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PubMedDate not supplied

Granulocyte-macrophage colony-stimulating factor: pleiotropic cytokine with potential clinical usefulness.

Granulocyte-macrophage colony-stimulating factor (GM-CSF) is a 23-kDa glycoprotein with remarkably diverse effects on immune and nonimmune cells. GM-CSF induces differentiation of granulocyte, macrophage, and eosinophil precursor cells. Proliferation of monocyte-macrophages, T lymphocytes, keratinocytes, and endothelial cells is also stimulated by GM-CSF. In addition, GM-CSF alters the functional properties of mature granulocytes, macrophages, eosinophils, and basophils. GM-CSF is produced by T lymphocytes, macrophages, and several cell types in extramedullary sites, where it may act in a paracrine manner to regulate the local response to antigenic challenge. Clinical trials of GM-CSF have been conducted in patients with AIDS, aplastic anemia, myelodysplastic syndromes, and sarcoma and following bone marrow transplantation and accidental radiation exposure. GM-CSF significantly increased circulating numbers of several myeloid cells and produced dose-dependent toxicity consisting primarily of myalgias, fever, fluid retention, and serosal effusions. Additional studies are needed to define the role of GM-CSF in treatment of patients with qualitative and quantitative dysfunction of immune cells.

Animals↗
PubMed2003

Serotonin, serotonin 5-HT(1A) receptors and dopamine in blood peripheral lymphocytes of major depression patients.

There are increasing evidences of cell markers present in the immune and the nervous systems. These include neurotransmitter receptors and transporters. Serotonin receptor subtypes are related to depression and also have been shown to be present in certain cells of the immune system. In the present report, we determined the presence of 5-HT(1A) receptors by the binding of the selective agonist 8-hydroxy-2-(di-n-propyl-amino)tetralin in lymphocytes of peripheral blood isolated by Ficoll/Hypaque gradients from controls and depressed patients. The capacity of these receptors was around 24 fmol/10(6) cells in both groups of subjects, without significant difference among them. The affinity was in the nM range and either differ between controls and patients. Serotonin, 5-hydroxyindoleacetic acid, dopamine and 3,4-dihydroxyphenylacetic acid were determined by HPLC with electrochemical detector. There were no significant differences between controls and major depression patients in the values obtained for rich and poor platelet plasma or in the isolated cells. However, there was a reduction in serotonin turnover rate indicated by an increase in the ratio serotonin/5-hydroxyindoleacetic acid, but not in that of dopamine, in lymphocytes of major depression patients. Thus, there is a serotonergic dysfunction in immune circulating cells of major depression patients, without changes in the number of 5-HT(1A) receptors, although the coupling of these receptors to transduction mechanisms could be affected and may be related to the alteration of 5-HT turnover rate.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1987

Thymectomy delays the development of hypertension in Okamoto spontaneously hypertensive rats.

Previous studies in rats have demonstrated that immune system dysfunction contributes to the aetiology of spontaneous hypertension. Chronic immunosuppression with cyclophosphamide attenuated the level of hypertension in Okamoto spontaneously hypertensive rats (SHR) by approximately 50%. Also, neonatal thymic implants delayed the development of spontaneous hypertension and significantly attenuated its level at the age of 22 weeks in SHR. In the present study, the effect of thymectomy at the age of 4 weeks on blood pressure was investigated in SHR and Wistar-Kyoto (WKY) rats. The removal of the thymus gland in 4-week-old SHR produced a significant reduction in systolic arterial pressure (SAP), diastolic arterial pressure (DAP) and mean arterial pressure (MAP) when rats were 16-19 weeks old, while no pressure reduction was observed in WKY rats. The decrease in arterial pressure of 16-week-old SHR was associated with a significant reduction in lymphocyte count at this age as compared with the control group. In 1-year-old SHR, thymectomized at the age of 4 weeks, there was no significant difference in arterial pressure or lymphocyte count compared with controls. These data support the hypothesis that an immune imbalance may be important in the development of spontaneous hypertension. We conclude that thymectomy at a young age (4 weeks) delays the development of hypertension in SHR.

Aging↗
PubMed1985

Defects in mononuclear phagocytic system (MPS) function in autoimmune MRL-lpr/lpr mice.

