Interrelationship of interleukin 6, C-reactive protein and Chlamydia pneumoniae IgG antibodies in patients with acute coronary syndromes

Background/Aim. Inflammation due to infection could be associated with the development of acute coronary syndromes, clinical manifestations of ongoing atherosclerosis in vessel walls. Our aim was determine whether interleukin 6, C-reactive protein and Chlamydia pneumoniae IgG antibodies are connected with the development of acute coronary syndromes, to evaluate their interrelationship and to examine whether they are predictive of new events and mortality. Methods. This prospective study included 211 subjects, of whom 111 were patients with acute coronary syndromes (60% male, mean age 59.42 years) and 100 were healthy controls (58% male, mean age 59.03 yuears). Blood samples were taken for analysis on admission, before the application of the therapy. Interleukin 6, high sensitivity C-reactive protein and Chlamydia pneumoniae IgG antibodies were measured, in a follow-up period of 30 days. Results. Levels of interleukin 6 (p < 0.001) and C-reactive protein (p < 0.001) were significantly higher among the patients with acute coronary syndromes than among controls. Chronic infection caused by Chlamydia pneumoniae was present in 72% of patients and in 22% of healthy controls (p < 0.001). There was a correlation between interleukin 6 and C-reactive protein, C-reactive protein and Chlamydia pneumoniae but not between Chlamydia pneumoniae and interleukin 6. Higher levels of interleukin 6 and C-reactive protein were seen with increasing body mass index, smoking exposure, presence of hypertension and diabetes, and decreasing ejection fraction. The patients with ST-segment elevation had higher examined markers than the patients without ST-segment elevation. Interleukin 6 and C-reactive protein were independently related to the clinical outcome. Conclusion. Interleukin 6, C-reactive protein and Chlamydia pneumoniae infection are connected with the development of acute coronary syndromes and may reflect a clinical outcome of the disease

The Prevalence of Antibodies Against Wheat and Milk Proteins in Blood Donors and Their Contribution to Neuroimmune Reactivities

The aim of this study was to look for the presence of IgG, IgM, and IgA antibodies against two widely consumed foods, wheat and milk, in a relatively large number of specimens. As wheat, milk, and their antigens have been found to be involved in neuroimmune disorders, we measured the co-occurrence of their antibodies against various neural antigens. We assessed the reactivity of sera from 400 donors to wheat and milk proteins, GAD-65, cerebellar, MBP, and MOG. Statistical analysis showed significant clustering when certain wheat and milk protein antibodies were cross-referenced with neural antibodies. Approximately half of the sera with antibody elevation against gliadin reacted significantly with GAD-65 and cerebellar peptides; about half of the sera with elevated antibodies against α + β-casein and milk butyrophilin also showed antibody elevation against MBP and MOG. Inhibition studies showed that only two out of four of the samples with elevated cerebellar or MOG antibodies could be inhibited by gliadin or α + β-casein, confirming individual variation in epitope recognition. We conclude that a subgroup of blood donors, due to a breakdown in immunological tolerance, may react and produce significant levels of antibodies (p-values less than 0.05) against wheat and milk antigens that cross-react with different neural antigens, which may have broader implications in the induction of neuroimmune reactivities

Detection of IgE, IgG, IgA and IgM antibodies against raw and processed food antigens

<p>Abstract</p> <p>Background</p> <p>Despite the first documented case of food allergy to cooked food in 1921 by Prausnitz and Kustner, all commercial food antigens are prepared from raw food. Furthermore, all IgE and IgG antibodies against dietary proteins offered by many clinical laboratories are measured against raw food antigens.</p> <p>Methods</p> <p>We developed an enzyme-linked immunosorbent assay for the measurement of IgE, IgG, IgA and IgM antibodies against raw and processed food antigens. Sera with low or high reactivity to modified food antigens were subjected to myelin basic protein, oxidized low density lipoprotein, and advanced glycation end products (AGE) such as AGE-human serum albumin and AGE-hemoglobin.</p> <p>Results</p> <p>Compared to raw food antigens, IgE antibodies showed a 3–8-fold increase against processed food antigens in 31% of the patients. Similarly, IgG, IgA and IgM antibodies against modified food antigens overall were found at much higher levels than antibody reactions against raw food antigens. Almost every tested serum with high levels of antibodies against modified food antigens showed very high levels of antibodies against myelin basic protein, oxidized low density lipoprotein, AGE-human serum albumin and AGE-hemoglobin.</p> <p>Conclusion</p> <p>We conclude that the determination of food allergy, intolerance and sensitivity would be improved by testing IgE, IgG, IgA and IgM antibodies against both raw and processed food antigens. Antibodies against modified food antigens, by reacting with AGEs and tissue proteins, may cause perturbation in degenerative and autoimmune diseases such as diabetes, atherosclerosis, inflammation, autoimmunity, neurodegeneration and neuroautoimmunity.</p

