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Biomedical subjects

Aristo Vojdani

Publications and source records attributed to Aristo Vojdani.

At least 19 recordsLinked to original sources
PubMed2006

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).

Journal Article↗
PubMed2006

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).

Journal Article↗
PubMed2006

Regulatory T cells, a potent immunoregulatory target for CAM researchers: the ultimate antagonist (I).

Over the past decade, great interest has been given to regulatory T (T(reg)) cells. A vast body of evidence has shown the existence and highlighted the importance of T(reg) cells in the active suppression of immune system responses. This form of immunoregulation is the dominant means utilized by the immune system to reach a harmony between reciprocal response processes in order to ensure adequate host defense with minimal host detriment. Therapeutically targeting T(reg) cells is a direct and powerful means to manipulate the immune system to achieve beneficial effects on various disease pathologies, including allergy, autoimmunity and cancer, as well as the facilitation of organ transplantation. This powerful target for immunoregulation is of much concern to practitioners and researchers of complementary and alternative medicine because it allows a great deal of control and certainty in dealing with the prevalence of debilitating immune system-related disorders for which there has been little remedy outside of Western Medicine.

Journal Article↗
PubMed2006

Hormone allergy.

BACKGROUND: Estrogen and progesterone have been associated in women with symptoms that include asthma, migraine, dermatitis and pain. OBJECTIVE: We suggest a connection between symptoms associated with hormone changes to a hormone antibody response. METHODS: For IgG, IgM and IgE antibodies to progesterone, blood samples were obtained from 288 healthy control subjects by a commercial lab in California. Blood from 270 patients in Texas with changes in symptoms associated with menstrual cycles was examined. For IgE antibodies to both progesterone and estrogen, blood samples were obtained from an additional 32 healthy control subjects who had no symptoms related to menses and from 98 patients with symptoms associated with menstrual cycles. The symptoms were asthma, migraines and joint pain. RESULTS: At 2 S.D. above the mean values of control subjects, a significant number of patients show high levels of IgG, IgM and IgE antibodies to progesterone and estrogen. CONCLUSIONS: This paper describes evidence of antibodies to the hormones estrogen and progesterone. Progesterone, estrogen and their metabolites, after binding to human tissue proteins, such as albumin or globulin, may act as antigens and promote Type 2 helper cell development, thereby regulating antibody synthesis and allergy. This leads to the possibility of treating a wide variety of disorders by determining hormone allergy and initiating desensitization. Two obvious applications for determination and treatment of hormone allergies are pre-menstrual asthma and menstrual migraines.

Adult↗
PubMed2005

Antibodies against Stachybotrys chartarum extract and its antigenic components, Stachyhemolysin and Stachyrase-A: a new clinical biomarker.

BACKGROUND: IgG and IgE antibodies against Stachybotrys extract have been reported in allergic patients and residents of water-damaged buildings. Detection of these antibodies in blood was partially attributed to cross-reacting proteins from other fungi. There is a need for a specific method to detect antibodies against characteristic components of S. chartarum. MATERIAL/METHODS: We measured IgG and IgE antibodies against Stachybotrys hemolysin and proteinase-Stachyrase-A by ELISA and ELISA-inhibition techniques. RESULTS: Of 50 reference sera with IgE greater than 500 IU ml and positive against different mold extracts used in this study, significant elevation in IgG or IgE antibodies against S. chartarum extract was present in 25 and 21 specimens. Of these specimens 20 (80%) and 10 (40%) were positive for IgG anti-Stachybotrys hemolysin and anti-Stachyrase-A, while 8 out of 21 sera (38%) and 17 out of 21 (81%) specimens were positive for IgE anti-Stachybotrys hemolysin and anti-Stachyrase-A respectively. Inhibition studies using Stachybotrys hemolysin and Stachyrase-A at a concentration of 50 microg/ml prevented binding of anti-Stachybotrys to S. chartarum extract. CONCLUSIONS: Detection of IgG as well as IgE antibodies against Stachybotrys hemolysin and Stachyrase-A and inhibition of anti-Stachybotrys binding to Stachybotrys antigens indicate that Stachybotrys hemolysin and Stachyrase-A are two major antigenic components of S. chartarum extract, which can be used in antibody assays. Measurement of antibodies against these characteristic components of S. chartarum may be considered for demonstration of exposure and possibly allergy to the fungus.

