2022 Impact Factor: 1.5
2023 CiteScore: 2.6
pISSN: 1735-1502
eISSN: 1735-5249
Chairman:
Mostafa Moin, M.D.
Editors-in-Chief:
Masoud Movahedi, M.D.
Vol 8, No 1 (2009)
Articles
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Viral myocarditis is a common cardiovascular disease, which has greatly threatened human health. However, up to now, the pathogenesis of viral myocarditis has been unclear, which leads to the lack of its effective treatments.
To investigate the role of chemokines in pathogenesis of viral myocarditis, mRNA expression for a panel of 19 chemokines detected by RT-PCR in myocardial tissue of BALB/c mice that were inoculated intraperitoneally with coxsackievirus B3. Moreover primary cultured cardiac myocytes were infected with coxsackievirus B3 following extraction of RNA, from myocytes the expression of 19 chemokines was detected by by RT-PCR.
Our results showed that there was much difference in the expression pattern of chemokines in myocardial tissue between infected mice with viral myocarditis and uninfected control mice. The expression of chemokines was varied significantly in clusters in myocardium post coxsackievirus B3 infection. There were also complexity and imbalance in the change of the expression of chemokines. In the meantime, Coxsackievirus B3 infection also influenced the expression pattern of chemokines in cardiac myocytes in vitro. However the expression of monocyte chemoattractant protein-1 alone was upregulated in cardiac myocytes post coxsackievirus B3 infection in the 19 detected chemokines.
The chemokine expression pattern changed in complexity and imbalance manner both in myocardium and in primary cultured cardiac myocytes after coxsackievirus B3 infection. Coxsackievirus B3 infection may start viral myocarditis by regulating the expression pattern of chemokines in cardiac myocytes. MCP-1 may be one of key chemokines in the initial stage of viral myocarditis. -
Insulin dependent diabetes mellitus (IDDM) results from irreversible loss of beta cells (β-cells) of the pancreas. A Streptozotocin (STZ)-induced diabetes in animal model mimics, in some aspects, recent onset IDDM. This study was conducted to investigate the effect of nicotinamide on experimentally-induced IDDM.
Thirty Spraque Dawley rats were divided into 3 groups; a control group, a diabetic group which received an intraperitoneal (i.p.) injection of 55 mg/kg STZ and a nicotinamide group (1g/kg/day) which were dosed orally for 3 days followed by (i.p.) STZ (55 mg/kg) with the nicotinamide treatment continuing for an additional 14 days.
Rats receiving STZ became diabetic after 2 weeks. This diabetic group showed hyperglycemia, and a very low level of C-peptide. Furthermore, pancreatic islets exhibited increased nitric oxide (NO) production together with an increased apoptotic index (as detected by TUNEL and electron microscopy). Nicotinamide treatment prevented STZ-induced diabetes, it also antagonized an increase in NO, and inhibited β-cell apoptosis. Fasting blood glucose, serum insulin and serum C-peptide were all within the normal range in the nicotinamide group.
The nicotinamide protection of β-cells may be facilitated via inhibition of apoptosis and nitric oxide generation. It is suggested that nicotinamide might be considered an effective agent for the prevention and treatment of IDDM in prediabetic, and early stages, of IDDM. -
Transforming growth factor-beta (TGF-β) is one of the most important cytokines implicated in growth, differentiation, repair and also the pathogenesis of the lung fibrosis by its stimulatory effect on extracellular matrix deposition. Pulmonary epithelial cells are considered as a source of TGF-β in lung. Substance P (SP), as a neuroimmunomodulator has elevated levels in inflamed airways and although it has significant role in the pathogenesis of the lung fibrosis, but its effect on transforming growth factor -beta (TGF-β) production of the lung epithelial cells (and so its regulatory potential) remains unclear.
In this study TGF-1 levels in supernatants of the normal (BEAS-2B) and cancerous (A549) lung epithelial cell line cultures at the presence of various concentrations of SP were examined and MTT assay was performed to evaluate cells viability.
We have observed that SP (without any other stimulator) significantly augments TGF-β production of both BEAS and A54 cells and this effect is inhibited by NK1-receptor antagonist (CP-96345). We have also observed that the viability of cells did not significantly affect at the presence of SP.
