Biomedical subjects

A Vojdani

Publications and source records attributed to A Vojdani.

At least 19 recordsLinked to original sources

PubMed2004

Immune response to dietary proteins, gliadin and cerebellar peptides in children with autism.

The mechanisms behind autoimmune reaction to nervous system antigens in autism are not understood. We assessed the reactivity of sera from 50 autism patients and 50 healthy controls to specific peptides from gliadin and the cerebellum. A significant percentage of autism patients showed elevations in antibodies against gliadin and cerebellar peptides simultaneously. For examining cross-reaction between dietary proteins and cerebellar antigens, antibodies were prepared in rabbits, and binding of rabbit anti-gliadin, anti-cerebellar peptides, anti-MBP, anti-milk, anti-egg, anti-soy and anti-corn to either gliadin- or cerebellar-antigen-coated wells was measured. In comparison to anti-gliadin peptide binding to gliadin peptide at 100%, the reaction of anti-cerebellar peptide to gliadin peptide was 22%, whereas the binding of anti-myelin basic protein (MBP), anti-milk, anti-egg and anti-soy to gliadin was less than 10%. Further examination of rabbit anti-gliadin (EQVPLVQQ) and anti-cerebellar (EDVPLLED) 8 amino acid (AA) peptides with human serum albumin (HSA) and an unrelated peptide showed no binding, but the reaction of these antibodies with both the cerebellar and gliadin peptides was greater than 60%. This cross-reaction was further confirmed by DOT-immunoblot and inhibition studies. We conclude that a subgroup of patients with autism produce antibodies against Purkinje cells and gliadin peptides, which may be responsible for some of the neurological symptoms in autism.

Adolescent↗

PubMed2003

Failure to detect Chlamydia pneumoniae by cell culture and polymerase chain reaction in major arteries of 93 patients with atherosclerosis.

To detect Chlamydia pneumoniae in punch specimens of the aortic wall of 61 patients undergoing coronary-aortic bypass graft, and carotid atheromas of 32 patients undergoing carotid endarterectomy, cell culture (HEp-2 cells) and two polymerase chain reaction assays in two different laboratories were used. All cultures and polymerase chain reaction tests for Chlamydia pneumoniae were negative. Further studies are required to explore the complex relationship between Chlamydia pneumoniae and atherosclerosis.

Aged↗

PubMed2003

Antibodies to myelin basic protein, myelin oligodendrocytes peptides, alpha-beta-crystallin, lymphocyte activation and cytokine production in patients with multiple sclerosis.

OBJECTIVE: To measure neurone-specific humoral and cellular immune parameters in MRI-positive patients with multiple sclerosis (MS). BACKGROUND: It has been postulated from animal models for MS and in situ evidence in MS patients that antibodies, activated T cells and proinflammatory cytokines are involved in the destruction of myelin sheaths and loss of oligodendrocytes in active areas. SUBJECTS AND METHODS: Blood samples were obtained from 20 healthy control subjects and 20 patients with abnormal MRI and clinical diagnosis of MS. Sera were tested for levels of IgG, IgM and IgA against myelin basic protein (MBP), myelin oligodendrocyte glycoprotein (MOG) peptides, and a small heat-shock protein, alpha-beta-crystallin. Lymphocytes were isolated and cultured in the presence or absence of MBP, MOG peptides and alpha-beta-crystallin, measured for stimulated T cells, cytokine production and compared with controls. RESULTS: Patients with MS showed the highest levels of IgG, IgM or IgA antibodies against one or all three tested antigens. Moreover, in the presence of MBP, MOG peptides or alpha-beta-crystallin, a significant percent- age of lymphocytes from MS patients underwent blast transformation, which resulted in high levels of interferon gamma (IFN-gamma), tumour necrosis factor alpha (TNF-alpha) and tumour necrosis factor beta (TNF-beta) production. Sensitivity of these assays was 60-80% and specificity, 65-70%. CONCLUSIONS: Detection of antibodies against MBP, MOG peptides, alpha-beta-crystallin, lymphocyte stimulation and production of proinflammatory cytokines in response to these antigens could be used as surrogate markers for the confirmation of MS diagnosis. A combination of antibodies, lymphocyte activation or cytokine production with abnormal MRI may significantly increase the sensitivity and specificity of MS diagnosis.