MRL-lpr/lpr mice develop an autoimmune disease similar to systemic lupus erythematosus. To determine whether mice of this strain develop defects in mononuclear phagocyte system (MPS) function similar to those observed in patients, the pattern of sequestration of labeled immune complexes was compared 90 min after infusion into MRL-lpr/lpr and into normal B6D2 mice. The amount of complexes persisting in the blood was increased, and the amount sequestered in the liver was significantly reduced in MRL-lpr/lpr mice in comparison to normal B6D2 controls. This defect was most evident in MRL-lpr/lpr mice of the ages of 25-26 weeks; mice of this age also demonstrated the greatest elevation of anti-DNA antibody levels. The role of the MRL strain background and of the lpr gene in determining this defect was investigated by analysis of MRL-+/-/+/- and of other lpr congenic strains (B6-lpr/lpr, AKR-lpr/lpr, and C3H-lpr/lpr). Both MRL-+/-/+/- and congenic lpr animals showed similar defects, although to a lesser degree than MRL-lpr/lpr mice. In contrast, MRL-lpr/lpr mice demonstrated normal clearance of heat-damaged red blood cells and heat-aggregated albumin. Thus MRL-lpr/lpr mice display a selective defect in MPS Fc receptor function and may provide a valuable model for elucidating the etiology and importance of MPS dysfunction in immune complex deposition disease.

Animals↗
PubMed1995

Human glioma-derived interleukin-10 inhibits antitumor immune responses in vitro.

Intracranial malignant gliomas are sequestered from the immune system yet are associated with broad suppression of host immunocompetence. Immune system dysfunction in patients with gliomas seems to be related to inhibitory mediators produced by glioma cells. We investigated the physiological roles of glioma-derived interleukin (IL)-10 in Class II expression of monocytes, cytokine secretion from lymphocytes, and T cell proliferation in vitro. We could detect the messenger ribonucleic acid transcript of IL-10 in four gliomas by the reverse-transcribed polymerase chain reaction. Glioma-derived IL-10 greatly down-regulated human lymphocyte antigens-DR expression on monocytes. The inhibitory effect of IL-10 on interferon-gamma and tumor necrosis factor-alpha was neutralized by the anti-IL-10 monoclonal antibody; however, the inhibitory effect on IL-2 was not neutralized. Next, supernatants of glioma cells remarkably suppressed T cell proliferation in a dose-dependent fashion; however, this inhibitory effect was not restored by adding anti-IL-10 monoclonal antibodies. The supernatant also inhibited the allocytolytic activity of lymphocytes that were not neutralized by anti-IL-10 monoclonal antibody. IL-10 plays an important role in cytokine synthesis; nevertheless, impaired T cell responsiveness cannot be solely explained by glioma-derived IL-10.

Brain Neoplasms↗
PubMed2006

Functional impairment of monocyte-derived dendritic cells in patients with severe chronic kidney disease.

BACKGROUND: Dendritic cells (DCs) are antigen-presenting cells that are pivotal for the initiation of the primary immune response. Patients with chronic kidney disease (CKD) with or without chronic intermittent haemodialysis (CIHD) show an impaired immune response. Dysfunction of DCs may underlie this phenomenon. METHODS: In this study, several different functions of monocyte-derived DCs (moDC) of patients with CKD class IV-V (glomerular filtration rate <30 ml/min) and patients on CIHD were studied in vitro and compared with age- and sex-matched healthy volunteers. RESULTS: We demonstrate that, independent of the maturation stimulus used, mature moDC from both groups of patients did not acquire the same level of terminal differentiation as moDC from controls, as shown by analysis of cell surface markers and the relative high macropinocytosis activity of moDC. The stimulation of allogeneic T-cells by immature moDC and mature moDC did not differ between patients and controls. However, in the presence of immature moDC or antigen-loaded maturated moDC from patients, less proliferation of autologous T-cells was observed in response to recall antigens. There was no difference between moDC from controls and patients in their ability to activate naive T-cells and to differentiate them into Th1 and Th2 cells. CONCLUSIONS: These results show that the terminal differentiation of moDC in patients with severe CKD is impaired. This impairment is not restricted to one maturation stimulus and is independent of treatment with haemodialysis.

Adult↗
PubMed2006

Microarray analysis of mercury-induced changes in gene expression in human liver carcinoma (HepG2) cells: importance in immune responses.