Infections, Toxic Chemicals and Dietary Peptides Binding to Lymphocyte Receptors and Tissue Enzymes are Major Instigators of Autoimmunity in Autism

Similar to many complex autoimmune diseases, genetic and environmental factors including diet, infection and xenobiotics play a critical role in the development of autism. In this study, we postulated that infectious agent antigens such as streptokinase, dietary peptides (gliadin and casein) and ethyl mercury (xenobiotic) bind to different lymphocyte receptors and tissue enzyme (DPP IV or CD26). We assessed this hypothesis first by measuring IgG, IgM and IgA antibodies against CD26, CD69, streptokinase (SK), gliadin and casein peptides and against ethyl mercury bound to human serum albumin in patients with autism. A significant percentage of children with autism developed anti-SK, anti-gliadin and casein peptides and anti-ethyl mercury antibodies, concomitant with the appearance of anti-CD26 and anti-CD69 autoantibodies. These antibodies are synthesized as a result of SK, gliadin, casein and ethyl mercury binding to CD26 and CD69, indicating that they are specific. Immune absorption demonstrated that only specific antigens, like CD26, were capable of significantly reducing serum anti-CD26 levels. However, for direct demonstration of SK, gliadin, casein and ethyl mercury to CD26 or CD69, microtiter wells were coated with CD26 or CD69 alone or in combination with SK, gliadin, casein or ethyl mercury and then reacted with enzyme labeled rabbit anti-CD26 or anti-CD69. Adding these molecules to CD26 or CD69 resulted in 28–86 % inhibition of CD26 or CD69 binding to anti-CD26 or anti-CD69 antibodies. The highest % binding of these antigens or peptides to CD26 or CD69 was attributed to SK and the lowest to casein peptides. We, therefore, propose that bacterial antigens (SK), dietary peptides (gliadin, casein) and Thimerosal (ethyl mercury) in individuals with pre-disposing HLA molecules, bind to CD26 or CD69 and induce antibodies against these molecules. In conclusion, this study is apparently the first to demonstrate that dietary peptides, bacterial toxins and xenobiotics bind to lymphocyte receptors and/or tissue enzymes, resulting in autoimmune reaction in children with autism. </jats:p

The Role of Th17 in Neuroimmune Disorders: Target for CAM Therapy. Part II

Decades of research went into understanding the role that Th1 autoreactive T-cells play in neuroinflammation. Here we describe another effector population, the IL-17-producing T-helper lineage (Th17), which drives the inflammatory process. Through the recruitment of inflammatory infiltration neutrophils and the activation of matrix metalloproteinases, IL-17, a cytokine secreted by Th17 cells, contributes to blood-brain barrier breakdown and the subsequent attraction of macrophages and monocytes into the nervous system. The entry of cells along with the local production of inflammatory cytokines leads to myelin and axonal damage. This activation of the inflammatory response system is induced by different pathogenic factors, such as gut bacterial endotoxins resulting in progressive neurodegeneration by Th17 cells. Through the understanding of the role of bacterial endotoxins and other pathogenic factors in the induction of autoimmune diseases by Th17 cells, CAM practitioners will be able to design CAM therapies targeting IL-17 activity. Targeted therapy can restore the integrity of the intestinal and blood-brain barriers using probiotics, N-acetyl-cysteine, α-lipoic acid, resveratrol and others for their patients with autoimmunities, in particular those with neuroinflammation and neurodegeneration