Adult↗

PubMed2002

Antibodies to neuron-specific antigens in children with autism: possible cross-reaction with encephalitogenic proteins from milk, Chlamydia pneumoniae and Streptococcus group A.

We measured autoantibodies against nine different neuron-specific antigens and three cross-reactive peptides in the sera of autistic subjects and healthy controls by means of enzyme-linked immunosorbent assay (ELISA) testing. The antigens were myelin basic protein (MBP), myelin-associated glycoprotein (MAG), ganglioside (GM1), sulfatide (SULF), chondroitin sulfate (CONSO4), myelin oligodendrocyte glycoprotein (MOG), alpha,beta-crystallin (alpha,beta-CRYS), neurofilament proteins (NAFP), tubulin and three cross-reactive peptides, Chlamydia pneumoniae (CPP), streptococcal M protein (STM6P) and milk butyrophilin (BTN). Autistic children showed the highest levels of IgG, IgM and IgA antibodies against all neurologic antigens as well as the three cross-reactive peptides. These antibodies are specific because immune absorption demonstrated that only neuron-specific antigens or their cross-reactive epitopes could significantly reduce antibody levels. These antibodies may have been synthesized as a result of an alteration in the blood-brain barrier. This barrier promotes access of preexisting T-cells and central nervous system antigens to immunocompetent cells, which may start a vicious cycle. These results suggest a mechanism by which bacterial infections and milk antigens may modulate autoimmune responses in autism.

Antigens↗

PubMed2000

New evidence for antioxidant properties of vitamin C.

This study was designed to examine the effect of 500 to 5,000 mg of ascorbic acid on DNA adducts, natural killer (NK) cell activity, programmed cell death, and cell cycle analysis of human peripheral blood leukocytes. According to our hypothesis, if ascorbic acid is a pro-oxidant, doses between 500 and 5,000 mg should enhance DNA adduct formation, decrease immune function, change the cell cycle progression, and increase the rate of apoptosis. Twenty healthy volunteers were divided into four groups and given either placebo or daily doses of 500, 1,000 or 5,000 mg of ascorbic acid for a period of 2 weeks. On days 0, 1, 7, 15, and 21, blood was drawn from them, and the leukocytes were separated and examined for intracellular levels of ascorbic acid, the level of 8-hydroxyguanosine, NK cell activity, cell cycle progression, and apoptosis. Depending on the subjects, between a 0% and a 40% increase in cellular absorption of ascorbic acid was observed when daily doses of 500 mg were used. At doses greater than 500 mg, this cellular absorption was not increased further, and all doses produced equivalent increases in ascorbic acid on days 1 to 15. This increase in cellular concentration of ascorbic acid resulted in no statistically meaningful changes in the level of 8-hydroxyguanosine, increased NK cytotoxic activity, a reduced percentage of cells undergoing apoptosis, and switched cell cycle phases from S and G2/M to G0/G1. After a period of 1 week, with no placebo or vitamin washout, ascorbic acid levels along with functional assays returned to the baseline and became equivalent to placebos. In comparison with baseline values, no change (not more than daily assays variation) was seen in ascorbate concentrations or other assays during oral placebo treatment. We concluded that ascorbic acid is an antioxidant and that doses up to 5,000 mg neither induce mutagenic lesions nor have negative effects on NK cell activity, apoptosis, or cell cycle.

Administration, Oral↗

PubMed1999

TNF-alpha and chronic fatigue syndrome.