Mercury is widely distributed in the biosphere, and its toxic effects have been associated with human death and several ailments that include cardiovascular diseases, anemia, kidney and liver damage, developmental abnormalities, neurobehavioral disorders, autoimmune diseases, and cancers in experimental animals. At the cellular level, mercury has been shown to interact with sulphydryl groups of proteins and enzymes, to damage DNA, and to modulate cell cycle progression and/or apoptosis. However, the underlying molecular mechanisms of mercury toxicity remain to be elucidated. Our laboratory has demonstrated that mercury exposure induces cytotoxicity and apoptosis, modulates cell cycle, and transcriptionally activates specific stress genes in human liver carcinoma cells. The liver is one of the few organs capable of regeneration from injury. Dormant genes in the liver are therefore capable of reactivation. In this research, we hypothesize that mercury-induced hepatotoxicity is associated with the modulation of specific gene expressions in liver cells that can lead to several disease states involving immune system dysfunctions. In testing this hypothesis, we used an Affymetrix oligonucleotide microarray with probe sets complementary to more than 20,000 genes to determine whether patterns of gene expressions differ between controls and mercury (1-3 microg/mL) treated cells. There was a clear separation in gene expression profiles between controls and mercury-treated cells. Hierarchical cluster analysis identified 2,211 target genes that were affected. One hundred and eighty-eight of these genes were up-regulated, among which forty eight were significant (p = 0.001) with greater than a two-fold change difference in the concentration range (1-3 microg/mL) of mercury-treated cells; twelve genes were moderately over-expressed with an increase of more than one fold (p = 0.004). 2,023 genes were down-regulated with only forty of them reaching statistically significant decline at p = 0.05 according to the Welch's ANOVA/Welch's t-test. Further analyses of affected genes identified genes located on all human chromosomes with higher than normal effects on genes found on chromosomes 1-14, 17-20 (sex-determining region Y)-box18SRY, 21 (splicing factor, arginine/serine-rich 15 and ATP-binding), and X (including BCL6-co-repressor). These genes are categorized as control and regulatory genes for metabolic pathways involving the cell cycle (cyclin-dependent kinases), apoptosis, cytokine expression, Na+/K+ ATPase, stress responses, G-protein signal transduction, transcription factors, DNA repair as well as metal-regulatory transcription factor 1, MTF1 HGNC, chondroitin sulfate proteoglycan 5 (neuroglycan C), ATP-binding cassette, sub-family G (WHITE), cytochrome b-561 family protein, CDC-like kinase 1 (CLK1 HGNC) (protein tyrosine kinase STY), Na+/H+ exchanger regulatory factor (NHERF HGNC), potassium voltage-gated channel subfamily H member 2 (KCNH2), putative MAPK activating protein (PM20, PM21), ras homolog gene family, polymerase (DNA directed), delta regulatory subunit (50 kDa), leptin receptor involved in hematopoietin/interferon-class (D200- domain) cytokine receptor activity and thymidine kinase 2, mitochondrial TK2 HGNC and related genes. Significant alterations in these specific genes provide new directions for deeper mechanistic investigations that would lead to a better understanding of the molecular basis of mercury-induced toxicity and human diseases that may result from disturbances in the immune system.

Cell Line, Tumor↗
PubMed1992

A single autosomal gene defect severely limits IgG but not IgM responses in B lymphocyte-deficient A/WySnJ mice.

