changes caused by estrogen might affect the function of immune system in fish.

Influence of prenatal psychosocial stress on cytokine production in adult women

The aim of the present study was to determine the association between prenatal stress and immune function in human adults. Peripheral blood mononuclear cells (PBMCs) from 34 healthy young women whose mothers experienced major negative life events during their pregnancy (Prenatal Stress, PS group, mean age 25, SD +/- 4.34 years), and from a female comparison group (n = 28, CG, mean age 24 +/- 3.40 years), were stimulated with phytohemagglutinin (PHA), and subsequent cytokine production was measured. A bias for T-helper 2 (Th2) cytokine production due to an overproduction of IL-4 relative to IFN-gamma after PHA stimulation was observed in PS subjects. In addition, IL-6 and IL-10 were also significantly elevated. To the best of our knowledge, this study is the first to suggest a direct association between prenatal stress exposure and alterations in immune parameters in adult women.

Characterisation of immunosuppression in rabbits after infection with myxoma virus

Myxoma virus (MXV) causes the systemic disease myxomatosis in the European rabbit. Despite many in vitro studies on the function of MXV immunomodulatory proteins and detailed molecular knowledge of virus, little is known about the dynamics of interaction of the virus with the integrated host-immune system during infection. In this study changes in haematological profile, changes in lymphocyte subset distribution and non-specific proliferation activity of lymphocytes from different lymphoid compartments on the 2nd, 4th, 6th, 9th and 11th day after experimental infection of rabbits with MXV strain Lausanne was characterised. The relationship between alterations of immune parameters and dynamic of virus dissemination through the body was investigated. Haematological changes included moderate leucopenia with significant lymphopenia, neutrophilia, monocytosis and eosinopenia. A decrease of T cells including CD4 + and CD8 + and increase of CD79α + were observed in draining popliteal lymph node 4 days after virus inoculation. From day 6, comparable changes were seen in collateral popliteal lymph node, spleen and peripheral blood. From day 9, the mentioned lymphocyte subsets tended to reach their original state in all of these lymphocyte compartments except draining popliteal lymph node. In thymus, MXV infection affected mainly CD4 +CD8 + double positive thymocytes. On the other hand, proliferation activity of lymphocytes determined by the proliferation assay with plant-derived mitogens was significantly reduced from day 4 or 6 and remained reduced until the end of experiment in all observed lymphoid organs. Presence of MXV in respective lymphoid compartments preceded changes in lymphocyte subset distribution or lymphocyte activity.

Immunoglobulin E (IgE) and Lymphocyte Subsets in Relation to Vitamins C and E in Cord Blood

TAB3-PD-02 Background: Epidemiologic studies have demonstrated beneficial effects of foods rich in antioxidants or antioxidant supplements on ventilatory function, respiratory symptoms, and atopy in children and adults. One plausible mechanism by which vitamin levels may influence health is through immunomodulation. Objective: To determine whether concentrations of vitamins C and E in cord blood are associated with alterations in immune parameters at birth. Methods: Mothers delivering in 2 districts in the Czech Republic between 1994 and 1998 were enrolled in the Immune Biomarker Study. Cord blood samples (n = 1397) were analyzed by flow cytometry to determine lymphocyte phenotypes (T lymphocytes: CD3+, CD4+, CD8+; B lymphocytes: CD19+; and natural killer cells: CD16+CD56+). Cord IgE was determined by Carrier-Polymer-System and maternal IgE by nephelometry for 463 births. Vitamin C was determined using spectrophotometry (n = 763) and vitamin E by high pressure liquid chromatography with UV detection (n = 642). Multiple linear regression was used to quantify the relations between vitamins C and E and lymphocyte proportions adjusting for questionnaire information (lifestyle, sociodemographic, reproductive) as well as delivery and meteorologic variables. Elevated cord serum IgE (>0.9 IU/mL) was predicted by multiple logistic regression models adjusting for district, year of birth, and elevated levels of maternal IgE (>100 IU/mL) as a proxy for maternal atopy (other covariates were not predictive). Results: Mean cord blood levels (μg/mL, ± SD) for vitamins E and C were 3.2 ± 2.0 and 13.9 ± 4.8, respectively. For a 1-μg (about half the SD)/mL increase in cord vitamin E, the percentage of cord CD19+ cells decreased −2.8% (95% CI, −5.4% to −0.3%) in a model adjusted for 45-day average ambient temperature. Models alternatively adjusting for 3-day temperature showed similar results. Associations were attenuated after control for season of delivery. Other lymphocyte subsets were not associated with cord vitamin E levels. For a 1-μg/mL increase in cord vitamin E, the odds of having an elevated cord IgE increased slightly (OR = 1.3; 95% CI, 1.0 to 1.6). Adjustment for maternal atopy, a strong predictor of cord IgE, had no impact here. Vitamin C levels were not associated with lymphocytes or IgE. Conclusion: Fetal vitamin E levels may affect the relative production of B cells and the concentrations of circulating IgE at birth. Other seasonal factors, such as pollen exposures or additional nutritional factors, may confound the association with lymphocytes. Further work is needed to clarify the independent and joint effects of these exposures.