Based upon the clinical presentation of chronic fatigue syndrome (CFS), we hypothesized that proinflammatory cytokines may play a role in the pathogenesis of the disease. We therefore undertook a retrospective cross-sectional study to examine the role of TNF-alpha in patients with CFS. Our results suggest a significant increase serum TNF-alpha in patients with CFS (P<0.0001) compared to non-CFS controls. This study supports the further examination of the role of proinflammatory mediators in CFS. Furthermore, the clinical testing of TNF-alpha blockers and other antiinflammatory agents for the treatment of this disease is warranted.

Adult↗

PubMed1999

Single aetiological agent may not be feasible in CFS patients.

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Fatigue Syndrome, Chronic↗

PubMed1999

Interferon-induced proteins are elevated in blood samples of patients with chemically or virally induced chronic fatigue syndrome.

Overlapping symptomatologies between Chronic Fatigue Syndrome (CFS) and Chemical Sensitivity have been observed by different investigators. Therefore, it is of great importance to develop biomarker(s) for possible differentiation between viral induced CFS (without sensitivity to chemicals) versus chemically induced CFS. Since interferon induced proteins 2-5A Synthetase and Protein Kinase RNA (PKR) have been implicated in the viral induction of CFS, the objective of this study was to utilize 2-5A and PKR activity for differentiation between CFS induced by either viruses or chemicals. Based on the CDC definition and criteria, twenty CFS patients who were positive for viral genome(s) (mainly HHV6; HTLVII, EBV, and CMV) and did not have any history of exposure to toxic chemicals were included in this study. As a comparison, the second group of patients consisted of twenty individuals from the same geographical area who were negative for viral genomes but had been exposed to methyl tertiary-butyl ether concentration of up to 70 ppb and benzene concentration up to 14 ppb. All patients complained of fatigue and other symptoms overlapping between the two groups. From all 40 patients, blood was drawn, leukocyte extract was prepared and assayed for 2-5A Synthetase and PKR activity. Clinical specimens which were positive for viral genomes showed from 2.2-38.7 fold increase in 2-5A activity and 1.3-13.5 fold increase in PKR activities over the background of the healthy controls. Similarly, the second group (negative for viral genomes, but exposed to chemicals) showed a 1.1-29.2 fold increase for 2-5A Synthetase and a 1.3-11.6 fold increase for PKR when they were compared to healthy subjects. To elucidate mechanisms involved in viral versus chemical induction of 2-5A Synthetase and PKR, MDBK cell lines were cultured either in the presence or absence of HHV6, MTBE, or Benzene, heat shock proteins and interferon-beta. 2-5A and PKR activities were measured in all the above conditions. A clear induction of 2-5A and PKR was observed when MDBK cells were exposed to HHV6, MTBE, and Benzene. This induction was more significant with HSP90, HSP70, and IFN-beta indicating their involvement in the mechanism of action. However, when MDBK cells were incubated either with MTBE + Benzene or HHV6 in the presence or absence of anti IFN-beta or anti-HSP-70, the activities of both 2-5A and PKR in HHV6 infected cells were inhibited by more than 90% due to addition of anti IFN-beta, and only 20% by addition of anti-HSP70. While in MTBE + Benzene exposed cells anti IFN-beta reduced the activity of these enzymes by 40% and anti-HSP70 by more than 90%. This variation in the induction of 2-5A and PKR by anti-HSP70 or IFN-beta indicates involvement of IFN-beta in viral induction 2-5A and PKR, and HSP involvement in chemical induction of these enzymes. We conclude that 2-5A and PKR are not only biomarkers for viral induction of CFS, but biomarkers to other stressors that include MTBE and Benzene.

2',5'-Oligoadenylate Synthetase↗

PubMed1998

Multiplex PCR for the detection of Mycoplasma fermentans, M. hominis and M. penetrans in cell cultures and blood samples of patients with chronic fatigue syndrome.