Antigen-stimulated B lymphocytes either differentiate into IgM-secreting plasma cells or into memory B cells that secrete other immunoglobulin isotypes upon antigen restimulation. The mechanisms that generate and maintain memory B cells are poorly understood. Previously, we described a severe B lymphocyte deficiency in adult strain A/WySnJ mice compared to subline A/J. Here we show that the single, autosomal co-dominant locus responsible for the deficiency also diminishes IgG-secreting B cell formation without interfering with IgM-secreting plasma cell differentiation. A/WySnJ secondary IgG1 responses to the protein antigens hemocyanin, bovine gamma-globulin, ovalbumin, lysozyme and beta-galactosidase were 6- to 50-fold lower than A/J responses. The defect also decreased secondary IgG2a and IgG3 responses, and primary IgG1 and IgG2a responses. The reduced A/WySnJ secondary IgG1 response was not due to differential response kinetics or dose responsiveness, and could not be augmented to A/J levels by repeated immunizations. Serum IgG1, IgG2a and IgG3 levels from nonimmune A/WySnJ mice were similarly reduced. The secondary IgG1 response and splenic B cell percentage showed significant positive correlation (r = 0.72) in F2 mice, suggesting that a single locus controlled both traits. In contrast, A/WySnJ mice made good primary IgM responses to hemocyanin, beta-galactosidase, and the thymus-independent antigen trinitrophenyl-Ficoll. The A/WySnJ splenic adherent cells were competent in antigen-presenting function, and A/WySnJ immune T cells proliferated in response to antigen and provided the requisite B cell stimulatory signals for an IgG1 response. Together, our results suggest that A/WySnJ mice have a genetic lesion that causes a selective IgG immune response dysfunction. The absence of IgG-secreting cell precursors or a defect in precursor activation or differentiation are two possible mechanisms which could precipitate a selective IgG response dysfunction. We propose that the defective A/WySnJ and normal A/J strain pair offer the opportunity to use a natural genetic variation as a tool to investigate B lymphocyte development and function.

Animals↗
PubMed1991

Coexistence of reduced function of natural killer cells and osteoclasts in two distinct osteopetrotic mutations in the rat.

Recent evidence suggesting that immune cells and their products (cytokines) play an important role in the regulation of skeletal development and function, particularly of the osteoclast, implies that immune cell dysfunction may be involved in the pathogenesis of certain skeletal disorders. The mammalian osteopetroses are a pathogenetically heterogeneous group of skeletal disorders characterized by skeletal sclerosis resulting from reduced osteoclast-mediated bone resorption. Using a 51Cr-release microcytotoxicity assay we demonstrated that splenic natural killer (NK) cell activity was significantly reduced in two distinctly different osteopetrotic mutations in the rat, osteopetrosis (op) and toothless (tl). To determine whether this reduction in NK cell-mediated cytotoxicity is caused by decreased cell number and/or function in these osteopetrotic mutants, we quantitated NK cells by analyzing mononuclear cell suspensions labeled for two-color fluorescence with OX8 and OX19 monoclonal antibodies in a fluorescence-activated cell sorter. Flow cytometry of these double-labeled cells revealed that the percentage of NK cells (OX8+/OX19- subset) in op and tl spleens was not significantly different from that of normal spleens. These results suggest that NK cells in these osteopetrotic mutants are functionally defective. Thus aberrations in osteoclast and NK cell function coexist in these mutations, and their developmental relationships deserve further study.

Animals↗
PubMed1988

The effect of zinc status on the immune function of diabetic rats.

To evaluate the role of zinc status in immune system dysfunction in diabetic animals, the interleukin-2 production and the lymphocyte mitogenic response to phytohaemagglutinin, concanavalin A and lipopolysaccharide were measured in streptozotocin-induced diabetic rats, diabetic rats treated with insulin and their non-diabetic controls maintained on low zinc, normal zinc and high zinc diets for 3 weeks. Unstimulated lymphocyte proliferation was significantly lower in diabetic rats compared to nondiabetic control rats maintained on normal zinc diet (1505 +/- 318 vs 3447 +/- 497 cpm) (p less than 0.005) or low zinc diet (546 +/- 191 vs 4011 +/- 628 cpm) (p less than 0.005). High zinc diet attenuated the difference between the diabetic rats (2404 +/- 833 cpm) and control rats (3929 +/- 713 cpm). Insulinised diabetic rats were similar to control rats. Phytohaemagglutinin-stimulated lymphocyte proliferation was not significantly altered with dietary zinc changes, but diabetic rats on low zinc diet had significantly lower (p less than 0.025) values compared to control rats on the same diet (41470 +/- 7874 vs 72308 +/- 8895 cpm). Insulinisation did not normalise phytohemaegglutinin-stimulated lymphocyte proliferation (40711 +/- 3666 cpm). Similarly, cells from diabetic rats on low zinc diet, unlike their controls, failed to respond to concanavalin A stimulation. Compared to control rats the diabetic rats on either low or normal zinc diets had lower lipopolysaccharide-stimulated lymphocyte proliferation. High zinc diet or insulinisation normalised mitogenic response of lymphocytes to lipopolysaccharide. Unlike the diabetic rats alterations in dietary zinc intake did not significantly affect the lymphocyte proliferation in control rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1996

Health and immunology study following exposure to toxigenic fungi (Stachybotrys chartarum) in a water-damaged office environment.

