Serum Levels Of IL-17A Research Articles

PAH-induced metabolic changes related to inflammation in childhood asthma.

Epidemiological studies have shown that PAHs may exert adverse effects on childhood asthma. However, the underlying molecular mechanism remains to be fully elucidated. This study aimed to investigate this process in view of metabolic pathways, especially one-carbon metabolism and tryptophan metabolism. Fifty asthmatic children and 50 control subjects were recruited for this study. Serum IgE and IL-17A levels were detected by ELISA. Serum PAH concentrations were measured by GC-MS. One-carbon-related metabolites and tryptophan metabolites were determined by UPLC-Orbitrap-MS. DNA methylation was analyzed by bisulfite sequencing PCR. ChIP assays were used to examine H3K4me3 enrichment on IL-17A gene. Multivariable linear regression was performed to evaluate the association between PAHs and childhood asthma mediated by intermediators. HE staining in lung tissue, IgE and IL-17A in BALF, metabolic profiles in urine, and Ahr, Il-17a, and Cyp1a1 gene expression were determined in PAH-exposed mice. Serum Fla level was associated with childhood asthma (OR = 1.380, 95% CI: 1.063-1.792), and had a great effect on one-carbon metabolites, especially SAH, SAM, and Ser, which exerted significant mediation effects on the relationship between the Fla concentration and asthma. Moreover, we did find significant mediation effects between serum Fla and asthma by LINE-1 DNA methylation and H3K4me3 levels in the IL-17A promoter region. The differential Trp metabolites, such as Trp, tryptamine, IA, IAA, indole, IAld, and IAAld, indicated that asthmatic children had increased indole-AhR pathway. Mediation analysis failed to show a mediator effect of Trp metabolites in the association between PAHs and childhood asthma. An animal study confirmed that PAH exposure increased methylation levels, and altered Trp metabolite-AhR-IL-17A axis, which may be influenced by gender. PAHs disturbed one-carbon metabolism to influence the methyl group refilling DNA methylation and histone methylation, and disturbed tryptophan metabolism to regulate Th17-cell differentiation, which may elevate serum IL-17A concentration in asthmatic children.

Interleukin-17A in Egyptian leprosy patients: a clinical, genetic, and biochemical study

BackgroundLeprosy represents a long-term communicable disease resulting from Mycobacterium leprae infection. IL-17A is one of the pro-inflammatory cytokines that protects humans against many fungal and bacterial pathogens. ObjectiveTo investigate IL-17A (rs2275913) gene polymorphism and its circulating level in leprosy patients, and to correlate the detected results with different clinical aspects of leprosy in the investigated patients. Methods60 patients with leprosy, and 29 age and sex-matched volunteers were investigated for IL-17A serum level and IL-17A single nucleotide polymorphism (SNP) by ELISA and RFLP-PCR respectively. ResultsIL-17A serum level was significantly higher in leprosy patients than in controls (p=0.034), and in TL than LL (p=0.017). IL-17A (rs2275913 A/G) G allele and GG genotype were associated significantly with LL (p=0.005and 0.001 respectively). IL-17A (rs2275913 A/G) AG genotype carriers demonstrated the highest IL-17A serum levels; however, its lowest levels were found in IL-17A (rs2275913 A/G) AA genotype carriers (p=0.005). Grade 2 disability (p=0.030) and positive slit skin smear (SSS) (p=0.005) were significantly associated with IL-17A (rs2275913 A/G) GG genotype. Study limitationsThe small number of studied subjects. ConclusionsIL -17A may have a pivotal role in leprosy pathogenesis. IL-17A (rs2275913) GG genotype plus G allele might be related to the development of LL in the Egyptian population.

Investigation of serum IL-12, IL-16, and IL-17A as diagnostic biomarkers in children with cow's milk protein allergy.