A multiplex polymerase chain reaction (PCR) was initially developed to detect the presence of mycoplasma genus DNA sequences in cell cultures and to differentiate between three human pathogenic mycoplasma species simultaneously. The assay in turn, proved to be a useful tool for the detection of mycoplasma infection in human DNA samples. One set of oligonucleotide primers which are specific for a highly conserved region among all members of the genus mycoplasma along with three other primer sets which are specific for Mycoplasma fermentans, Mycoplasma hominis andMycoplasma penetrans species were used in this assay. The sensitivity of detection was determined by infecting peripheral blood mononuclear cells (PBMC) of healthy individuals with known bacterial copy numbers from each species, extracting the DNA, and subjecting 1 microgram of DNA from each sample to 40 cycles of amplification. By using agarose gel electrophoresis the detection level was determined to be 7, 7, 9 and 15 mycoplasma cells per microgram of human genomic DNA for M. genus,M. fermentans, M. hominis and M. penetrans, respectively. The assay was applied to DNA extracted from the PBMCs of individuals suffering from chronic fatigue syndrome (CFS) (n=100) as determined by the Center for Disease Control (CDC) criteria, and compared to healthy individuals (n=100). The percentage of M. genus infection was found to be 52% in CFS patients and only 15% in healthy individuals. Mycoplasma fermentans, M. hominis andM. penetrans were detected in 32, 9 and 6% of the CFS patients while they were detected in 8, 3 and 2% of the healthy control subjects, respectively. This assay provides a rapid and cost efficient procedure to screen either cell cultures or clinical samples for the presence of three potentially pathogenic species of mycoplasma with a high level of sensitivity and specificity.

Blood↗

PubMed1998

Putting chemical and environmental sensitivities in perspective.

Chemical sensitivity has been recognized for an extended period. Over the last 30 years or more, there has been a growing number of chemicals to which humans are being exposed. Some people have become sensitive to one or more of these chemicals and present this sensitivity in a wide variety of signs or symptoms. Single or multiple organ systems may become involved. This article is intended to give an overview on the existence and recognition of chemical sensitivities and how they may be diagnosed and treated. The important item is to educate physicians to the existence of chemical sensitivity and to consider this in their differential diagnosis when the patient presents with the signs, symptoms, or clinical pattern that is explained.

Allergens↗

PubMed1998

Detection of Mycoplasma genus and Mycoplasma fermentans by PCR in patients with Chronic Fatigue Syndrome.

Mycoplasma fermentans and other Mycoplasma species are colonizers of human mucosal surfaces and may be associated with human immunodeficiency virus infection. While many infectious agents have been described in different percentages of patients with Chronic Fatigue Syndrome (CFS), little is known about the prevalence of mycoplasmas and especially M. fermentans in CFS patients. A polymerase chain reaction (PCR)-based assay was used to detect Mycoplasma genus and M. fermentans genomes in peripheral blood mononuclear cells (PBMC) of CFS patients. Blood was collected from 100 patients with CFS and 50 control subjects. The amplified products of 717 bp of Mycoplasma genus, and 206 bp of M. fermentans were detected in DNA purified from blood samples in 52% and 34% of CFS samples, respectively. In contrast, these genomes were found in only 14% and 8% of healthy control subjects respectively (P < 0.0001). All samples were confirmed by Southern blot with a specific probe based on internal sequences of the expected amplification product. Several samples, which were positive for Mycoplasma genus, were negative for M. fermentans indicating that other Mycoplasma species are involved. A quantitative PCR was developed to determine the number of M. fermentans genome copies present in 1 microg of DNA for controls and CFS patients. Mycoplasma copy numbers ranging from 130 to 880 and from 264 to 2400 were detected in controls and CFS positive subjects, respectively. An enzyme immunoassay was applied for the detection of antibodies against p29 surface lipoprotein of M. fermentans to determine the relationship between M. fermentans genome copy numbers and antibody levels. Individuals with high genome copy numbers exhibited higher IgG and IgM antibodies against M. fermentans specific peptides. Isolation of this organism by culture from clinical specimens is needed in order to demonstrate specificity of signal detected by PCR in this study.

Adult↗

PubMed1998

Downregulation of RNase L inhibitor correlates with upregulation of interferon-induced proteins (2-5A synthetase and RNase L) in patients with chronic fatigue immune dysfunction syndrome.