Antibodies, Fungal↗
PubMed2004

Heat shock protein and gliadin peptide promote development of peptidase antibodies in children with autism and patients with autoimmune disease.

Searching for a mechanism underlying autoimmunity in autism, we postulated that gliadin peptides, heat shock protein 60 (HSP-60), and streptokinase (SK) bind to different peptidases resulting in autoantibody production against these components. We assessed this hypothesis in patients with autism and in those with mixed connective tissue diseases. Associated with antigliadin and anti-HSP antibodies, children with autism and patients with autoimmune disease developed anti-dipeptidylpeptidase I (DPP I), anti-dipeptidylpeptidase IV (DPP IV [or CD26]) and anti-aminopeptidase N (CD13) autoantibodies. A significant percentage of autoimmune and autistic sera were associated with elevated immunoglobulin G (IgG), IgM, or IgA antibodies against three peptidases, gliadin, and HSP-60. These antibodies are specific, since immune absorption demonstrated that only specific antigens (e.g., DPP IV absorption of anti-DPP IV), significantly reduced IgG, IgM, and IgA antibody levels. For direct demonstration of SK, HSP-60, and gliadin peptide binding to DPP IV, microtiter wells coated with DPP IV were reacted with SK, HSP-60, and gliadin. They were then reacted with anti-DPP IV or anti-SK, anti-HSP, and antigliadin antibodies. Adding SK, HSP-60, and gliadin peptides to DPP IV resulted in 27 to 43% inhibition of the DPP IV-anti-DPP IV reaction, but DPP IV-positive peptides caused 18 to 20% enhancement of antigen-antibody reactions. We propose that (i) superantigens (e.g., SK and HSP-60) and dietary proteins (e.g., gliadin peptides) in individuals with predisposing HLA molecules bind to aminopeptidases and (ii) they induce autoantibodies to peptides and tissue antigens. Dysfunctional membrane peptidases and autoantibody production may result in neuroimmune dysregulation and autoimmunity.

Adolescent↗
PubMed2004

Cellular and humoral immune abnormalities in Gulf War veterans.

We examined 100 symptomatic Gulf War veterans (patients) and 100 controls for immunologic assays. The veterans and controls were compared for the percentage of T cells (CD3); B cells (CD19); helper:suppressor (CD4:CD8) ratio; natural killer (NK) cell activity; mitogenic response to phytohemagglutin (PHA) and pokeweed mitogen (PWM); level of immune complexes; myelin basic protein (MBP) and striated and smooth muscle autoantibodies; and antibodies against Epstein-Barr virus, cytomegalovirus, herpes simplex virus type 1 (HSV-1), HSV-2, human herpes Type 6 (HHV-6), and Varicella zoster virus (VZV). The percentage of T cells in patients versus controls was not significantly different, whereas a significantly higher proportion of patients had elevated T cells compared with controls. The percentage of B cells was significantly elevated in the patients versus the controls. The NK cell (NK) activity was significantly decreased in the patients (24.8 +/- 16.5 lytic units) versus the controls (37.3 +/- 26.4 lytic units). The percentage of patients with lower than normal response to PHA and PWM was significantly different from controls. Immune complexes were significantly increased in the patients (53.1 +/- 18.6, mean +/- SD) versus controls (34.6 +/- 14.3). Autoantibody titers directed against MBP and striated or smooth muscle were significantly greater in patients versus controls. Finally, the patients had significantly greater titers of antibodies to the viruses compared with the controls (p < 0.001). These immune alterations were detected 2-8 years after participation in the Gulf War. The immune alterations are consistent with exposure to different environmental factors. We conclude that Gulf War syndrome is a multifaceted illness with immune function alterations that may be induced by various factors and are probably associated with chronic fatigue syndrome.