Cow's milk protein allergy (CMPA) is an abnormal immune response caused by milk proteins and is most common in infancy and early childhood. Statistics revealed up to 7.5% of children suffered from milk allergy. Its clinical symptoms were characterized by diversity, non-specificity, and can affect multiple systems, including the digestive tract, skin, and respiratory tract. In this study, we aimed to investigate the effects of IL-12, IL-16, and IL-17A on diagnosing and monitoring CMPA in children for clinical treatment. A total of 158 infants with CMPA and 89 healthy babies were recruited and evaluated. Demographic and clinical information of all participants were recorded. An extensive analysis of inflammatory cytokine levels, including IL-12, IL-16, and IL-17A, was performed in blood samples from 247 infants younger than 9 months. Meanwhile, the serological specificity immunoglobulin E (sIgE) levels were evaluated. In addition, the area under the curve (AUC) values of IL-12, IL-16, and IL-17A in differentiating CMP from healthy babies were measured by receiver operating characteristic analysis. Finally, the correlation between sIgE and IL-12, IL-16, and IL-17A levels were detected using Spearman correlation analysis. Compared with healthy control, infants who developed CMPA had decreased IL-12, increased IL-16, and IL-17A. Moreover, a significant correlation between serum IL-12, IL-16, IL-17A and sIgE levels was observed in the CMPA group. In addition, AUC values of IL-12, IL-16, and IL-17A in discriminating CMPA from healthy infants were 0.8425, 0.9196, and 0.8813, respectively. Finally, IL-12 was increased while IL-16 and IL-17A levels were decreased in the CMPA group after three months of milk avoidance treatment. We found that IL-12, IL-16, and IL-17A levels in children with CMPA were associated with SCORAD scores, sIgE levels, and disease severity, functioning as valuable disease-monitor markers in CMPA.

Brain microglia activation and peripheral adaptive immunity in Parkinson’s disease: a multimodal PET study

BackgroundAbnormal activation of immune system is an important pathogenesis of Parkinson’s disease, but the relationship between peripheral inflammation, central microglia activation and dopaminergic degeneration remains unclear.ObjectivesTo evaluate the brain regional microglia activation and its relationship with clinical severity, dopaminergic presynaptic function, and peripheral inflammatory biomarkers related to adaptive immunity.MethodsIn this case–control study, we recruited 23 healthy participants and 24 participants with early-stage Parkinson’s disease. 18F-PBR06 PET/MR for microglia activation, 18F-FP-DTBZ for dopaminergic denervation, total account of T cells and subpopulations of T helper (Th1/Th2/Th17) cells, and the levels of serum inflammatory cytokines were assessed. Sanger sequencing was used to exclude the mix-affinity binders of 18F-PBR06-PET.ResultsCompared to healthy controls, patients with Parkinson’s disease had an increased 18F-PBR06-PET standardized uptake value ratio (SUVR) in the putamen, particularly in the ipsilateral side of the motor onset. 18F-PBR06-PET SUVR was positively associated with 18F-FP-DTBZ-PET SUVR in the brainstem and not associated with disease severity measured by Hoehn and Yahr stage, MDS-UPDRS III scores. Patients with Parkinson’s disease had elevated frequencies of Th1 cells and serum levels of IL10 and IL17A as compared to healthy controls. No significant association between peripheral inflammation markers and microglia activation in the brain of PD was observed.ConclusionParkinson’s disease is associated with early putaminal microglial activation and peripheral phenotypic Th1 bias. Peripheral adaptive immunity might be involved in microglia activation in the process of neurodegeneration in PD indirectly, which may be a potential biomarker for the early detection and the target for immunomodulating therapy.

Fecal microbiota transplantation versus glucocorticoids for the induction of remission in mild to moderate ulcerative colitis