Chronic Fatigue Immune Dysfunction Syndrome (CFIDS) is a disorder characterized by debilitating fatigue associated with immunological abnormalities and cognitive impairments. The recently cloned RNase L Inhibitor (RLI) gene encodes a specific protein which is believed to regulate 2-5A synthetase and RNase L activity via the formation of a latent heterodimeric protein complex. In the present study, we investigated the levels of 2-5A synthetase, RNase L and RLI in patients with CFIDS as compared to healthy controls. Quantitative Competitive PCR (Q/C PCR) analysis showed a statistically significant decrease in RLI mRNA present in the peripheral blood lymphocytes (PBL) of patients with CFIDS (n = 25, mean = 569, S.E = 154) as compared to RLI mRNA level present in peripheral blood lymphocytes (PBL) of healthy controls (n = 15, mean = 2296, S.E = 506; p < 0.0001). The decrease in RLI mRNA in CFIDS individuals correlated directly with RLI and RLI: RNase L protein ratio while showing an inverse relationship to the 2-5A synthetase and RNase L activity. This RLI mRNA and protein deficiency in CFIDS patients may explain the increase in activity of RNase L found in CFIDS patients. The unidirectional decrease in RLI message and protein levels in CFIDS individuals may contribute to the destabilization of the latent RLI:RNase L heterodimeric protein complex, resulting in the excessive activation of RNase L shown in this study. The increased activation of RNase L may result in an increased cellular RNA turnover and subsequent inhibition of protein synthesis; thus resulting in general fatigue, myalgia muscle weakness and other symptomatologies shown in CFIDS patients. Furthermore, this data supports the hypothesis that the antiviral 2-5 oligoadenylate synthetase (2-5OAS) overexpression in individuals with CFIDS correlates with an increase in RNase L activity and with a decrease in RNase L inhibitor.

2',5'-Oligoadenylate Synthetase↗

PubMed1997

Methyl tertiary-butyl ether antibodies among gasoline service station attendants.

Occupational exposure to petroleum products (gasoline) and elevated blood levels of MTBE have been demonstrated among gasoline station attendants. While MTBE and its metabolites have been considered environmentally inert, immunologically these materials could be reactive. This study was conducted to assess the immunological reactivity of humans to MTBE. Blood samples from 24 gasoline station attendants and 12 healthy controls were examined for levels of IgG, IgM, IgA, and IgE against MTBE by ELISA. In the gasoline-exposed group 7 out of 24 exhibited optical densities or antibody levels of 3-15-fold (OD 0.6-2.68) of the levels detected in controls (OD < 0.2). The detected antibodies both against MTBE-BSA or MTBE-HSA were of IgG and IgM but not IgA or IgE isotypes. These antibodies at much lower levels (OD of 0.45) were detected in only 1 of the 12 healthy control groups. The specificity of these antibodies was evidenced by absorption of MTBE antibodies in different sera using the same haptenic group bound to a different carrier. These results indicate that immune reactions to MTBE do occur through hapten carrier reactions which, in some individuals, end with specific IgG and IgM production.

Antibodies↗

PubMed1997

Elevated apoptotic cell population in patients with chronic fatigue syndrome: the pivotal role of protein kinase RNA.