Adult↗
PubMed2004

Detection of trichothecene mycotoxins in sera from individuals exposed to Stachybotrys chartarum in indoor environments.

To date, no study has effectively demonstrated a direct human exposure to mycotoxins in mold-contaminated buildings. Therefore, the authors investigated the presence of trichothecene mycotoxins in sera from individuals exposed to indoor molds (specifically Stachybotrys chartarum). Sera from occupants of contaminated (test samples, n=44) and uncontaminated (control samples, n=26) buildings were analyzed using a competitive enzyme-linked immunosorbent assay (ELISA) highly specific for macrocyclic trichothecenes. Twenty-three samples were significantly different (p < 0.05) from normal human serum tested in the same manner, whereas only 1 of the control samples tested positive. Mass spectrometry analysis could not confirm the presence of intact S. chartarum macrocyclic trichothecenes. The authors hypothesize that this result was caused by uncharacterized ELISA-reactive metabolic breakdown products. Data from this study suggest that trichothecene mycotoxins can be demonstrated in the tissues of certain individuals exposed to S. chartarum in contaminated buildings.

Air Pollution, Indoor↗
PubMed2004

Cross-reactivity of Aspergillus, Penicillium, and Stachybotrys antigens using affinity-purified antibodies and immunoassay.

In this study, the author examined the cross-reactivities of Stachybotrys chartarum, Aspergillus niger/fumigatus, and Penicillium notatum with affinity-purified rabbit sera. The molds were grown for expression of maximum numbers of antigens, after which they were extracted and mixed with commercially available extracts. The mixture was used for antibody preparation in rabbits, measurement of antibody levels, and for the demonstration of the degree of cross-reactivity. Control rabbits were injected with saline, yet they produced significant levels of immunoglobulin G antibodies against all mold extracts tested. The author interpreted this result to mean that sera obtained from rabbits immunized with pure mold extracts likely reflected cross-reactivity with other molds. Therefore, only affinity-purified antibodies and the most sensitive immunoassay technique (i.e., enzyme-linked immunosorbent assay [ELISA]) were used for the cross-inhibition studies. The antigenic cross-reactivities were as follows: (a) between Aspergillus and Penicillium, 19.6-21.0%; (b) between Stachybotrys and Aspergillus, 8.2-8.7%; and (c) between Stachybotrys and Penicillium, 7.0-9.6%. The findings of this study demonstrate that cross-reactivity studies between different molds require the use of affinity-purified antibodies and a sensitive and quantitative assay with untreated antigens. With the use of such an assay, it was determined that the cross-reactivity between Stachybotrys, Aspergillus, and Penicillium was at approximately 10%, which is less widespread than previously believed.

Animals↗
PubMed2003

Biochemical changes in the serum of patients with chronic toxigenic mold exposures: a risk factor for multiple renal dysfunctions.

This paper analyzes and presents the biochemical abnormalities in the sera of patients presenting with chronic mycosis in order to investigate the relationship with the risks of multiple renal disorders. The study population (n = 10) consisted of six females and four males (mean age 36.3 years) exposed by toxic molds in their homes and offices for an average of 2.8 years. The control group comprised ten people, five males and five females (mean age 35.9 years) without any known exposures to toxic molds. Blood samples were obtained from both the patients and the controls and were processed using specific biochemical methods that included enzyme-linked immunoabsorbent assay (ELISA). There were biochemical abnormal concentrations in creatinine, uric acid, phosphorus, alkaline phosphotase, cholesterol, HDH, SGOT/AST, segmented neutrophils, lymphocytes, total T3, IgG and IgA immunoglobulins with significant differences between patients and controls. These abnormalities were consistent with multiple renal disorders. The major complaints of the mycosis patients were headaches, pulmonary symptoms, allergic reactions, memory loss, skin rashes, blurred vision symptoms, fatigue, and runny nose. These findings were depictive of a strong association of chronic mycosis with abnormal renal indicators. It was concluded that, although this research was a pilot investigation, based on the overall results, people exposed to chronic indoor environmental toxic molds were at risk of multiple renal complications.