There is growing concern about adverse health effects of fungal bio-aerosols on occupants of water-damaged buildings. Accidental, occupational exposure in a nonagricultural setting has not been investigated using modern immunological laboratory tests. The objective of this study was to evaluate the health status of office workers after exposure to fungal bio-aerosols, especially Stachybotrys chartarum (atra) (S. chartarum) and its toxigenic metabolites (satratoxins), and to study laboratory parameters or biomarkers related to allergic or toxic human health effects. Exposure characterization and quantification were performed using microscopic, culture, and chemical techniques. The study population (n = 53) consisted of 39 female and 14 male employees (mean age 34.8 years) who had worked for a mean of 3.1 years at a problem office site; a control group comprised 21 persons (mean age 37.5 years) without contact with the problem office site. Health complaints were surveyed with a 187-item standardized questionnaire. A comprehensive test battery was used to study the red and white blood cell system, serum chemistry, immunology/antibodies, lymphocyte enumeration and function. Widespread fungal contamination of water-damaged, primarily cellulose material with S. chartarum was found. S. chartarum produced a macrocyclic trichothecene, satratoxin H, and spirocyclic lactones. Strong associations with exposure indicators and significant differences between employees (n = 53) and controls (n = 21) were found for lower respiratory system symptoms, dermatological symptoms, eye symptoms, constitutional symptoms, chronic fatigue symptoms and several enumeration and function laboratory tests, mainly of the white blood cell system. The proportion of mature T-lymphocyte cells (CD3%) was lower in employees than in controls, and regression analyses showed significantly lower CD3% among those reporting a history of upper respiratory infections. Specific S. chartarum antibody tests (IgE and IgG) showed small differences (NS). It is concluded that prolonged and intense exposure to toxigenic S. chartarum and other atypical fungi was associated with reported disorders of the respiratory and central nervous systems, reported disorders of the mucous membranes and a few parameters pertaining to the cellular and humoral immune system, suggesting a possible immune competency dysfunction.

Adult↗
PubMed1998

Thyroid abscess due to Rhodococcus equi in a patient infected with the human immunodeficiency virus.

A case of thyroid abscess due to Rhodococcus equi in an HIV-positive patient with previous pulmonary abscess is reported. Rhodococcus equi is a gram-positive rod that can cause infections in both immunocompetent and immunocompromised patients, though it occurs more frequently in patients with dysfunctional cellular immune systems. Several cases of Rhodococcus equi infection in persons infected with HIV have been reported. In these patients Rhodococcus equi usually invades the lungs, producing pneumonia. These infections often relapse, accompanied by intermittent bacteremia, despite conventional treatment. Extrapulmonary abscesses can occur.

AIDS-Related Opportunistic Infections↗
PubMed2006

Association between breast cancer and autoimmune thyroid disorders: no increase of lymphocytic infiltrates in breast malignant tissues.

An association between thyroid autoimmunity and breast cancer (BC) has been consistently reported, but the cause of this association is still unknown. The role of lymphocytic infiltration (LI) in breast tumorigenesis is controversial and several data suggest that in BC an increase of lymphoid cell infiltrates or a dysfunctional local immune response may be detected very early during tumor development. Chronic autoimmune thyroiditis is characterized by different degrees of LI in thyroid gland and BC cells share some antigenic properties similar to those detected in thyroid tissue, such as sodium iodide symporter (NIS) and peroxidase activity. The aim of this study was to evaluate the frequency and amount of LI in malignant and in normal peritumoral breast tissues, as expression of autoimmune morphological changes, in a group of BC patients with thyroid autoimmunity. We suppose that an increased LI in breast tissues of this group of patients may help explain the association between BC and thyroid autoimmunity. The study group included 26 BC patients with thyroperoxidase antibodies positivity (TPOAb+), 14 of them (53.8%) with Hashimoto's thyroiditis (HT), and 30 BC patients with no evidence of thyroid autoimmune disorders. Malignant and surrounding normal breast tissues were assessed for LI. The amount of LI was scored as very scanty or scanty (LI S) and moderate or marked (LI M), independently by two expert pathologists. LI S was detected in 19/26 (73.1%) BC tissues from patients with TPOAb positivity and LI M in 7 (26.9%). All BC patients with HT had LI S. LI S was detected in 25/30 (83%) and LI M in 5/30 (17%) of BC tissue from patients with no thyroid autoimmunity. The difference in the amount of LI of BC tissues in patient with or without autoimmune thyroid disorders was not significant. The LI was generally absent or very scanty in remote breast tissue in all cases. In conclusion, in breast malignancies the presence of humoral and/or clinical evidence of thyroid autoimmunity is not associated to autoimmune morphological changes of cancer and peritumoral normal tissue. The LI does not seem to have any role in tumorigenesis in patients with BC and thyroid autoimmunity.