ObjectiveTo compare efficacy and safety of fecal microbiota transplantation (FMT) with glucocorticoid as induction therapy in ulcerative colitis (UC).MethodsThe patients with active mild to moderate UC were recruited into the single-center, prospective cohort study. The patients were treated with either FMT (FMT group) or glucocorticoids (GCs group). Patients received FMT administration for 3 days. The primary outcome was clinical and endoscopic remission at week 12. Inflammatory parameters were assessed by routine blood tests. Safety was assessed by adverse events recorded. The serum levels of TNF-α, IFN-γ, IL-1β, IL-4, IL-5, IL-6, IL-10 IL-8, IL-12p70, IL-13, IL-17A and IL-23 following FMT were measured by Luminex multiplex assay.ResultsOf the 122 patients, 62 patients were treated with FMT and 60 with glucocorticoids. 34 patients in FMT group (54.8%) and 29 in GCs group (48.3%) reached the primary outcome (p = 0.30). The incidence of adverse events in GCs group (35/60, 58.3%) was significantly higher than that in FMT group (14/62, 22.6%) and two serious adverse events were observed following GCs. Patients in FMT group were stratified into responders (RE) and non-responders (NR) groups. The level of TNF-α and IL-6 decreased significantly in RE group, while IL-10 decreased significantly in NR group.ConclusionFMT therapy was as effective as glucocorticoids to induce remission in active mild to moderate UC, accompanied by fewer adverse events. The modification of serum TNF-α, IL-6 and IL-10 might be related to the efficacy of FMT in UC.Trial registration This study was registered with ClinicalTrials.gov (NCT02435160). Registered on 6 April, 2015. https://clinicaltrials.gov/ct2/results?cond=&term=NCT02435160&cntry=&state=&city=&dist=

Concerted regulation of OPG/RANKL/ NF‑κB/MMP-13 trajectories contribute to ameliorative capability of prodigiosin and/or low dose γ-radiation against adjuvant- induced arthritis in rats

BackgroundProdigiosin (PDG) is a microbial red dye with antioxidant and anti-inflammatory properties, although its effect on rheumatoid arthritis (RA) remains uncertain. Also, multiple doses of low dose γ- radiation (LDR) have been observed to be as a successful intervention for RA. Thus, the purpose of this study was to investigate the ameliorative potential of PDG and/or LDR on adjuvant-induced arthritis (AIA) in rats. MethodsThe anti-inflammatory and anti-arthritic effects of PDG and/or LDR were examined in vitro and in vivo, respectively. In the AIA model, the arthritic indexes, paw swelling degrees, body weight gain, and histopathological assessment in AIA rats were assayed. The impact of PDG (200 µg/kg; p.o) and/or LDR (0.5 Gy) on the levels of pro- and anti-inflammatory cytokines (IL-1β, TNF-α, IL-6, IL-18, IL-17A, and IL-10) as well as the regulation of osteoprotegrin (OPG)/ receptor activator of nuclear factor κB ligand (RANKL)/ nuclear factor-κB (NF-κB)/MMP-13 pathways was determined. Methotrexate (MTX; 0.05 mg/kg; twice/week, i.p) was administered concurrently as a standard anti-arthritic drug. ResultsPDG and/or LDR markedly diminished the arthritic indexes, paw edema, weigh loss in AIA rats, alleviated the pathological alterations in joints, reduced the levels of pro-inflammatory cytokines IL-1β, TNF-α, IL-6, IL-18, IL-17A, and RANKL in serum and synovial tissues, while increasing anti-inflammatory cytokines IL-10 and OPG levels. Moreover, PDG and/or LDR down-regulated the expression of RANKL, NF-κBp65, MMP13, caspase-3, and decreased the RANKL/OPG ratio, whereas OPG and collagen II were enhanced in synovial tissues. ConclusionPDG and/or LDR exhibited obvious anti-RA activity on AIA.

Critical roles of RGS16 in the mucosal inflammation of ulcerative colitis.

BackgroundUlcerative colitis is a chronic and progressive inflammatory disorder. The regulator of the G-protein signaling (RGS) is involved in the pathogenesis of several immune system disorders. RGS16, a member of the RGS protein superfamily, has been shown to play critical roles in several immune system-related diseases. However, the roles of RGS16 in ulcerative colitis remain to be elucidated.MethodsWe analyzed the expression of RGS16 in peripheral blood mononuclear cells (PBMCs) and inflamed mucosa of ulcerative colitis patients using quantitative reverse transcription-PCR, western blotting and immunohistochemistry. We performed Spearman’s correlation to analyze the correlation between RGS16 expression and the ulcerative colitis endoscopic index of severity (UCEIS), Mayo index, erythrocyte sedimentation rate (ESR) and serum tumor necrosis factor alpha (TNF-a) and IL-17A levels. Further, PBMCs were stimulated with inflammatory cytokines in vitro.ResultsRGS16 expression significantly increased in the colonic mucosa and PBMCs from patients with ulcerative colitis and significantly correlated with the Mayo index, UCEIS, ESR and serum TNF-α and IL-17A levels. TNF-α upregulated RGS16 expression in PBMCs in a dose- and time-dependent manner via the nuclear factor kappa beta (NF-kB) signaling pathway. Moreover, anti-TNF treatment with infliximab significantly decreased RGS16 expression in PBMCs and intestinal mucosa of patients with ulcerative colitis.ConclusionOur study revealed a novel mechanism by which RGS16 expression in ulcerative colitis is positively correlated with disease activity. Thus, RGS16 might serve as a potential therapeutic marker for the treatment of ulcerative colitis.