It can be concluded that SP can directly modulate the release of TGF-β from human bronchial epithelial cell line and thereby participates in various lung functions or pathologic conditions. -
Variety of positive as well as negative regulatory signals are provided by antigen presenting cell in particular by dendritic cells. In this research, we studied the capacity of dendritic cells to expand antigen-specific T regulatory cells.We also investigated the role of TGF-beta in induction inhibitory functions of dendritic cells in mixed leukocyte reactions.
Dendritic cells were generated from blood CD14+ monocytes with granulocyte-Monocyte colony stimulating factor and interleukin-4 with or without TGF-beta (TGF-β-GM-DC or GM-DC). CD4+ T cell were isolated to assess lymphocyte proliferation by lymphocyte transformation test assay and the ratio of CD4+FOXp3+ CD25+ T cells were determined by fluorescene-activated cell sorter.
T cell proliferation responses in GM-DC showed a significance antigen-specific proliferative response comparing with TGFβ-GM -DC. T Cell proliferation was inhibited in co-culture system containing DC-treated TGF-β.
It can be suggested that the expsansion of T regulatory by TGF-β-GM-DC provides a means for antigen specific control of unwanted immune reactions. -
The aim of this study was to examine the association of 22 cytokine gene polymorphism in Macedonians with chronic obstructive pulmonary disease (COPD).
The sample of the population comprised of 301 normal respondents and 62 patients with COPD. Cytokine genotyping was performed by polymerase chain reaction with sequence-specific priming (PCR-SSP).
Positive (susceptible) association was found between patient with COPD and IL-1α -889/C allele; where as negative (protective) association among was found for the following alleles IL-1β +3962/C; IL-12B -1188/A; IFNγ +874/T; IL-2 -330/G; IL-4 -1098/G and IL-4-33/C. We found positive (susceptible) association between patients with COPD and following genotypes: IL4 -33/T:T; IFNγ +874/A:A; IL-4 -1098/T:T ; IL-1α -889/C:C; IL-1β +3962/C:T; IL-12B -1188/C:C; IL-4Rα +1902/G:G; IL-10 -1082/G:G; IL-2 -330/T:T; IL-4 -590/C:C; and IL-1α -889/C:T. Negative (protective) association between patients with COPD and following genotypes was found: IFNγ +874/A:T; IL-4 -33/C:T; IL-4 -1098/G:T; IL-2 -330/G:T; IL-1β +3962/C:T; IL-4 -590/C:T; IL-10 -1082/A:G; and IL-4 -33/C:C. Positive (susceptible) association between patients with COPD and following haplotypes was found: IL-4/TCT; IL-10/ATC; and IL-2/TG, and negative (protective) association was found between the patients with COPD and haplotypes for: IL-4/TTC; and IL-4/GCC.
It could be concluded that several cytokine polymorphisms are positively (susceptible), or negatively (protective) associated with COPD in Macedonians. -
X-linked Agammaglobulinemia (XLA) is a hereditary immunodeficiency, characterized by an early onset of recurrent bacterial infections, hypogammaglobulinemia and markedly reduced B lymphocytes number.
In order to determine the association of neutropenia among Iranian patients with XLA, hospital records of 30 patients with confirmed XLA in Children Medical Center Hospital, were reviewed.
Eight out of 30 XLA patients (26.7%) developed neutropenia during the course of the disease. In two patients, episodes of neutropenia were identified before or at the time of diagnosis of XLA. Other six patients whom were not visited regularly and did not receive periodical immunoglobulin replacement therapy experienced neutropenia after diagnosis of XLA.
Neutropenia in XLA is mainly associated with infection and is resolved with intravenous immunoglobulin replacement and antibiotics therapy. -
Several studies reported the appearance of asthma and autoimmune conditions in the same patient, but the clinical significance of this association was not yet assessed.
One hundred asthmatic patients were observed for one year evolution with death, severe exacerbations, intake of > 1000 micrograms of beclometasone or equivalent (high ICS) and FEV1 decline >100 ml, in relation with ANA (ELISA), sputum and blood eosinophilia (EO), NSAID intolerance, BMI >25, chronic rhinosinusitis, smoking status and FEV1 <30% predicted (low FEV1).
