Thyroid nodules (TNs) are distinct lesions inside the thyroid that can be determined from the adjacent thyroid parenchyma on ultrasonography. Complement activation, autoantibody generation, persistent inflammation, and immune-complex deposition are the hallmarks of systemic lupus erythematosus (SLE), a complicated systemic autoimmune condition that damages tissues and organs. The current study aimed to detect TNs prevalence in SLE patients, and possible malignancy in a sample of Egyptian population. This cross-sectional study included 80 cases diagnosed with systemic lupus erythematosus, attending the Endocrinology and Rheumatology outpatient clinics at Ain-Shams University Hospital, to detect the prevalence of TNs in a sample of Egyptian SLE cases. There was a positive relation between Systemic Lupus Erythematosus Disease Activity Index (SELDAI) score and TNs, also positive relation between SELDAI score and prevalence of malignancy. There was a higher remarkable number, 13 patients (43.3%), of TNs cases among the group with abnormal thyroid functions. In conclusion, the percent of thyroid malignancy among patients with SLE is the same as in general population, so that SLE itself did not increase the risk of thyroid malignancy. Also, the percent of TNs among cases with SLE was the same as in the general population. Activity of SLE in terms of SLEDAI score has relation with TNs and malignancy. Cases with SLE and TNs are more susceptible to thyroid dysfunctions.
Common variable immunodeficiency (CVID) is one of the primary immunodeficiency disorders. The phenotype of peripheral blood memory B cells is a useful tool in the classification of patients into clinically and functionally relevant groups. This study aimed to assess the level of naïve and switched memory B cells level and their correlation with the clinical phenotypes and complications in patients with CVID. This case control study included 30 adult patients with CVID and 30 normal controls, matched for age and sex. Complete blood count, cluster of differentiation 3 (CD3)+, CD4+, CD8+ T cells and CD19+27-IgD+ for naïve B cells and CD19+27+IgD- switched memory B cells levels were assessed. The mean age of the onset of symptoms was 16.9±15.1 years, the mean age of diagnosis was 27.30±14.39 years, with a diagnostic delay of 10.43±10.29 years, and the body mass index was significantly lower in CVID group. Infections including (upper respiratory tract infection, chronic diarrhea, pneumonia and bronchiectasis) were the most frequent phenotypes. CD4+, CD4+/CD8+ T cells, CD19+ and CD19+27+IgD- switch memory B cell, IgG, IgA, and IgM were significantly lower in CVID group than in the control group (p < 0.001 and p < 0.015, respectively). CD8+ T cells and CD19+27-IgD+ naïve B cells were significantly higher in the CVID group (p < 0.001). CD19+27-IgD+ naïve B cells level was significantly lower in cases with bronchiectasis with low baseline serum IgG in lymphadenopathy group (p=0.049), and higher level of CD3+ T cells in cases with splenomegaly. There was no significant difference in laboratory results in CVID patients presented with autoimmune diseases, Granulomas nor enteropathy. In conclusion, high level of CD19+27-IgD+ naïve and low level of CD19+27+IgD- switch memory B cells are characteristic features of CVID. Moreover, the reduced CD19+27-IgD+ naïve B cells level can be a predictor of the development of bronchiectasis in CVID patients.
Type 1 Diabetes Mellitus (T1DM) is a chronic progressive autoimmune disease characterized by destruction of insulin-producing beta cells in the pancreas. The immune system plays a critical role in this illness, particularly regarding micro ribonucleic acid (miRNA) expression and cytokines levels. This study aimed to investigate the role of miRNA-155 and interleukin-2 (IL-2) in diagnosis of T1DM with related to antibodies against glutamic acid decarboxylase 65 (anti-GAD65) and Connecting peptide (C-peptide). This case-control study involved 120 participants, of whom 80 were T1DM patients and 40 apparently healthy subjects as controls. The patients' age ranged from 3 to 17 years of both sexes, collected from the Department of Diabetic in Al-Sader medical city in AL- Najaf Al-Ashraf province during October 2023 till February 2024. Their diagnoses were made based on clinical and serological parameters. Blood samples were collected from all participants to detect IL-2 serum level by an enzyme linked immunosorbent assay and miRNA155 by the reverse transcription polymerase chain reaction (RT-PCR), whereas anti-GAD65 and C-peptide diagnosis by a chemiluminescence immunoassay. The results showed that serum IL-2 was significantly lower in T1DM patients (330.66 ±129.92 ng/ml) compared to the control group (960.67 ±188.05 ng/ml). The expression of miR-155 was significantly higher in the patients' group (2.61 ± 1.17) versus the control group (1.0 ± 0.71) (p < 0.001). The serum level of anti-GAD antibodies among patients with T1DM was significantly higher than in controls (375.01 U/ml vs 5.66 U/ml). While the serum level of C-peptide in the patients was lower than in controls. In conclusion, the elevated expression of miRNA-155, along with significantly reduced blood IL-2 levels in T1DM patients indicates their potential as valid biomarkers for the diagnosis and progress of T1DM.