OBJECTIVES: A prominent feature of chronic fatigue syndrome (CFS) is a disordered immune system. Recent evidence indicates that induction of apoptosis might be mediated in a dysregulated immune system by the upregulation of growth inhibitory cytokines. Therefore, the purpose of this study was to evaluate the apoptotic cell population, interferon-alpha (IFN-alpha) and the IFN-induced protein kinase RNA (PKR) gene transcripts in peripheral blood lymphocytes (PBL) of CFS individuals, as compared to healthy controls. SUBJECTS AND METHODS: PBL were isolated from CFS (n = 29) and healthy control individuals (n = 15) and subjected to quantitative analysis of apoptotic cell population and cell cycle progression by flow cytometry. Quantitative competitive polymerase chain reaction (Q/C PCR) and Western blot analysis were used to assess the levels of PKR mRNA and protein in control and CFS individuals. In addition, circulating IFN-alpha was measured by ELISA assay. RESULTS: Increased apoptotic cell population was observed in CFS individuals, as compared to healthy controls (26.6 +/- 12.9% and 9.9 +/- 4.2%, respectively). The increased apoptotic subpopulation in CFS individuals was accompanied by an abnormal cell arrest in the S phase and the G2/M boundary of the cell cycle as compared to the control group (8.6 +/- 1.2 to 22.8 +/- 2.4 and 3.6 +/- 0.82 to 24.3 +/- 3.4, respectively). In addition, CFS individuals exhibited enhanced PKR mRNA and protein levels (mean basal level 3538 +/- 1050 and 2.7 +/- 0.26, respectively) as compared to healthy controls (mean basal level 562 +/- 162 and 0.89 +/- 0.18, respectively). In 50% of the CFS samples (n = 29) treated with 2-aminopurine (2-AP) (a potent inhibitor of PKR) the apoptotic population was reduced by more then 50%. CONCLUSIONS: PKR-mediated apoptosis in CFS individuals may contribute to the pathogenesis and the fatigue symptomatology associated with CFS.

2-Aminopurine↗

PubMed1997

Abnormal apoptosis and cell cycle progression in humans exposed to methyl tertiary-butyl ether and benzene contaminating water.

1. In this study we hypothesized that in individuals with certain genetic makeup, MTBE, benzene or their metabolites act as adducts and may induce programmed cell death. 2. Our study involved a group of 60 male and female subjects who were exposed to MTBE and benzene-contaminated water concentrations up to 76 PPB for MTBE and 14 PPB for benzene, for a period of 5 to 8 years. For comparison, we recruited a control group consisting of 32 healthy males and females with similar age distribution and without a history of exposure to MTBE or benzene. 3. Peripheral blood lymphocytes (PBL) of both groups were tested for the percentage of apoptotic cells and cell cycle progression using flow cytometry. 4. When apoptotic lymphocytes from exposed individuals were compared to apoptotic lymphocytes from the control group, statistically-significant differences between each mean group were detected (26.4 +/- 1.8 and 12.1 +/- 1.3, respectively), indicating an increased rate of apoptosis in 80.5% of exposed individuals (P < 0.0001, Mann-Whitney U-Test). MTBE and benzene-induced apoptosis is attributed to a discrete block within the cell cycle progression. Because cell cycle analysis showed that in PBL from chemically-exposed individuals, between 20-50% of cells were accumulated at the S-G2/M boundaries. 5. One of the signaling molecules which mediates programmed cell death is nuclear factor Kappa-B (NF-kappa B). NF-kappa B was examined as one of the many molecular mechanisms for mediating cell death by MTBE and benzene. Indeed, addition of inhibitors of NF-kappa B activation pyrrolidine dithiocarbamate (PDTC), to the lymphocytes of the chemically-exposed group was capable of inhibiting programmed cell death by 40%. This reversal of apoptosis almost to the control level by inhibitor of NF-kappa B activation may indicate involvement of this signaling molecule in MTBE and benzene induction of programmed cell death.

Adolescent↗

PubMed1997

Enhancement of natural killer cell activity and T and B cell function by buffered vitamin C in patients exposed to toxic chemicals: the role of protein kinase-C.

After exposure to many toxic chemicals, NK function can be decreased significantly. Weeks or months later, natural killer (NK) function can rebound to normal levels in some and can be suppressed for prolonged periods of time in other patients. In view of this, we decided to study the effect of buffered vitamin C on NK, T and B cell function in patients who had been exposed to toxic chemicals. After the first blood draw, 55 patients immediately ingested granulated buffered vitamin C in water at a dosage of 60 mg/Kg body weight. Exactly 24 hours later, blood was again drawn for a follow-up study of NK, T and B cell function. Vitamin C in high oral dose was capable of enhancing NK activity up to ten-fold in 78% of patients. Lymphocyte blastogenic responses to T and B cell mitogens were restored to the normal level after vitamin C usage. Signal transduction enzyme protein kinase C (PKC) appeared to be involved in the mechanism of induction of NK activity by vitamin C. We conclude that immune functional abnormalities can be restored after toxic chemical exposure by oral usage of vitamin C.