Lymphocyte Population Changes at Two Time Points during the Acute Period of COVID-19 Infection

We previously observed an increase of serum interleukins (IL) and a reduction of most lymphocyte subpopulations in hospitalized COVID-19 patients. Herein, we aimed to evaluate the changes in serum IL-6, IL-10, and IL-17A levels and cytometric lymphocyte profiles in 144 COVID-19 patients at admission and after one week, also in relation to steroid treatment before hospitalization. After one week of hospitalization, we found that: (i) total lymphocytes were increased in all patients; (ii) neutrophils and IL-6 were reduced in mild/moderate patients; (iii) B lymphocytes were increased in severe patients; (iv) T lymphocyte populations increased in mild/moderate patients. In the eight patients that died during hospitalization, total leukocytes increased while T, T helper, T cytotoxic, T regulatory, and NK lymphocytes showed a reducing trend in five of the eight patients. Even if seven days are too few to evaluate the adaptive immunity of patients, we found that the steroid therapy was associated with a reduced COVID-19 inflammation and cytokine activation only in patients with severe disease, while in patients with less severe disease, the steroid therapy seems to have immunosuppressive effects on lymphocyte populations, and this could hamper the antiviral response. A better knowledge of cytokine and lymphocyte alterations in each COVID-19 patient could be useful to plan better treatment with steroids or cytokine targeting.

Evaluation of interleukin -17a levels in Iraqi patients with type 2 diabetes mellitus

Type 2 Diabetes mellitus (T2DM) is one of the major non-communicable diseases worldwide. Interleukin-17 (IL-17, also known as IL-17A) is a key cytokine that links T cell activation to neutrophil mobilization and activation. In the cytokine storm, up-regulation of T-helper 17 cell cytokine IL-17A, and maybe also IL-17F, is primarily responsible for the immunopathology. This study aims to assess the Interleukin-17 A levels among the susceptibility of T2DM Iraqi diabetic patients as well as to determine the Interleukin-17 A levels among those patients and controls. A total of 70 participants 50 confirmed type 2diabetic patients and 20 apparently healthy individuals as controls were selected using a convenient sampling method. Evaluation of serum levels of IL-17A were performed using by enzyme-linked immunosorbent assay technique (ELISA) using a Human- IL-17A kit. (Elabscience Company /china). The results of the current study indicated that the levels of this interleukin were higher in the sera of patients with type 2 diabetes compared to healthy controls, although there were no significant differences, in patients (243.7233±38.45944), vs. controls (148.8930±11.79280), P= 0.135. We conclude that there may be a correlation between high levels of IL-17A and T2DM.

854 Bermekimab, anti-IL-1α antibody, inhibits skin injury induced response in healthy subjects

Interleukin-1 alpha (IL-1α) is constitutively expressed in epithelial cells located at barrier sites, such as skin, lung and gut. Upon cellular death, injury or infection, IL-1α is released. Serum levels of IL-1α are largely undetectable in healthy volunteers (HV), or atopic dermatitis (AD) and hidradenitis suppurativa (HS) patients, while levels in the skin, especially in the epidermis and exudates from HS tunnels, are highly concentrated. Bermekimab (BMK) is a first-in-class fully human anti-IL-1α monoclonal antibody that has been tested in Ph2A AD & HS studies.