Neonatal sepsis is an important cause of morbidity and mortality. High mobility group box1 protein (HMGB1) is a cytokine that can mediate inflammation. The aim of this research was to investigate the role of HMGB1 in diagnosis and prognosis of late onset neonatal sepsis. This observational case-control study included 80 newborn infants ≥37 weeks of gestation. Newborn infants were assigned into two groups: the late-onset neonatal septic group included 40 infant cases, and the control group included 40 newborn infants. Clinical sepsis score, hematological sepsis score and serum level of C-reactive protein were assessed and blood culture performed. HMGB1 was measured by an enzyme-linked immunosorbent assay. There was a significant increase of HMGB1 in the late-onset neonatal septic group than the control group (p < 0. 001). The best cut off point of HMGB 1 to discriminate against the late-onset sepsis cases from the control newborn infants was > 68 ng/ml with a sensitivity of 97.5%, specificity of 95%, positive predictive value of 95.1% and negative predictive value of 97.4% with total accuracy of 0.99%. The values of HMGB1 were not affected by gestational age, birth weight, postnatal age or gender. There were no significant differences in mean values between survival and non-survival cases. The best cut off value to predict mortality in the late onset sepsis group was >167.8 ng/ml with a sensitivity of 60% and specificity of 54.29%. In conclusion, this study suggested that HMGB1 is a promising marker for diagnosis of late onset neonatal sepsis in full term infants, on the contrary HMGB1 could not predict mortality in neonatal septic patients.
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that may cause severe complications. This study aimed to investigate the frequency of critical complications in SLE patients requiring intensive care unit (ICU) admission and to identify potential risk factors affecting their outcomes. The study included 50 SLE patients admitted to the Critical Care Unit. All patients underwent a comprehensive medical history, physical examination and laboratory investigations. Disease activity was assessed using the modified new version of the SLE disease activity index (SLEDAI-2K). Both the Acute Physiology and Chronic Health Examination-II (APACHE-II) score and the Sequential Organ Failure Assessment score (SOFA score) were calculated within 24-hour period post-admission. Patients were followed until hospital discharge or demise. The mean age of the studied patients was 33.62 years, with a range of 20 to 47 years. The most leading causes of admission were lupus nephritis (44%) and pneumonia (24%). Of these patients, 12 (24%) patients developed different forms of complications. Of the patients, 80% survived, while 20% experienced a fatal outcome. The predictors of mortality were older age (odds ratio 1.59), complications (odds ratio 2.09), and high APACHE-II scores (odds ratio 3.11). In conclusion, patients with SLE admitted to the critical care unit were liable for complications in the presence the following risk factors; old age, high disease activity and high APACHE-II.
Systemic lupus erythematosus (SLE) is a systemic autoimmune disease. Anti-double stranded DNA (anti-dsDNA) detection is essential for diagnosis and assessment of disease severity and lupus nephritis. Variable laboratory tests for Anti-dsDNA detection have different qualities affecting the results and the disease diagnosis. This study aimed to compare the performance of four different methods of detection of anti-dsDNA among SLE patients in Sohag Governorate. This Case -control study was done in Sohag University Hospital during the period from March 2021 to June 2022 and included 81 cases diagnosed with SLE according to the ACR/EULAR 2019 classification criteria for SLE. We compared serum anti-dsDNA antibody levels by different commercially available kits including Crithidia luciliae indirect immunofluorescence assay (CLIFT), chemiluminescence immunoassay (CLIA), enzyme linked immunosorbent assay (ELISA) and dot immunoassay results. ELISA showed the highest positivity (75.3%), followed by CLIA (61.7%), dot immunoassay (49.4%) and CLIFT (48.1%), respectively. Combining the four methods of detection, 45.7% of the cases showed positive by all of the four detection methods. Most of the other cases were at least positive in two or three tests. Only 17.3% of the cases were negative by all of the four detection methods. None of the subjects in the control group were positive by any test. In conclusion for the detection of anti-dsDNA antibodies, ELISA showed the highest sensitivity. However, the combination of more than one method revealed higher sensitivity.