Regulatory T Cells, a Potent Immunoregulatory Target for CAM Researchers: Modulating Allergic and Infectious Disease Pathology (II)

Regulatory T (T(reg)) cells maintain dominant control of immune responses to foreign materials and microbes. Appropriate T(reg) cell suppression of immune responses is essential for the maintenance of efficacious defensive responses and the limitation of collateral tissue damage due to excess inflammation. Allergy and infection are well studied and frequent afflictions in which T(reg) cells play an essential role. As such, they provide excellent models to communicate the significance and relevance of T(reg) cells to complementary and alternative medicine (CAM)

Regulatory T Cells, a Potent Immunoregulatory Target for CAM Researchers: Modulating Tumor Immunity, Autoimmunity and Alloreactive Immunity (III)

Regulatory T (T(reg)) cells are the major arbiter of immune responses, mediating actions through the suppression of inflammatory and destructive immune reactions. Inappropriate T(reg) cell frequency or functionality potentiates the pathogenesis of myriad diseases with ranging magnitudes of severity. Lack of suppressive capability hinders restraint on immune responses involved in autoimmunity and alloreactivity, while excessive suppressive capacity effectively blocks processes necessary for tumor destruction. Although the etiology of dysfunctional T(reg) cell populations is under debate, the ramifications, and their mechanisms, are increasingly brought to light in the medical community. Methods that compensate for aberrant immune regulation may not address the underlying complications; however, they hold promise for the alleviation of debilitating immune system-related disorders. The dominant immunoregulatory nature of T(reg) cells, coupled with recent mechanistic knowledge of natural immunomodulatory compounds, highlights the importance of T(reg) cells to practitioners and researchers of complementary and alternative medicine (CAM)

Heterogeneous Collaborative Sensor Network for Electrical Management of an Automated House with PV Energy

In this paper we present a heterogeneous collaborative sensor network for electrical management in the residential sector. Improving demand-side management is very important in distributed energy generation applications. Sensing and control are the foundations of the “Smart Grid” which is the future of large-scale energy management. The system presented in this paper has been developed on a self-sufficient solar house called “MagicBox” equipped with grid connection, PV generation, lead-acid batteries, controllable appliances and smart metering. Therefore, there is a large number of energy variables to be monitored that allow us to precisely manage the energy performance of the house by means of collaborative sensors. The experimental results, performed on a real house, demonstrate the feasibility of the proposed collaborative system to reduce the consumption of electrical power and to increase energy efficiency

The production of hydrolysates from industrially defatted rice bran and its surface image changes during extraction

BACKGROUND This research employed mild-subcritical alkaline water extraction (SAW) technique to overcome the difficulty of active compounds extractability from an industrially defatted rice bran (IDRB). Mild-SAW (pH 9.5, 130 °C, 120 min) treatment, followed by enzymatic hydrolysis (Protease G6) were applied to produce rice bran hydrolysate (RBH). Response surface methodology was used to identify proteolysis conditions for maximizing protein content and ABTS radical scavenging activity (ABTS-RSA). The microstructural changes during the extraction occurring in the IDRB were monitored. The selected RBH was characterised for protein recovery, yield, antioxidant activities, phenolic profile and hydroxymethylfufural (HMF) content. RESULTS Optimal proteolysis conditions were at 20 mL kg-1 IDRB (E/S) for 6 h. Under these conditions, the yield, ABTS-RSA, Ferric reducing antioxidant power and the total phenolic content of the RBH were 46.1%, 294.22 μmol trolox g-1, 57.72 μmol FeSO4 g-1, and 22.73 mg gallic acid g-1, respectively, with relatively low HMF level (0.21 mg g-1). The protein recovery was 4.8 times greater than the recovery obtained by conventional alkaline extraction. Its major phenolic compounds were p-coumaric and ferulic acids. The microstructural changes of IDRB confirmed that the mild-SAW/Protease G6 process enhanced the release of active compounds. CONCLUSION The process of mild-SAW followed by proteolysis promotes the release of active compounds from IDRB