Adult↗
PubMed2003

Combination of high-dose intravenous immunoglobulins and itraconozole in treating chronic mycotic demyelinating optic neuritis.

Mycotic demyelinating optic neuritis is a neurological disorder of the visual system caused by mycotoxins released by indoor toxic molds. Although the health effect of indoor toxic mold on the population worldwide is now one of the "emerging diseases", its involvement in chronic demyelinating optic neuritis has not been reported. Most of the neurological and immunologic abnormalities associated with toxic mold mycotoxins are very difficult to treat successfully, especially neural demyelination of the central and peripheral nervous systems. This paper presents the case of a 42-year-old white female, in whom chronic demyelinating optic neuritis with persistent visual defects due to chronic exposure to toxic molds was diagnosed at the age of 34 years. In spite of all the therapeutic services given to her for over 8 years, her illness persisted and was difficult to treat. However, we successfully treated her with a combination of intravenous immune globulin (IVIG) and itraconozole (Sporanox) when all other treatment modalities failed. This is probably the first report where persistent toxic mold-induced neurological and immunologic disorders were successfully treated with a combination of itraconozole and IVIG.

Adult↗
PubMed2003

Neurophysiological effects of chronic indoor environmental toxic mold exposure on children.

The phenomenon of building-related diseases is attracting much research interest in recent years because of the extent to which it affects people with compromised immune systems, especially children. In this study, we reported the neurological findings in children who attended our Center because of chronic exposure to toxic molds. Clinical neurological and neurobehavioral questionnaires were administered with the cooperation of the children's parents. The children then underwent a series of neurophysiological tests including electroencephalogram (EEG), brainstem evoked potential (BAEP), visual evoked potential (VEP), and somatosensory evoked potential (SSEP). The results showed high levels of abnormalities in the analysis of the subjective responses derived from the questionnaires. The EEG examination was abnormal in seven out of ten of the patients compared to the controls with only one in ten with episodes of bihemispheric sharp activity. In all the patients, there was frontotemporal theta wave activity that seemed to indicate diffuse changes characteristic of metabolic encephalopathies. Also, there was highly marked 1 to 3 Hz delta activity that was asymmetrical in the right hemisphere of the brain in three out of ten patients. The waveforms of BAEP showed abnormalities in 90% of the patients with both 15' and 31' check sizes compared to none in the controls. There were significant delays in waveform V in a majority of the patients representing dysfunctional cognitive process and conductive hearing loss in both ears. VEP showed clear abnormalities in four in ten of the patients with P100 amplitudes and latencies decreased bilaterally. In all the patients, there was slowing of conduction in the right tibial at an average of 36.9 ms and there was significant decrease in amplitude of response at the proximal stimulation site. Sensory latencies obtained in the median, ulnar, and sural nerves bilaterally showed abnormalities in five out of ten compared to none in the controls. The median, ulnar, and sural sensory potentials were abnormal in six out of ten patients. There was prolongation of the median distal sensory latencies bilaterally at an average of 4.55 ms on the right and an average of 6.10 ms on the left as compared to the ulnars of 2.55 ms bilaterally. There was no abnormality in the controls. These findings represent evidence of diffuse polyneuropathy to which three patients demonstrated borderline slow motor conduction at an average of 41.1 ms. Overall, the objective neurophysiological measurements (EEG, BAEP, VEP, and SSEP) were abnormal, indicating significant neurological deficits in all the patients. Our findings revealed the extent to which toxic molds can affect the neurological and behavioral status of children. Further work should be encouraged in this regard.