Polycystic ovarian syndrome (PCOS) is a hormonal, reproductive, metabolic disorder, affect female at reproductive age. PCOS is associated with hormonal and immunological defect, and chronic low-grade inflammation, that affect some proteins expression, like cytotoxic T Lymphocyte Associate protein 4 (CTLA-4), programmed death-1 (PD-1), epiregulin (EREG) in association with T-cell activation. These immunological parameters may indicate autoimmune diseases and PCOS. CTLA-4 and PD-1 are immune checkpoints that regulate the immunity during the chronic inflammation, by suppressing T-cells activation, natural killer cell, B-cell production. Epiregulin, a member of the epidermal growth factor (EGF) family, is released in response to luteinizing hormone(LH) released from granulosa cells in ovaries. There is an indirect link between PCOS and epiregulin in chronic low-grade inflammation. The purpose of this study was to indicate the role of CTLA-4, epiregulin, and PD-1 in women with polycystic ovarian syndrome, also the estimation of some related hormones level in PCOS, like prolactin, testosterone anti-Mullerian hormone (AMH). This study included 65 patients with PCOS and 56 normal controls (healthy women). Their average ages were from 20 to 45 years. The study subjects were from the private women's infertility clinics at the Medical City Hospital, Baghdad. The study lasted from November 2024 to January 2025. Metformin, vitamin D, and oral contraceptives were prescribed by consultant to patients. The blood samples were collected and CTLA-4, PD-1, EREG were measured by enzyme-linked immunosorbent assay (ELISA) technique. The results showed a significant decrease in CTLA-4 in patients (46.04 ±4.51) than in controls (70.46 ±9.41), (p≤0.01). Also, there was no difference in PD-1 level in patients (250.37 ±23.37), and controls (247.81 ±29.80), (p>0.05). EREG showed a significant increase in patients (1099.12 ±138.51), compared to controls (835.02 ±48.62), (p≤0.05). In addition, prolactin hormones recorded a significant increase in patients (154.86 ±27.22) compared to controls (13.91 ±1.50), (p≤0.05). While for the testosterone hormone there was a significant decrease in patients (16.36 ±2.58), as compared to controls (28.73 ±1.75), (p≤0.05). The AMH showed no difference between patients (5.79 ±0.40), and controls (4.18 ±0.44), (p>0.05). In conclusion, based on the current findings, the decrease in CTLA-4, and the increase in EREG in the patient's group was associated with low-grade inflammation like PCOS.
Diabetic nephropathy (DN) is one of the most worrisome complications of diabetes, causing significant social and economic impacts. Genetic polymorphisms in vitamin D receptor (VDR) gene may lead to genomic instability and increase susceptibility to end-stage renal disease (ESRD). In this research, we aimed to identify the association of genetic variants: ApaI "rs7975232" and FokI "rs10735810" in the VDR gene with nephropathy stages in diabetic patients. This case-control hospital-based study included 200 Egyptian participants divided into a group of 150 patients with type 2 diabetes mellitus (T2DM), divided into three subgroups according to albumin/creatinine ratio, and 50 age and sex matched participants as a normal control group. Genetic variants in the VDR gene were detected using restriction fragment length polymerase chain reaction to evaluate their association with kidney disease stage and bone density in T2DM patients. Our results revealed that aa genotype and a allele frequency in ApaI "rs7975232" and ff genotype and f allele frequency in FokI "rs10735810" were more frequent in diabetic patients than in the normal control group (p < 0.001). In addition, our results revealed that T2DM patients with the ApaI aa genotype and a allele were at a higher risk of developing ESRD as they were almost 13-fold higher than those with the (Aa/AA) genotype and A allele. Also, we found that carriers of the ff genotype and f allele of FokI are at 17-fold and 7-fold higher risk of ESRD than carriers of the non-ff genotype. In conclusion, our study findings indicated that the FokI f allele and the ApaI a allele variant of VDR gene could be used as molecular biomarkers to predict the risk of diabetes and nephropathy stages in Egyptian patients.