Adult↗
PubMed2004

Vascular endothelial and basic fibroblast growth factor serum levels in patients with Behçet's disease.

Behçet's disease (BD) is a systemic vasculitis of unknown aetiology. Its pathogenesis is related to endothelial cell dysfunction, humoral immune defects, and immune system dysregulation. The aim of this study was to investigate the possible role of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) in the pathogenesis of BD. We also investigated whether disease activity, age, or duration of BD correlates with VEGF and bFGF. We studied 33 patients and 20 healthy controls. Vascular endothelial growth factor and bFGF serum levels were measured by enzyme-linked immunosorbent assay. We measured acute phase reactants, including erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP). The mean serum VEGF level was significantly higher in patients with BD (398.8+/-222.2 pg/ml) than the control group (193.0+/-122.4 pg/ml) (P=0.002). The levels were similar in both active and inactive BD (P=0.675) but did not correlate with disease duration, CRP, ESR, or age (P>0.05 for each). The bFGF was below detection limits in 18 of 33 patients with BD and ten of 20 controls, and its mean serum level was higher in BD patients (42.4+/-76.9 pg/ml) than controls (29.0+/-9.1 pg/ml), but this difference was not statistically significant (P=0.232). The bFGF levels were similar in both active and inactive BD (P=0.09) and, in patients, correlated with disease duration and CRP (r=0.58, P=0.02; r=-0.57, P=0.02, respectively) but not with ESR or age (P>0.05 for each). Vascular endothelial growth factor may be more important in the pathogenesis of BD than bFGF. Neither growth factor is an activity criterion or inflammatory marker in BD.

Adult↗
PubMed1985

Polyclonal induction of immunoglobulin synthesis by feline leukocytes as identified in a reverse hemolytic plaque assay.

Optimal conditions of culture and assay for identification of feline immunoglobulin-secreting mononuclear cells were determined for the staphylococcal protein A-reverse hemolytic plaque assay (SpA-RHPA). Hemolytic plaques were most distinct and numerous when peripheral blood mononuclear cells were stimulated with 6.9 micrograms/ml pokeweed mitogen for 7 days. Immunoglobulin-secreting cells were identified morphologically within a zone of hemolysis utilizing a 1:5 dilution of rabbit anti-cat IgG and a 1:30 dilution of guinea pig complement as developing reagents. The SpA-RHPA system should contribute to an understanding of normal feline T- and B-lymphocyte interactions and will likely aid in the identification and understanding of immune cell dysfunctions associated with chronic feline leukemia virus infection.

Animals↗
PubMed1990

Frequent isolation of HHV-6 from saliva and high seroprevalence of the virus in the population.

Human herpesvirus-6 (HHV-6) was recovered at high frequency (greater than 85%) from the saliva of both healthy individuals and those infected with the human immunodeficiency virus (HIV). The level of isolation mirrored the high prevalence of antibodies to HHV-6 found in sera obtained from residents of diverse areas of the world. Seroconversion occurred between 1 and 3 years of age; seroprevalence ranged between 80% and 100% among adults under 40 and decreased to 35% between ages 62 and 88. Serum titres in healthy individuals remained stable during periods of virus shedding. Immune cellular dysfunction in patients was associated with high geometric mean HHV-6 antibody titres. These observations suggest that HHV-6 infection takes place within the first 3 years of life, and strongly implicate oral shedding as a common means of transmission of this newly described herpesvirus.