Adjuvants, Immunologic↗

PubMed1996

Cytomegalovirus DNA identified in skin biopsy specimens of patients with vitiligo.

BACKGROUND: Viral infections have been implicated in the pathogenesis of a variety of autoimmune diseases. OBJECTIVE: This investigation was undertaken to determine the presence or absence of viral genomes in the depigmented and uninvolved skin of patients with vitiligo. METHODS: A polymerase chain reaction assay was used to detect viral genomes in paraffin-embedded skin biopsy specimens. Twenty-nine patients with vitiligo and 22 control subjects were included. Biopsy specimens were screened in a blinded fashion for a panel of DNA and RNA viruses including herpes simplex, varicella-zoster, cytomegalovirus (CMV), Epstein-Barr, HIV, and human T-cell lymphotropic virus. RESULTS: CMV DNA was identified in 38% of the patients studied. Twenty-one percent had indeterminate results. Results in all control subjects were negative. Polymerase chain reaction screening for identification of other viral genomes was negative. Although not statistically significant, data trends suggested a correlation between the presence of CMV DNA in biopsy specimens and active vitiligo of relatively brief duration. In addition, CMV-positive patients had a statistically significant increased frequency of other concurrent autoimmune diseases. CONCLUSION: CMV DNA in the depigmented and uninvolved skin of some patients with vitiligo and its absence in control subjects suggest that vitiligo may indeed be triggered by a viral infection in select patients.

Adult↗

PubMed1996

Immunological cross reactivity between Candida albicans and human tissue.

An old concept to account for autoimmunity is the existence of immunologic cross reactions, or shared determinants between an exogenous agent and self antigen. To study molecular mimicry between the Candida antigen and an autoantigen, sera from clinical specimens were screened, based on seronegativity or positivity for thyroid, ovary and adrenal antibodies. Compared with tissue antibody negative sera and sera from healthy controls, samples from positive tissue antibody subjects exhibited significantly higher levels of Candida IgG (P < 0.001) IgM (P < 0.001) and IgA (P < 0.01) antibodies. While Candida antibodies were elevated in 60% of tissue antibody positive samples, these antibodies were present in only 7.5% of tissue antibody negative subjects and in 10% of healthy controls. Since PAGE electrophoresis showed similar bands mobility in Candida and different tissues, these positive antibodies and rabbit anti Candida antibodies were reacted in immunodiffusion and Western Blot Assay against Candida and tissue antigens, simultaneously. The results of immunodiffusion showed a clear precipitation line against tissue antigens when rabbit anti Candida or human positive Candida serum was used. Similarly, Western Blot Assays with rabbit or human anti Candida serum showed several positive bands with Candida and one or two positive bands with different tissues. The common antigens were located in the regions of 72 and 36 KD. The 72 KD was detected in capsule antigens, placenta, ovary, adrenal, thymus, liver, pancreas, spleen, brain and kidney, but not in sperm or epithelial cell antigen. The 36 KD antigen was positive in placenta, spleen adrenal, pancreas and capsule tissues. Absorbtion of sera containing high levels of Candida antibodies with tissue antigens caused 10-15% reduction in antibody titers. Moreover, treatment of thyroid antibody positive sera with C. Albicans caused a similar reduction in thyroid antibody levels. These reductions in antibody levels are an additional support for cross reactivity between C. Albicans and mammalian tissues. A demonstration of immunological cross reactivity between Candida and human tissues may be associated with the possible pathogenic role of Candida Albicans in the development of autoimmune diseases which warrants further investigation.

Adrenal Glands↗