Chronic spontaneous urticarial (CSU) is defined as the appearance of wheals and /or angioedema for a total duration of six weeks or more. CSU affects approximately 15-25% of the population, influencing the quality of patients' life. This study aimed to evaluate interleukin 13 (IL-13) versus transforming growth factor Beta (TGF-ß) as a prognostic factor in the management of CSU. The study was designed as a cohort study, including 40 patients with CSU recruited from the allergy and immunology outpatient clinic at Ain Shams University Hospitals from 2022 and 2023. Also, the study included 25 normal subjects as a control group, matched with patients for age and sex, were recruited from healthy relatives of patients, hospital workers and nursing staff. Serum IL-13 and TGF-ß were measured by an enzyme linked immunosorbent assay (ELISA) at baseline, six-month follow-up after receiving subcutaneous allergen immunotherapy. The mean serum level of IL-13 at the start was 30.6 pg/ml and 22.1 pg/ml after 6 months , which was significantly higher in the CSU group than in the control group (4.7 pg/ml) (p < 0.001). The mean serum level of TGF-ß at the start was 106.6 ng/ml and 114.9 ng/ml after 6 months , which was significantly higher in the CSU group than in the control group (59.1 ng/ml)(p < 0.001). We concluded that IL-13 had a much better diagnostic performance in differentiating CSU cases from controls. While TGF-ß had significant moderate prognostic performance in predicting partial/complete response from non-response after receiving immunotherapy.
The aetiology and pathophysiology of systemic lupus erythematosus (SLE), are yet unclear. Autoantibodies that target various organs and tissues are produced as a result of SLE patients' poor immunological tolerance. Sirtuin-1 (SIRT1) is a histone deacetylase that has a major role in immune responses, apoptosis, and cell differentiation, through alteration of various signalling cascades, including nuclear factor κ-light chain enhancer and activator protein 1 of activated B cells cascades. According to recent data, SIRT1 is an immune system regulator factor, and its impaired action probably play a role in SLE pathogenesis. This study intended to determine whether SIRT1 can be an indicator for SLE severity and activity. This study comprised 30 SLE patients, with a mean age of 28.23 ± 5.21 years and 3.21 ± 1.2 years as duration of the disease. The normal control group consisted of 30 matched adults, aged 27.3±6.22 years (p=0.266). There was a significantly increase in the mean±SD of SIRT1 in SLE patients (28.72±5.83), compared to the control group (22.1±5.59) (p<0.05). Serum SIRT1 was significantly correlated to disease duration, SLEDAI, Katz score, ESR, CRP and renal biopsy classes. However, it was negatively correlated to C3, C4 and there was no correlation with age. A significant elevation was noted in the mean±SD of SIRT1 in active SLE patients (22.7 ± 13.77) compared to inactive SLE patients (6.02±11.27) (p <0.05). Also, the mean±SD of SIRT1 was significantly raised in patients with high SLE disease severity (17.94 ± 15.64) in contrast to those with low SLE disease severity (10.78±13.76) (p<0.05). In conclusion, SIRT1 serum levels were higher in patients with SLE, both with high and low disease severity. Thus, SIRT1 may be a serological indicator for the severity and activity of SLE.
Systemic lupus erythematosus (SLE) is an autoimmune disease of complicated and multifactorial pathogenesis. Interleukin 33 (IL-33) may play a role in the development of SLE through upregulation of toll like receptor 4 (TLR-4). The objective of this study was to investigate the association of IL- 33 serum levels and relative expression of TLR 4 with SLE development and clinical outcome. This case-control study included 80 SLE patients and 80 normal controls. Ribonucleic acid (RNA) was extracted from peripheral blood mononuclear cells. The serum level of IL 33 was measured by the enzyme linked immunosorbent assay (ELISA) and relative expression of TLR-4 determined by real time polymerase chain reaction. Clinical findings and SLE activity were evaluated for all patients. IL-33 serum levels and relative expression of TLR-4 were significantly higher in SLE patients when compared with controls (p < 0.001). There were statistically significant differences in the mean IL-33 serum levels and mRNA expression of TLR 4 among disease activity groups. They were proportionally increased with SLE activity where the highest concentrations existed in the highest disease activity patients (p < 0.001). A positive correlation was found between IL-33 serum levels and mRNA expression of TLR-4 in SLE patients (r=0.86 and p≤0.001). In conclusion, elevated IL-33 serum levels inducing increased expression of TLR-4 could be constituted as an important factor in the pathogenesis and activity of SLE.