Acquired Immunodeficiency Syndrome↗
PubMed2005

Oral fungal infections.

Candidiasis is the most common oral fungal infection diagnosed in humans. Candidiasis may result from immune system dysfunction or as a result of local or systemic medical treatment. Because oral candidiasis is generally a localized infection, topical treatment methods are the first line of therapy, especially for the pseudomembranous and erythematous variants. Patients with dental prostheses should also be advised to disinfect the prosthesis routinely during the candidal treatment period, because the prosthesis may serve as a source of reinfection. Additionally, patients should be advised that oral hygiene aids, such as toothbrushes and denture brushes, may also be contaminated and should be discarded or disinfected. A disinfecting solution of equal parts of hydrogen peroxide and water may be used. Likewise, 2% chlorhexidine gluconate solution may be used asa disinfecting solution for dental prostheses and oral hygiene aids. Occasionally the clinician encounters a more resistant form of oral candidiasis such as the hyperplastic variant or a variant that does not respond to topical therapy. Appropriate systemic therapy should be employed for the treatment of these infections. Additionally, a biopsy should be undertaken in individuals with the hyperplastic variant of Candida because there is some degree of risk for malignant transformation. Deep fungal infections should be managed in association with appropriate medical specialists to rule out other systemic involvement. The dental health care provider plays an important part in the diagnosis and management of fungal disease, and therefore clinicians should be aware of the presenting signs and symptoms or oral fungal disease.

Antifungal Agents↗
PubMed2006

Abnormal Fas/FasL and caspase-3-mediated apoptotic signaling pathways of T lymphocyte subset in patients with systemic lupus erythematosus.

OBJECTIVES: To explore the relationships between Fas-FasL-mediated signaling pathway and apoptosis disturbance of T lymphocyte subset in patients with SLE. METHODS: Flow cytometry was used to determine the percentage of apoptotic lymphocytes and necrotic lymphocytes by AnnexinV-FITC/PI double staining. Cell surface expression rates of Fas, FasL, and intracellular expression rates of activated caspase-3 were evaluated by two-color flow cytometry analysis in peripheral T lymphocyte subsets of SLE patients with inactive disease (n=22) and with active disease (n=17). The serum concentration of anti-nucleosome antibodies in SLE patients were assayed by ELISA immunoassay methods. Health volunteers (n=13) served as controls. RESULTS: The percentage of early apoptotic cells was enhanced in patients with active disease (P=0.001, vs. control) and in patients with inactive disease (P=0.004, vs. control). Compared with health control, the percentage of necrotic cells was significant higher in patients with active disease (P=0.001). The percentages of CD4(+)T cells expressing Fas (P=0.023, vs. control) and FasL (P=0.001, vs. control) were increased in patients with active disease. But there were no obvious differences of expression rates of Fas and FasL on T cell subset between two disease groups (P>0.05). In patients with active disease the percentage of CD4(+)T cells or CD8(+)T cells expressing intracellular activated caspase-3 significantly increased compared to inactive disease patients (P=0.018, P=0.027, respectively) and health controls (P=0.001, P=0.001, respectively). The serum concentration of anti-nucleosome antibodies was strikingly higher in patients with active disease (P=0.002, vs. patients with inactive disease; P=0.001, vs. control, respectively), however, the serum concentration of anti-nucleosome antibodies was not obviously different between patients with inactive disease and health control group (P=0.473). The percentage of apoptotic cells correlated with the serum concentration of anti-nucleosome antibodies in SLE patients (r(s)=0.350, P=0.031). CONCLUSIONS: Apoptosis of T lymphocyte subset in SLE patients increases. CD4(+)T cells are a state of active apoptosis. Fas/FasL-mediated apoptotic pathways are especially important for CD4(+)T cells undergoing apoptosis in SLE patients with active disease. Increased Fas expression results in a higher susceptibility to Fas-mediated apoptosis, which contributes to the increased levels of intracellular activated caspase-3 and accelerates apoptosis of T lymphocytes. The degree of lymphocytic apoptosis disturbance correlates with the level of anti-nucleosome antibodies in the circulation. Acceleration of lymphocytic apoptosis plays important roles in immune pathologic injury and immune regulation dysfunction.

Adolescent↗