Adolescent↗
PubMed2003

Mixed mold mycotoxicosis: immunological changes in humans following exposure in water-damaged buildings.

The study described was part of a larger multicenter investigation of patients with multiple health complaints attributable to confirmed exposure to mixed-molds infestation in water-damaged buildings. The authors present data on symptoms; clinical chemistries; abnormalities in pulmonary function; alterations in T, B, and natural killer (NK) cells; the presence of autoantibodies (i.e., antinuclear autoantibodies [ANA], autoantibodies against smooth muscle [ASM], and autoantibodies against central nervous system [CNS] and peripheral nervous system [PNS] myelins). A total of 209 adults, 42.7 +/- 16 yr of age (mean +/- standard deviation), were examined and tested with (a) self-administered weighted health history and symptom questionnaires; (b) standardized physical examinations; (c) complete blood counts and blood and urine chemistries; (d) urine and fecal cultures; (e) thyroid function tests (T4, free T3); (f) pulmonary function tests (forced vital capacity [FVC], forced expiratory volume in 1 sec [FEV1.0], and forced expiratory flow at 25%, 50%, 75%, and 25-75% of FVC [FEF25, FEF50, FEF75, and FEF2(25-75)]); (g) peripheral lymphocyte phenotypes (T, B, and NK cells) and mitogenesis determinations; and (h) a 13-item autoimmune panel. The molds-exposed patients reported a greater frequency and intensity of symptoms, particularly neurological and inflammatory symptoms, when compared with controls. The percentages of exposed individuals with increased lymphocyte phenotypes were: B cells (CD20+), 75.6%; CD5+CD25+, 68.9%; CD3+CD26+, 91.2%; CD8+HLR-DR+, 62%; and CD8+CD38+, 56.6%; whereas other phenotypes were decreased: CD8+CD11b+, 15.6% and CD3-CD16+CD56+, 38.5%. Mitogenesis to phytohemagglutinin was decreased in 26.2% of the exposed patients, but only 5.9% had decreased response to concanavalin A. Abnormally high levels of ANA, ASM, and CNS myelin (immunoglobulins [Ig]G, IgM, IgA) and PNS myelin (IgG, IgM, IgA) were found; odds ratios for each were significant at 95% confidence intervals, showing an increased risk for autoimmunity. The authors conclude that exposure to mixed molds and their associated mycotoxins in water-damaged buildings leads to multiple health problems involving the CNS and the immune system, in addition to pulmonary effects and allergies. Mold exposure also initiates inflammatory processes. The authors propose the term "mixed mold mycotoxicosis" for the multisystem illness observed in these patients.

Adult↗
PubMed2003

Antibodies to molds and satratoxin in individuals exposed in water-damaged buildings.

Immunoglobulin (Ig)A, IgM, and IgG antibodies against Penicillium notatum, Aspergillus niger, Stachybotrys chartarum, and satratoxin H were determined in the blood of 500 healthy blood donor controls, 500 random patients, and 500 patients with known exposure to molds. The patients were referred to the immunological testing laboratory for health reasons other than mold exposure, or for measurement of mold antibody levels. Levels of IgA, IgM, and IgG antibodies against molds were significantly greater in the patients (p < 0.001 for all measurements) than in the controls. However, in mold-exposed patients, levels of these antibodies against satratoxin differed significantly for IgG only (p < 0.001), but not for IgM or IgA. These differences in the levels of mold antibodies among the 3 groups were confirmed by calculation of z score and by Scheffé's significant difference tests. A general linear model was applied in the majority of cases, and 3 different subsets were formed, meaning that the healthy control groups were different from the random patients and from the mold-exposed patients. These findings indicated that mold exposure was more common in patients who were referred for immunological evaluation than it was in healthy blood donors. The detection of antibodies to molds and satratoxin H likely resulted from antigenic stimulation of the immune system and the reaction of serum with specially prepared mold antigens. These antigens, which had high protein content, were developed in this laboratory and used in the enzyme-linked immunosorbent assay (ELISA) procedure. The authors concluded that the antibodies studied are specific to mold antigens and mycotoxins, and therefore could be useful in epidemiological and other studies of humans exposed to molds and mycotoxins.