Chronic spontaneous urticaria (CSU) is a significant clinical condition characterized by an undetermined etiology, with some of its manifestations being attributed to immunological factors. The antibacterial properties of the cathelicidin leucine-leucine-37 (LL-37) can potentially contribute to the development of autoimmune disorders. Evaluating serum level of cathelicidin in CSU, particularly in its autoimmune aspect, will provide novel insights into pathogenesis. This study assessed serum cathelicidin levels in CSU patients and determined the association between serum cathelicidin and urticaria activity score (UAS). This case-control study involved 40 CSU patients and 40 sex and age-matched controls. Total IgE, serum cathelicidin levels, and antithyroid antibodies were measured. An autologous serum skin test was done, and the UAS was assessed. The levels of LL-37 exhibited a statistically significant difference between the investigated groups, with downregulated levels observed in the case group. A statistically significant negative association exists between the urticaria severity index and serum cathelicidin. Additionally, we detected a statistically insignificant correlation between serum cathelicidin and age, disease duration, hemoglobin, white blood cells, eosinophils, total IgE, antithyroglobulin antibody, and antithyroid peroxidase antibody. A significant association was also detected between urticaria severity and serum cathelicidin. In conclusion, LL-37 level contributes to many autoimmune diseases, and recent studies have pointed to its role in allergic diseases. CSU is a critical skin disease and needs more research to identify the triggers to open the gate for new treatment.
This review article aims to discuss neuroimmune interactions by emphasizing the role of central and peripheral immunities in central nervous system (CNS) protection and function, as well as how abnormalities in this relationship may be implicated in the genesis of neurodegenerative diseases (NDDs). Immune elements that play roles within the CNS both during stable and infectious states are described. Innate CNS immunity is explored as a distinct entity comprised of the brain blood barrier, CNS parenchyma, and resident immune cells-microglia and astrocytes, whose roles in antigen recognition and clearance and neuromodulation are further enumerated. Due to the inability of the CNS to independently initiate an adaptive immune response, the necessary recruitment and regulation of elements from the peripheral immune system (PIS) are described in a process that, in chief, utilizes resident antigen-presenting cells to prime naïve T-cells, which later enter the CNS through areas of access to the cerebrospinal fluid. The previous modes of interaction especially enable microglia, astrocytes, and T-cells to play part in neurodevelopment and plasticity, and the proposed mechanisms by which they participate in synaptic pruning, neurogenesis, and memory are examined. In addition to its protective role, the PIS has also been shown to play a regulatory role in the CNS, where it drives responses that optimize immune function, such as fever and sickness behavior. Due to the high level of involvement of the immune system within the CNS, dysregulations of the immune system are thought to be implicated in numerous NDD pathogeneses, where neuroinflammation both causes and is caused by immune reactions. Alzheimer's disease, Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis are particularly discussed.
Penicillin, the most well-known β-lactam antibiotic, is thought to cause allergic responses in 0.7-10% of the human population. Atopic and other allergy illnesses are believed to be developed and regulated in part by excessive secretion of Interleukin-4 (IL-4) and interferon-γ (IFN-γ). In this study, the frequency of penicillin allergy was analyzed by IL-4 and IFN-γ using the enzyme linked immunosorbent assay in 45 patients with an allergy to penicillin and 45 apparently healthy subjects as a control group. Also, we determined the IL-4 receptor α gene (IL-4 Rα) by using tetra primer-amplification refractory mutation system based polymerase chain reaction (T-ARMS-PCR). The findings demonstrated that IFN-γ and IL-4 levels in serum of the patients in the experimental group were significantly higher than in the control group. Although IFN-γ levels were lower than IL-4 in the patients and controls, patients exhibited higher IFN-γ concentrations compared to control subjects. The IL-4 receptor α (Rα) genotype distribution in patients and control groups revealed that genotypes AA, GA, and GG were present in 26 (57.78%), 11 (24.44%), and 8 (17.78%) patient subjects, while in the control group they were present in 17 (37.78%), 21 (46.67%), and 7 (15.56%) subjects. As a result, it seemed that patients had a higher frequency of genotype AA than the control group. In conclusion, penicillin allergy is influenced by IL-4 and IFN-γ, and IL-4 Rα gene polymorphism revealed that AA and GA genotypes may be linked to β-lactam allergy, whereas GG genotypes may offer a strong defense against β-lactam allergy.