Characterization of a small molecule modulator of inflammatory cytokine production

In the present study, the effect(s) of the immunomodulatory drug GLS-1027 on various cell types involved in inflammation were investigated. GLS-1027 reduced LPS-stimulated secretion of pro-inflammatory cytokines by macrophage or monocytic cells and cell lines. This reduction was likely due in part to decreased activation of NF-κB family transcription factors and inhibition of p38 MAPK signaling in GLS-1027-treated cells. Independent from its effects on macrophages, GLS-1027 inhibited dendritic cell maturation and differentiation of naïve CD4+ T cells into Th17 cells, reducing the production of typical pro-inflammatory cytokines associated with both processes. In vivo administration of GLS-1027 prevented the development of type 1 diabetes in NOD mice which correlated with reduced serum levels of IL17A in GLS-1027 treated animals and reduced ex vivo production of IL17A from both spleen and lymph-node cells. Overall, our data show that GLS-1027 can reduce inflammation through multiple actions, including the reduction of pro-inflammatory cytokine production by innate immune cells, the inhibition of dendritic cells maturation, and the inhibition of Th17 cells polarization.

Gastric Th17 Cells Specific for H+/K+-ATPase and Serum IL-17 Signature in Gastric Autoimmunity.

Human gastric autoimmunity [autoimmune gastritis (AIG)] is characterized by inflammation of the gastric mucosa and parietal cell loss. The gastric parietal cell proton pump H+/K+-adenosine triphosphatase (H+/K+-ATPase) is the major autoantigen in AIG. Our work aimed to investigate the gastric H+/K+-ATPase-specific T helper 17 (Th17) responses in AIG and serum interleukin (IL)-17 cytokine subfamily in AIG patients, in healthy subjects [healthy controls (HCs)], and in patients with iron deficiency anemia (IDA) without AIG. We analyzed the activation of gastric lamina propria mononuclear cells (LPMCs) by H+/K+-ATPase and the IL-17A and IL-17F cytokine production in eight patients with AIG and four HCs. Furthermore, we compared serum levels of IL-17A, IL-17F, IL-21, IL-17E, IL-22, and IL-23 in 43 AIG patients, in 47 HCs, and in 20 IDA patients without AIG. Gastric LPMCs from all AIG patients, but not those from HCs, were activated by H+/K+-ATPase and were able to proliferate and produce high levels of IL-17A and IL-17F. AIG patients have significantly higher serum IL-17A, IL-17F, IL-21, and IL-17E (393.3 ± 410.02 pg/ml, 394.0 ± 378.03 pg/ml, 300.46 ± 303.45 pg/ml, 34.92 ± 32.56 pg/ml, respectively) than those in HCs (222.99 ± 361.24 pg/ml, 217.49 ± 312.1 pg/ml, 147.43 ± 259.17 pg/ml, 8.69 ± 8.98 pg/ml, respectively) and those in IDA patients without AIG (58.06 ± 107.49 pg/ml, 74.26 ± 178.50 pg/ml, 96.86 ± 177.46 pg/ml, 10.64 ± 17.70 pg/ml, respectively). Altogether, our results indicate that IL-17A and IL-17F are produced in vivo in the stomach of AIG patients following activation with H+/K+-ATPase and that serum IL-17A, IL-17F, IL-21, and IL-17E levels are significantly elevated in AIG patients but not in patients without AIG. These data suggest a Th17 signature in AIG and that IL-17A, IL-17F, IL-21, and IL-17E may represent a relevant tool for AIG management.

Role of IL-17A in enhancing liver fibrosis induced by TGF-β1 and IL-13 in Schistosoma mansoni infected mice