Alterations in immune parameters in foundry and pottery workers

To assess the immune competence of workers occupationally exposed to mainly silica, peripheral blood lymphocytes, serum immunoglobulins (IgG, IgA and IgM), C3 and C4 complement protein concentrations of foundry and pottery workers were evaluated and compared to healthy controls with no history of silica and other chemical exposure. The absolute number and percentage of functionally different subsets of peripheral blood mononuclear lymphocytes, i.e. T, T-suppressor and natural killer cells were unchanged. However, T-helper lymphocytes in pottery ( P<0.05) and B cells in foundry ( P<0.01) workers were significantly lower when compared to their controls. In addition, silica-exposed foundry workers had a significant reduction in the IgG, IgA and IgM levels. No significant differences were observed in the serum complement C3 and C4 levels of the workers. These results suggest that human chronic exposure to mainly silica and other chemicals originating from foundry and pottery settings may be detrimental to the immune system.

Alterations in Immune Parameters Associated with Low Level Methylmercury Exposure in Mice

Methylmercury (MeHg) is a known toxicant and continues to be a significant environmental contaminant. While the neurotoxicity and developmental toxicity of MeHg are well established, the immunotoxic effects of MeHg are just now being studied and described. This study evaluated strain and gender specific effects of low level, prolonged MeHg exposure in mice. Mice were exposed to MeHg in the drinking water (0, 3 or 10 ppm) for 4 weeks. Splenocytes and thymocytes were evaluated for alterations in immunophenotype, GSH levels, and intracellular Ca2+ flux after mitogen stimulation. MeHg exposure resulted in alterations in splenocyte and thymocyte subsets and a dose dependent decrease in GSH levels (as measured by monochlorobimane fluorescence and flow cytometry) of all splenocyte subsets. This decrease in GSH was further confirmed by biochemical assay in splenocytes. In addition, there was a dose response related decrease in mitogen stimulated Ca2+ flux and in the percentages of CD4+ splenocytes and CD8+ splenocytes from mice exposed to 10 ppm of MeHg. These results suggest that low-level chronic MeHg exposure may cause immune disfunction by disturbing thiol redox balance, transmembrane signaling and splenic cellularity.

Bacterial Modulation of the Lung Response to Coal Mine Dust

Occupational exposure to coal mine dust is correlated with the development of a number of respiratory diseases. The mechanisms through which dust causes these conditions are incompletely understood but probably involve the inflammatory, growth regulatory and immune functions of leukocytes, particularly those of pulmonary macrophages. A number of studies have also examined the role of infection as a co-factor in dust-induced lung disease (Seaton, 1984). Numerous reports in the literature describe alterations in immune parameters following occupational inhalation exposure to mineral dusts, including coal. It is also well known that infection or exposure to the products of some bacteria can lead to a series of changes in macrophage structure, metabolism and function; a process known as activation (Adams and Hamilton, 1984). Infection can alter the lung response to mineral dusts (Chiappino and Vigliani, 1982). It is likely that the toxic properties of dust components, particularly silica, on pulmonary macrophages potentiate mycobacterial and other infections (Snider, 1978). It has also been shown that smoke inhalation caused lung injury in rats only when there was a concurrent, remote inflammatory stress induced by intraperitoneal injection of glycogen (Thorn et al., 1994). Co-exposure or sequential exposure of workers to infection and dust could result in potentiation of lung damage.

Dietary Fructo-oligosaccharide Modulates Large Intestinal Inflammatory Responses toClostridium difficilein Antibiotic-compromised Mice

Intestinal inflammatory parameters and microbiological changes were examined in antibiotic-compromised mice in response to Clostridium difficile , a causative agent of pseudomembranous colitis. C57BL/6NHsd mice were treated orally with a broad- spectrum antibiotic and then fed a low-residue diet (Ensure®) with or without the fermentable substrate fructo-oligosaccharide (FOS). Animals were infected with C. difficile 6 d after antibiotic treatment. Three days after antibiotic challenge, total anaerobes were lower for antibiotic-treated mice than for controls (no antibiotic) in the Ensure-fed group. However, when the diet was supplemented with FOS, total anaerobe concentrations were higher for antibiotic-treated mice than for controls. Levels of C. difficile were higher for antibiotic-treated animals on day 12 in the FOS-supplemented group and in both diet groups 4 d post-infection. Toxin A litres were significantly elevated 1 d and 4 d post C. difficile challenge only in the antibiotic treated mice not receiving FOS. Antibiotic effects on intestinal immune cell populations were also dependent on diet. Dendritic and γδ T-cell numbers in the caecum were increased by antibiotic treatment in mice fed Ensure only, while tissue concentrations of the bioactive lipid prostaglandin E 2 were decreased. Alternatively, antibiotic treatment increased macrophage numbers in the caecum of FOS-supplemented mice without affecting dendritic and γδ T-cell numbers or prostaglandin E 2 concentrations. Notably, alterations in immune parameters in response to antibiotic were observed predominantly in the caecum, where bacterial density is highest and where C. difficile -induced lesions are localised in the mouse. Keywords: Clostridium difficile , colonisation resistance, intestinal microbiota, intestinal immune system, caecum.