Iranian Journal of Allergy, Asthma and Immunology
Volume:6 Issue: 2, Jun 2007

The E-selectin mediates the interaction of activated endothelial cells with leukocytes and plays a fundamental role in the pathogenesis of asthma. It has been suggested that an S/R (Serine128Arginine) polymorphism of E-selectin alters ligand binding function. Our purpose in this study was to determine whether this Serine128Arginine polymorphism influences the risk of asthma and also to analyze the possible correlation of disease severity in Iranian patients with polymorphism of E-selection. We studied human E-selectin gene polymorphism in 172 asthmatic patients and 173 healthy volunteers by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). To determine the severity of the asthma’s situation, a questionnaire was prepared requesting the following information: age, sex, clinical signs and symptoms and past medical history. After the participants filled in the questionnaire, all active or ex-smoker patients were excluded. A trained observer assessed airway reversibility, peak flowmetry and spirometry in asthmatic patients. We found increased serum levels of soluble E-selectin (sE-selectin) in asthmatic patients compared with healthy subjects (P<0. 0001). Frequencies of the SS, SR, and RR genotypes were found as 66.3%, 31.4%, and 2.3% in the patients and 91.9%, 8.1%, and 0.0% in control subjects, respectively. The 128Arg allele was more prevalent in patients than controls (OR 5.78; 95% CI, 3.07-10.86, P<0.0001). However, in this study the polymorphism was not associated with circulating sE-selectin levels. We found a direct correlation between the level of sE-selectin and the severity of asthma (P=0.001). On the other hand, there was a close relation between 128Arginine carriage and disease severity (P<0.0001). These results suggest that the Ser128Arg polymorphism of the E-selectin gene is a genetic factor that may be associated with the severity of asthma.

Predominantly antibody deficiencies are a category of primary immunodeficiency diseases, which consist of several rare disorders such as common variable immunodeficiency (CVID) and X-linked agammaglobulinemia (XLA). We evaluated the effects of CVID and XLA patients’ sera as a source of microenviromental factors on maturation and function of monocyte-derived DCs. Blood was collected from 10 CVID and 5 XLA patients before immunoglobulin replacement therapy and also from 8 healthy volunteers in order to obtain necessary sera for this study. Monocyte derived DCs were generated from blood cells obtained from healthy volunteers in the presence of GM-CSF, IL-4 and 10% serum concentrations from cases and controls. Immature DCs were incubated with monocyte conditioned medium (MCM) and TNF-a in order to generate mature DCs. Interleukin 18 (IL-18) production by CD40L-activated mature DCs was measured after 24 hours of culture in vitro.IL-18 production by DCs generated in the presence of CVID and XLA patients’ sera were 6.75±2.59 and 7.08±1.75 ng/ml, respectively, which were significantly higher than normal serum conditioned DCs (3.55±0.68) ng/ml. These results suggest that the sera of patients with predominantly antibody deficiencies may contain soluble factor(s) that can induce a significant increase in IL-18 production by DCs.

Immune and inflammatory responses mediated by cytokines, play important roles in the pathophysiology of asthma. These responses are associated with overexpression of Th2 cytokines such as IL-4 and IL-13. These two cytokines use common receptors for signaling that lead to identical immunological effects and regulation of the Th1/Th2 balance. The aim of this study was to determine whether patients with allergic asthma display overexpression of IL-4 and IL-13 genes.Using RT-PCR, we examined the expression of IL-4 and IL-13 genes in twenty asthmatic cases and twenty normal individuals. Total levels of serum IgE and IL-4 were also determined by ELISA method.Expression of IL-13 gene in 70% of patients with allergic asthma was higher than controls (P=0.01). There was no correlation between the expression of IL-13 gene and total level of serum IgE (P=0.07). Expression of IL-4 gene was detected in 30% of the patients and none of the normal individuals as determined by RT-PCR (P=0.01). Mean of serum IgE levels in patients and controls were 84.9 IU/ml and 62.2 IU/ml, respectively. Level of serum IgE was more than 100 IU/ml in 30% of patients (P=0.03). Mean of serum IL-4 levels in patients and controls were 15.73 pg/ml and 13.07 pg/ml, respectively. There was a relation between levels of serum IgE and IL-4 in 73% of cases.The results showed that there was a correlation between the expression of IL-4 gene and the level of serum IL-4. Levels of serum IgE and IL-4 were considerably higher in asthmatics than non-asthmatic controls.

Iran is one of several countries that has regions of high dose natural ionizing radiation. Two well-known villages in the suburb of Ramsar Town in the Caspian Sea strip, Taleshmahaleh and Chaparsar, have background radiation that is 13 times higher than normal. This radiation is the result of Radium 226 and Radon gas both of which are highly water soluble.While people living in these regions do not suffer from any major health problems, we decided to study the their immune responses to infection and inflammation in order to determine if their habitat affects their immune defense mechanisms as a way of compensating for their exposure to high dose environmental ionizing radiation.Our results showed that the total serum antioxidant level in the exposed people was significantly lower than the individuals not exposed to high dose natural ionizing radiation. The exposed individuals also had higher lymphocyte-induced IL-4 and IL-10 production, and lower IL-2 and IFN-g production. In addition, neutrophil NBT, phagocytosis, and locomotion were higher in the exposed group. In contrast, lymphocyte proliferation in response to PHA was unaffected.We conclude that the immune system of individuals exposed to high dose ionizing radiation has adapted to its environment by shifting from a Type 1 to a Type 2 response to promote anti-inflammation. This may be because inflammatory Type 1 responses generate more free radicals than Type 2 responses, in addition to the free radicals generated as a result of high environmental radiation. Thus, the serum total antioxidant level in the exposed residents was lower than the unexposed group.