Background: Schistosoma mansoni liver fibrosis is a complicated multicellular process involving numerous cytokines, chemokines, and growth factors. TGF-b1 and IL-13 have been identified as critical pro-fibrotic mediators in many studies. IL-17A was linked to enhanced TGF-b1 and IL-13-induced pathologies. Objective: This case-control study aimed to explore the effect of IL-17A on TGF-b1 and IL-13-induced liver fibrosis during experimentally schistosomiasis mansoni infection. Material and Methods: A total of forty laboratory-bred female C57BL/6 mice were divided into four equal groups, G1 non-infected, G2 infected wild type (WT), G3 infected/anti-IL-17 mAb and G4 treated mice. Mice were infected percutaneously with 40±5 cercariae per mouse. Neutralizing IL-17 mAb was administered to G3 intraperitoneally 3 weeks after infection and then every third day until 2 days before sacrification; mice of G4 were treated with a single dose of praziquantel. Serum levels of TGF-b1, IL-13, IL-17A and proinflammatory cytokines were measured by ELISA. Liver granulomas were identified by hematoxylin-eosin stain and measured by an ocular micrometer. Results: There was a significantly increased serum concentration of TGF-b1, IL-13, and IL-17A in infected WT mice, but praziquantel treatment reduced cytokine levels.

Evaluation of Serum IL-17A Levels in Diabetes with Chronic Periodontitis Patients

IL-17A cytokine is a most studied member of the IL-17 cytokine family and its increased production is associated with autoimmune disease and chronic inflammation including periodontitis. This study was aimed to evaluate the serum IL-17A levels in chronic periodontitis patients with or without diabetes. The study was carried out in 168 subjects and consisted of 6 groups wherein group 1 consisted of 28 Type 1 diabetes patients with periodontitis, group 2 consisted of 28 Type 1 diabetes patients without periodontitis, group 3 consists of 28 Type 2 diabetes patients with periodontitis, group 4 consists of 28 Type 2 diabetes patients without periodontitis, group 5 consists of 28 Non-diabetic patients with chronic periodontitis, group 6 consists of 28 Non-diabetic patients without periodontitis (control group). The Sample of 3 ml venous blood was collected from cubital fossa of each subject and analyzed by using ELISA kit. Overall comparison of IL-17A level in between the groups showed that, there was a significant difference (p value < 0.001) among the groups with highest mean level (5.02±0.45) for group-3 (T2DM+CP) followed by group-5 (only CP) and lowest (1.21±0.49) in group-6 (healthy). The serum IL-17A is significantly high in chronic periodontitis and type 2 diabetes with chronic periodontitis.

Role of vitamin D, interleukin-17A and interleukin-10 levels in women with recurrent miscarriage

Background: RPL is a common early pregnancy complication that is characterized as three or more pregnancy losses occurring before the 20th week of gestation. RPL is a common early pregnancy complication that is characterized as three or more pregnancy losses occurring before the 20th week of gestation. Recurrent miscarriage (RM) is a common occurrence, affecting 15–25% of all pregnancies. The study's goal was to assess vitamin D, interleukin-17a, and interleukin-10 levels in women who had several miscarriages and investigate the relationship between biomarkers to determine the final outcome of pregnancy. Methods: A case control study that included three study groups; thirty five women with RPL, thirty non-aborted pregnant (NAP) women and twenty five apparently healthy women. Patients were selected from those attending Bint Al-Huda Teaching Hospital and Suq Al-Shuyukh General Hospital at Thi-Qar Province (Iraq) during the period between October 2021 and July 2022 after stringent application of the eligibility criteria. Serum samples was collected form each subjects and was evaluated for serum VD, IL-17A and IL-10 levels via enzyme-linked immunosorbent assay (ELISA). Results: The results revealed that serum VD and IL-10 levels in the RPL group were significantly lower than in the healthy control group (HC).

Integrated Analysis of the Alterations in Gut Microbiota and Metabolites of Mice Induced After Long-Term Intervention With Different Antibiotics