The assessment of systemic lupus erythematosus (SLE) disease activity is considered a challenge to patients and physicians. In the last few years, there was evidence that progranulin (PGRN) may be involved in the pathogenesis of SLE, so, it might be a suitable marker for the assessment of disease activity. In this study, we aimed to identify the role of PGRN in SLE pathogenesis and its association with disease activity and organ damage. This case-control study included 50 SLE patients, 20 patients with autoimmune diseases other than SLE, and 20 apparently healthy adults as a control group. The concentration of serum PGRN was assayed in all studied participants by using quantitative enzyme-linked immunosorbent assay. The results showed that serum PGRN levels were significantly higher among SLE patients when compared to the group of patients with autoimmune diseases other than SLE, as well as when compared to the control group. There was a significant positive correlation of serum PGRN levels of SLE patients with erythrocyte sedimentation rate, 24 hours urine protein, SLE disease activity index (SLEDAI)-2k score, and SLICC/ACR damage index (SDI) score; while there was a negative correlation with C3, C4 and hemoglobin concentrations. Thus, we concluded that serum PGRN could be a useful biomarker of SLE disease activity.
The early and efficient diagnosis of sepsis in critically ill children remains a difficult task as the clinical signs are nonspecific. Complete blood count parameters and C‑reactive protein have low sensitivity., Also, the difficulty of its diagnosis may be due to decreased positive values of blood culture and the need for longtime to detect blood culture results. The serum Amyloid A (SAA) protein level in the blood increases earlier and up to 1000‑fold in response to inflammation. This study aimed to assess the role of SAA as diagnostic and prognostic marker in pediatric sepsis in the first 24 hours after pediatric intensive care unit (PICU) admission. This case-control study included 45 children with sepsis admitted at PICU from May 2023 to March 2024 and 45 children with matched age and sex as controls. We investigated SAA level in the same time with routine laboratory investigations of both groups. SAA level was higher in the patient group, ranged from 0.9 to 47.2 µg/m, with median 4.54 µg/ml, as compared to the control group with median 0.58 µg/ml ranged from 0 to 2.3 µg/ml. (p ≤0.001). Also, SAA level was significantly lower in the survived group with median 13.6 µg/ml, ranged from 5.7 to 20 µg/ml than the non-survived group with a median of 32.3 µg/ml; ranged from 30.3 to 47.2 µg/ml. In conclusion, we found that SAA was extremely high in critical and extremely critical ill patients which can be used as a predictor of mortality in severe sepsis among children.
Rheumatoid arthritis (RA) is a chronic autoimmune disease of multifactorial etiology which is linked to interactions between host and environmental factors. Previous studies showed that nasal carriage of the enterotoxigenic Staphylococcus aureus and increased expression of micro RNA-146a (miRNA-146a) may have a role in RA pathogenesis and severity. The objectives of this study were to evaluate the prevalence of nasal colonization by the enterotoxigenic S. aureus in RA patients and to correlate serum levels of staphylococcal enterotoxin and miRNA-146a relative expression in all the study participants with disease severity in RA patients. In this case-control study, after S. aureus isolation from nasal swabs of all participants, the prevalence of nasal colonization by enterotoxigenic S. aureus was assessed by the enzyme-linked immunosorbent assay (ELISA). Also, serum staphylococcal enterotoxin level was measured by ELISA. The quantitative reverse transcription polymerase chain reaction was used to assess serum miRNA-146a relative expression level. Assessment of RA disease activity was achieved according to the Disease Activity Score in 28 joints (DAS 28). Enterotoxigenic nasal S. aureus carriage rate was significantly higher in RA patients than control subjects (p < 0.001). RA patients showed a significantly higher mean value of serum levels of staphylococcal enterotoxin and miRNA-146a relative expression when compared to controls (p < 0.001 for both) and the highest mean value of both were found in RA patients with high disease activity (p < 0.001). There was a significant positive correlation between the relative expression level of miRNA-146a and serum level of staphylococcal enterotoxin in RA patients. In conclusion, staphylococcal enterotoxins and miRNA-146a could have a significant role in RA pathogenesis and both correlate with disease activity.