This study examined the possible effects of lycopene at physiological dosage and body fat mass on the humoral immune response in patients with type 2 diabetes mellitus (T2DM). A total of 35 patients with Typ2 diabetes mellitus from both sexes aged 54±9 yrs from the Iranian Diabetes Society were introduced into a double blind placebo controlled clinical trial conducted for 2 months. After a 2-week lycopene free diet washout period, patients were allocated to either lycopene supplementation group (10mg/d) (n=16) or placebo age- and sex matched group (n=19) for 8 weeks. Patients were instructed to keep their diets and physical activities as unchanged as possible. Lycopene supplements increased serum lycopene levels (p<0.001). While intake of dietary energy and nutrients did not change in either groups, the ratio of total antioxidant capacity to malondialdehyde increased significantly in the lycopene group (p=0.007). There was an inverse correlation between serum levels of lycopene and those of IgG (r= -0.338, p=0.008). On the contrary, changes of serum levels of lycopene directly correlated with those of IgM (r=0.466, p=0.005). Interestingly, changes of the amount of fat mass correlated directly with those of serum IgG (r=0.415, p=0.044) but inversely with of serum IgM (r= -0.469, p=0.021). While truncal fat might promote adaptive humoral immunity, lycopene probably by inhibiting MDA-LDL formation might attenuate T cell dependent adaptive (pro-atherogenic) humoral immune response. These findings may have preventive implications in long term diabetic complications, notably atherogenesis.

The pathogenetic mechanism of nasal polyps remains unknown, although allergy has been cited as an important factor in the etiology of nasal polyposis. Currently there is no definite histological criterion for differentiation of allergic from inflammatory nasal polyp. However, in a few studies, tissue eosinophil count has been used for this. This study aimed to find out the agreement rate of skin prick test and tissue eosinophil count in patients with nasal polyposis. Twenty five patients (18 males, 7 females) with nasal polyp were enrolled in this study. For each patient tissue sample from polyp material was taken for histopathological investigation. Moreover, skin prick test was performed for each patient using eleven common aeroallergens.Skin prick test was positive in 48% of the patients. Tissue eosinophil count of more than 50% was found in 75% of skin prick positive and in 69.2% of skin prick negative patients. Also tissue eosinophil count of more than 50% was found in 69.2% of patients with typical allergic symptoms as well as 75% of patients without allergic symptoms. No agreement was found between skin prick tests and tissue eosinophil counts in patients with nasal polyp. Also no difference was found between the tissue eosinophil counts in allergic and non allergic patients. Considering these results, it can be concluded that having a high tissue eosinophil count in patients with nasal polyp does not indicate that the polyp is allergic.

Neonatal sepsis is a disease of infants who are less than 1 month of age. These infants are clinically ill, and their blood culture are positive for bacteria. The reported incidence of neonatal sepsis for all infants is 1 to 10 per 1000 live births. The mortality rate is 4.2-26%. The clinical signs are not specific and diagnosis of neonatal sepsis is one of the most difficult tasks in clinical medicine. The aim of this work was determination of CD11b sensitivity and specificity for early detection of neonatal sepsis. We studied 65 neonates with gestational age of 27 to 38 weeks who were suspected for sepsis within the 28 days of life. Whole blood was obtained from neonates to determine CD11b expression on peripheral blood neutrophils by flow cytometry. C-Reactive protein (CRP) was measured qualitatively. Neonates were divided into two groups. Classification was based on the result of the blood culture. In the sepsis group all of the neonates (n = 8) showed positive blood culture and clinical symptoms. In the suspected group (n = 57) the neonates showed clinical signs but blood cultures were negative. Sensitivity and specificity of CD11b were 75%, 100% respectively. Also positive and negative predictive values of CD11b were 100% and 86% respectively.Results of present study and previous studies showed that measurement of neutrophil surface markers can be useful for diagnosis of infection in the early phases. Also, the quantitative measurement of CRP in addition to CD11b further enhances the ability to diagnose infections and improves sensitivity and negative predictive value by 100%.

Progesterone induced dermatitis is a rare disorder. It typically occurs in females due to an autoimmune phenomenon to endogenous progesterone production, but can also be caused by exogenous intake of a synthetic progestin. Here in, we present a case of autoimmune progesterone anaphylaxis (AIPA) observed in an adolescent female. The patient is an 18-year-old Caucasian female with no significant past medical history and no prior exogenous hormone use, who presented to her primary care physician complaining of cyclic skin eruptions with dyspnea, cough and respiratory distress. She noted that her symptoms occurred monthly, just prior to her menses. An intradermal skin test using 0.1 cml of progesterone was performed. The patient developed a 15mm wheal after 15 minutes, confirming the diagnosis of AIPA. The patient was started on a continuous regimen of an oral conjugated estrogen (0.625mg). The skin eruptions and respiratory symptoms have not returned since the initiation of this therapy.Autoimmune progesterone dermatitis manifests via the occurrence of cyclic skin eruptions. Women with the disorder commonly present with dermatologic lesions in the luteal phase of the menstrual cycle, if there are any other organ involvement in addition to skin (e.g. lung, GI) the reaction should be called as autoimmune progesterone anaphylaxis. Diagnosis of AIPA is confirmed by performing a skin allergen test using progesterone.