ObjectivesWe aimed to study the effect of antibiotic-induced disruption of gut microbiome on host metabolomes and inflammatory responses after long-term use of antibiotics.MethodsA total of three groups of 3-week-old female C57BL/6 mice (n = 44) were continuously treated with vancomycin (VAN), polymyxin B (PMB), or water, respectively, for up to 28 weeks. Fecal samples collected at different time points were analyzed by bacterial 16S rRNA gene sequencing and untargeted metabolomics by ultraperformance liquid chromatography coupled with quadrupole time-of-flight tandem mass spectrometry (UPLC Q-TOF MS). Serum cytokines (IFN-γ, IL-2, IL-10, IL-13, IL-17A, and TNF-α) were determined by multiplex immunoassay.ResultsTreatment by VAN or PMB did not affect the average body weight of mice. However, a heavier caecum observed in VAN-treated mice. Compared with PMB-treated and control mice, VAN treatment induced more rapid dysbiosis of gut microbiota and dysmetabolism. Instead of Bacteroides, VAN-treated mice had a compositional shift to Proteobacteria and its species Escherichia coli and Verrucomicrobia and its species Akkermansia muciniphila. The shift was accompanied by decreased richness and diversity in microbiota. PMB-treated mice had an increased Firmicutes, and the diversity was shortly increased and further decreased to the baseline. Decreased levels of short-chain and long-chain fatty acids, bile acids, L-arginine, dopamine, L-tyrosine, and phosphatidylcholine (all p < 0.05) were observed in VAN-treated mice. In contrast, significantly increased levels of amino acids including L-aspartic acid, beta-alanine, 5-hydroxy-L-tryptophan, L-glutamic acid, and lysophosphatidylcholines (all p < 0.05) were found. These changes occurred after 3-week treatment and remained unchanged up to 28 weeks. For PMB-treated mice, metabolites involved in the metabolic pathway of vitamin B6 were decreased, whereas glycocholic acid and chenodeoxycholic acid were increased (all p < 0.05). After 8-week treatment, VAN-treated mice had significantly higher levels of serum IFN-γ, IL-13, and IL-17A, and PMB-treated mice had higher levels of IL-13 and IL-17 compared to control mice. At 28-week treatment, only IL-17A remained high in PMB-treated mice.ConclusionThis study showed that the antibiotic-induced alterations in gut microbiota contribute to host inflammatory responses through the change in metabolic status, which are likely related to the type, rather than timing of antibiotic used.

Evaluation of IL17A, FGF21 and CXC12 in Post-menopause Iraqi Sample with Osteoporosis and Osteopenia

Osteoporosis (OP) is a systemic skeletal disorder that is characterized by reduced bone mass and micro-architectural deterioration of bone tissue, with a consequent increase in bone fragility and susceptibility to fracture. The most frequent osteoporotic fractures are fractures of the hip, wrist, and spine. The exact causes of OP are still unknown; several factors contribute to the disorder. Subjects and Methods: This study consists of patient groups, this group (Group A) was composed of 80 postmenopausal women with OP and osteopenia and the patient group was subdivided into two group; First group (GroupA1) was composed of 50 postmenopausal women with OP and the second group (Group A2) composed of (30) Postmenopausal Women with osteopenia. In addition, to control group (20), 5 mL of venous blood sample were collected from each patient and healthy control in the population study, and the blood sample was transferred to a clean gel tube, left at room temperature for at least 30 minutes for clotting, then centrifuged for 5–10 minutes at 3000 rpm. Then, separated and divided into aliquots to obtain the serum, then its kept frozen at -20°C until analysis. The obtained serum was used to measure IL17A, FGF21, CXC12, calcium, and alkaline Phosphatase (ALP). Measurement of IL17A, FGF21 and CXC12 levels were performed by ELISA. The total calcium and serum ALK were measured by spectrophotometric-based method. Results: Serum levels of IL17A, FGF21 and CXC12 are significantly increased in Group A and subgroup (A1 and A2). Serum levels of total calcium and ALP are non-significant in Group A and sub group patients. Significant negative correlation between serum levels of IL17A and T score, FGF21 and T score, CXC12 and T score, IL 17A and Z score, IL17A and Calcium. Conclusions: Serum levels of IL17A, FGF21 and CXC12 is significantly increased in Group A and subgroup patients. Serum levels of total calcium and ALP are non-significant in Group A and sub group patients. Significant negative correlation exists between serum levels of IL17A and T score, FGF21 and T score, CXC12 and T score in Groups A and A1.