Hypertension belongs to the category of serious health concerns among overweight people that are frequently attributed to chronic low-grade inflammation. The present study investigated the significance of the selected pro-inflammatory cytokines interleukin-17 (IL-17), interleukin-40 (IL-40), and tumor necrosis factor-alpha (TNF- α) as the markers of inflammation in non-smoking overweight men with hypertension. This case control study included 70 adult men (40 hypertensive and 30 age matched controls). Anthropometric parameters, arterial blood pressure, lipid profile, liver enzymes, renal function markers, aldosterone, cortisone, and serum cytokines were investigated. The concentrations of cytokines were determined through the enzyme-linked immunosorbent assay procedures. Body weight, body mass index, systolic and diastolic blood pressure, among hypertensive participants, were significantly higher in the cases than the controls (p≤0.01). Hypertensive subjects had significantly high serum concentrations of TNF-α, IL-17 and IL-40, which are indicators of a strong pro-inflammatory condition. Also, hypertensive patients were characterized by dyslipidemia and raised liver enzyme activity, raised aldosterone and cortisone levels, and slight but significant rises in serum creatinine. The results indicated that hypertension among overweight non-smoking men is interrelated with immune response, metabolic dysregulation as well as endocrine dysregulation. It is interesting to note that IL-40 was also a candidate novel inflammatory biomarker in addition to the previously known cytokines, TNF- α and IL- 17. The study findings revealed that the inflammatory and immune-endocrine pathways could be a new chance in the early management and detection of obesity-related hypertension.
Gestational diabetes mellitus (GDM) is a metabolic disorder that poses significant risks during pregnancy. The TCF7L2 gene, previously linked to type 2 diabetes, has also been associated with GDM. This study investigated the frequency of TCF7L2 single nucleotide polymorphism (SNP) alleles and their correlation with metabolic parameters in women with GDM. The study, evaluated the TCF7L2 intron polymorphisms rs7903146 and rs11196205 in 45 GDM patients and 45 control pregnant females. GDM patients, with mean age of 30.5 ± 4.6 years, had lower sex hormone-binding globulin and serum magnesium levels than controls. The study found significant associations between GDM and both SNPs. For rs7903146, the TT genotype increased GDM risk by 19.6-fold, while the CT+TT genotypes increased the risk by 8.2-fold under the dominant genetic model. The T allele raised GDM risk by a factor of 9.3. For rs11196205, the GC and CC genotypes increased GDM risk by 12.6-fold and 10.7-fold, respectively. Under the dominant genetic model, the G/C or C/C genotypes increased GDM risk by 11.7-fold, and the C allele raised GDM risk by a factor of 8.9. In conclusion, compared to the control group, the GDM of the study individuals was substantially related to the (rs7903146) (T>C) and (rs11196205) C>G SNPs.
Celiac disease (CD) is one of the most common autoimmune disorders. It is triggered by exposure to dietary gluten proteins resulting in small intestine mucosal injury. Previous studies showed that CD is highly associated with human leukocyte antigens (HLA) class II DQ heterodimers, mainly HLA-DQ2.5 and HLA-DQ8. The aim of the work was to evaluate the distribution of the CD associated risk HLA-DQ haplotypes in CD patients, CD patients with Type 1 diabetes mellitus (T1DM) comorbidity, in at-risk and healthy individuals in an Egyptian cohort. The study included 124 individuals, divided into 4 groups. They were 28 CD patients, 21 CD and T1DM patients diagnosed with T1DM comorbidity, 50 at-risk group including relatives of CD patients and T1DM patients and finally 25 normal individuals as controls. The multiplex ligation-dependent probe amplification (MLPA) assay was performed using peripheral blood DNA. HLA-DQ2.5 was the most frequent haplotype among CD patients (69.3%) and among the combined groups in the cohort population (58.1%), either homozygous or heterozygous (together with HLA-DQ8 or -DQ2.2).HLA-DQ8 was the second most frequent haplotype followed by HLA-DQ2.2 and HLA-DQ7.5. In the control group, two individuals carried HLA-DQ2.3 and one carried a single DQB1*02:01 allele. In the at-risk group, 7 individuals were negative for all the haplotypes investigated. In conclusion, CD is a multifactorial disease where HLA-DQ haplotypes are a major genetic predisposing factor for both development and progress of the CD disease.