After 1 year of observation, there were 5 deaths, 28 severe asthma exacerbations requiring hospitalisations, 24 cases requiring high inhaled corticosteroid intake, and 19 patients with fast FEV1 decline (>100 ml/year). Multiple regression analysis pointed out several different independent risk factors for severe asthma evolution: for death presence of ANA (P=0.037), NSAID intolerance (P<0.001) and low FEV1 (P=0.021); for evolution with severe exacerbations ANA (p=0.011), sputum EO (P<0.001), smoking (P=0.044) and NSAID intolerance (P=0.022); for high ICS intake ANA (P=0.036), sputum EO (P=0.026) and low FEV1 (P=0.006); for FEV1 decline >100 ml ANA (P=0.006), sputum EO (P=0.037), BMI>25 (P=0.046) and NSAID intolerance (P=0.017)
The presence of ANA is an independent risk factor in asthma for evolution with death, severe exacerbations, high inhaled corticosteroid intake and FEV1 decline >100 ml. -
Anti-desmoglein 3 and 1 autoantibodies are involved in the pathogenesis of pemphigus diseases. Our objective was to assess the value of ELISA in the diagnosis of pemphigus and its correlation with the severity of pemphigus vulgaris.
Based on clinical presentation and histopathologic confirmation for the diagnosis of the pemphigus, 38 patients took part in the study. Sera of the patients were tested by desmoglein 1 and desmoglein 3 ELISA. Also, direct immunofluorescence was performed for all patients which revealed positive results in 36 patients (94.7%).
ELISA was positive in 37 of 38 pemphigus patients (Sensitivity: 97.3%). The relationship between desmoglein 1 index values and skin severity was statistically significant (p<0.05). Desmoglein 3 index values increased with oral severity although this was not statistically significant. Iranian patients similar to Indian patients had higher positive anti-desmoglein 1 autoantibodies.
Desmoglein-ELISA test is appropriate in the diagnosis of pemphigus. Desmoglein 1 index value is statistically correlated with the severity of pemphigus vulgaris. -
Mutations in any of four known NADPH-oxidase components lead to CGD. X-linked CGD (X-CGD) is caused by defects in CYBB, the gene that encodes gp91-phox. Autosomal recessive (AR) CGD is caused by defects in the genes for p47 phox, p22-phox or p67-phox. The aim of this study was to screen the molecular defect in the fetus of an X-CGD carrier mother and postnatal confirmation of the results.
In a family whose first-born child died from X-CGD, fetal DNA was obtained from an ongoing pregnancy by chorionic villus sampling (CVS). Direct sequencing was used to detect the previously identified CYBB gene mutation. The NADPH oxidase activity in the neutrophils from the carrier mother and from the newborn was analyzed by the DHR assay.
Our studies predicted that the fetus in question was not affected by chronic granulomatous disease, which was demonstrated to be correct at birth. For prenatal screening in a pregnant X-CGD carrier, direct sequencing is a good method for detecting the mutation in the fetal DNA. Postnatal confirmation of results with the DHR assay is more practical than mutation screening to show whether the newborn have normal NADPH oxidase activity or does not. -
The purpose of this study was to evaluate the transverse and vertical dimensions of the palate of children with allergic rhinitis (AR). There was no significant difference for intermolar and intercanine distances between two groups in primary and mixed dentitions. Palate depth in children with allergic rhinitis was statistically more than in children without any respiratory disease. Cross bite was more prevalent in study group. It seems that the main influence of alteration of breathing pattern from nasal to mouth occurs on the vertical plane.
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Estrogens foster immunological processes driven by CD4+ Th2 cells and B cells and androgens foster Th1 CD4+ and CD8+ cell activity. Higher levels of IFN-gamma and IL-2 and lower levels of IL-4 and IL-10 are detected in the phytohemagglutinin-stimulated lymphocyte culture supernatants of men compared with women. It is documented that the physiologic levels of estrogens produced during the luteal phase of the menstrual cycle shift the female immune system toward a Th2-type response and that the Th1 cytokines are increased in postmenopausal women. However, the Th1 immune response is also surprisingly stronger in women, hence affording them a better protection against infections. Nickel sensitivity, a Th1 immune reaction, seems to be more common in women even if men wear earrings. Further, not only the Th2 but also the Th1 autoimmune diseases are generally more common in women than men. How do women advance a stronger Th1 response than men? It is suggested that in contrast to the paradigm that estrogens lead to a Th2 bias, estrogens can enhance Th1 cytokine production also. However, the discrepant effects of estrogens are difficult to be reconciled from a molecular viewpoint and hence are not advocated by all authors. This paper provides an explanation: The effects of dehydroepiandrosterone on