Characterization of IL-10-producing regulatory B cells in thymoma

Background Regulatory B cells (Bregs) are a subset of B cells that secrete interleukin 10 (IL-10) and play a vital role in suppressing the immune response. The aim of this study was to evaluate the proportion of Bregs in patients with thymoma. Methods The proportions of subgroups of Bregs in 23 patients with thymoma and 15 healthy controls were detected by flow cytometry. The serum IL-2, IL-4, IL-6, IL-10, IL-17A, IFN-γ, and TNF-α levels of the subjects were measured using a cytometric bead array (CBA). Results The proportions of circulating IL-10+ B cells, IL-10+CD24hiCD38hi Bregs, and IL-10+CD24hiCD27+ Bregs and the serum IL-10 level were significantly higher in patients with thymoma than in the control group and were negatively correlated with the Karnofsky Performance Scale (KPS) score. The serum levels of cytokines IL-2, IL-6, IFN-γ, and TNF-α were higher and serum IL-17A level was lower in patients with thymoma. Patients with advanced-stage thymoma exhibited significantly higher proportions of IL-10-producing Bregs and a higher serum IL-10 level. After tumour resection, the frequency of circulating IL-10+CD24hiCD38hi Bregs and the serum IL-10 level were significantly decreased in patients with thymoma. The serum IL-10 levels exhibited the best accuracy in assessing the risk of thymoma occurrence in this study. Conclusions The expression of IL-10 produced by Bregs is increased in patients with thymoma, particularly those with advanced-stage disease, which may suggest that Bregs are involved in the pathogenesis and progression of thymoma.

Association of Serum Vitamin D Levels, IL-17a Levels with Disease Severity among 3- to 18-year-old Children with Asthma in the Philippine General Hospital

Background. Previous studies show that Vitamin D has an inverse relationship with asthma severity, symptoms, exacerbations, medication usage, and a direct relationship with lung function. IL-17A was found to be increased in asthmatics, which was inhibited by Vitamin D. Associations found between vitamin D, IL-17A, and asthma may support the future role of vitamin D in the treatment of asthma in children.&#x0D; Objective. To compare vitamin D and IL-17A levels between children with and without asthma and determine their association with asthma severity&#x0D; Study Design. Cross-sectional study&#x0D; Methods. There were 44 participants, aged 3 to 18 years: 22 with asthma (12 non-severe, 10 severe) and 22 without asthma. Participants with any disease-altering vitamin D metabolism, intake of vitamin D supplementation, and recent infection were excluded. Serum vitamin D and IL-17A levels were measured in all participants.&#x0D; Results. There was no significant difference in mean vitamin D levels between participants with asthma (29.6 ± 12.6 ng/mL) and without asthma (27.6 ± 9.5 ng/mL) (p = 0.55) as well as between participants with non-severe asthma (29.8 ± 14.0 ng/mL) and severe asthma (29.4 ± 11.5 ng/mL) (p = 0.95). The overall prevalence of hypovitaminosis D (&lt; 30ng/mL) is 61.4%; 59.1% among those with asthma and 63.6% without asthma. The prevalence of vitamin D insufficiency and/or deficiency did not significantly differ between those with and without asthma (all p-value &gt; 0.05); prevalence ratios were: 1.05 for vitamin D insufficiency, 0.58 for vitamin deficiency, and 0.92 for vitamin D insufficiency and deficiency combined. There was also no significant difference in the prevalence of vitamin D insufficiency and/or deficiency between severe and non-severe asthma (all p-values &gt; 0.05), with prevalence ratios: 0.74 for vitamin D insufficiency, 0.50 for vitamin D deficiency, and 0.75 for vitamin D insufficiency and deficiency combined. Serum IL-17A levels were below the minimum detectable levels in 96% of the participants using the MILLIPLEX Map Human TH17 Magnetic Band Panel; hence, could not be analyzed.&#x0D; Conclusion. The mean serum vitamin D levels do not differ between children with asthma and healthy controls. There was no significant relationship between mean vitamin D levels and asthma severity. There was no association between the prevalence of vitamin D insufficiency and/or deficiency and asthma and its severity. The overall prevalence of hypovitaminosis D in this study is 61.4%. Serum IL-17A levels were undetectable in 96% of the study population.

Pediatric Research Challenge, Alignment with the National Research Agenda

Pediatric Research Challenge, Alignment with the National Research Agenda