Adult↗
PubMed2003

Saliva secretory IgA antibodies against molds and mycotoxins in patients exposed to toxigenic fungi.

Upper respiratory exposure to different environmental antigens results first in the activation of mucosal immunity and production of IgA antibodies in different secretions including saliva. Despite this there is no study, which addresses secretory antibodies against molds and mycotoxins. The purpose of this study was to evaluate mold-specific salivary IgA in individuals exposed to molds and mycotoxins in a water-damaged building environment. Saliva IgA antibody levels against seven different molds and two mycotoxins were studied in 40 patients exposed to molds and in 40 control subjects. Mold-exposed patients showed significantly higher levels of salivary IgA antibodies against one or more mold species. A majority of patients with high IgA antibodies against molds exhibited elevation in salivary IgA against mycotoxins, as well. These IgA antibodies against molds and mycotoxins are specific, since using molds and mycotoxins in immune absorption could reduce antibody levels, significantly. Detection of high counts of molds in water-damaged buildings, strongly suggests the existence of a reservoir of mold spores in the environment. This viable microbial activity with specific mold and mycotoxin IgA in saliva may assist in the diagnosis of mold exposure. Whether mold and mycotoxin specific IgA antibodies detected in saliva are indicative of the role of IgA antibodies in the late phase of type-1 hypersensitivity reaction or in type-2 and type-3 delayed sensitivities is a matter that warrants further investigation.

Adult↗
PubMed2003

Neural autoantibodies and neurophysiologic abnormalities in patients exposed to molds in water-damaged buildings.

Adverse health effects of fungal bioaerosols on occupants of water-damaged homes and other buildings have been reported. Recently, it has been suggested that mold exposure causes neurological injury. The authors investigated neurological antibodies and neurophysiological abnormalities in patients exposed to molds at home who developed symptoms of peripheral neuropathy (i.e., numbness, tingling, tremors, and muscle weakness in the extremities). Serum samples were collected and analyzed with the enzyme-linked immunosorbent assay (ELISA) technique for antibodies to myelin basic protein, myelin-associated glycoprotein, ganglioside GM1, sulfatide, myelin oligodendrocyte glycoprotein, alpha-B-crystallin, chondroitin sulfate, tubulin, and neurofilament. Antibodies to molds and mycotoxins were also determined with ELISA, as reported previously. Neurophysiologic evaluations for latency, amplitude, and velocity were performed on 4 motor nerves (median, ulnar, peroneal, and tibial), and for latency and amplitude on 3 sensory nerves (median, ulnar, and sural). Patients with documented, measured exposure to molds had elevated titers of antibodies (immunoglobulin [Ig]A, IgM, and IgG) to neural-specific antigens. Nerve conduction studies revealed 4 patient groupings: (1) mixed sensory-motor polyneuropathy (n = 55, abnormal), (2) motor neuropathy (n = 17, abnormal), (3) sensory neuropathy (n = 27, abnormal), and (4) those with symptoms but no neurophysiological abnormalities (n = 20, normal controls). All groups showed significantly increased autoantibody titers for all isotypes (IgA, IgM, and IgG) of antibodies to neural antigens when compared with 500 healthy controls. Groups 1 through 3 also exhibited abnormal neurophysiologic findings. The authors concluded that exposure to molds in water-damaged buildings increased the risk for development of neural autoantibodies, peripheral neuropathy, and neurophysiologic abnormalities in exposed individuals.

Adult↗