Periostin in Angiogenesis and Inflammation in CRC—A Preliminary Observational Study

Background and Objectives: To assess the periostin level and the concentrations of pro-inflammatory cytokines: TNFα, IFN-γ, IL-1β and IL-17 in tumor and marginal tissues of CRC and to investigate the influence of periostin on angiogenesis by MVD (microvessel density) and concentration of VEGF-A in relation to clinicopathological parameters of patients. Materials and Methods: The study used 47 samples of tumor and margin tissues derived from CRC patients. To determinate the concentration of periostin, VEGF-A, TNFα, IFNγ, IL-1β and IL-17, we used the commercially available enzyme- linked immunosorbent assay kit. MVD was assessed on CD34-stained specimens. The MVD and budding were assessed using a light microscope Results: We found significantly higher concentrations of periostin, VEGF-A, IFN-γ, IL-1 β, IL-17 and TNFα in the tumor samples compared with surgical tissue margins. The tumor concentrations of periostin were correlated with tumor levels of VEGF-A, IFN-γ, IL-1β and TNFα. We observed significant correlation between margin periostin and VEGF-A, IFN-γ, IL-17 and TNFα in tumor and margin specimens. Additionally, we found a significantly negative correlation between periostin tumor concentration and microvessel density at the invasive front. Tumor periostin levels were also correlated positively with tumor budding. Conclusions: Periostin activity may be associated with pro-inflammatory cytokine levels: TNFα, IFN-γ, IL-1β and IL-17. Our results also suggest the role of periostin in angiogenesis in CRC and its upregulation in poorly vascularized tumors. Further research on the regulations between periostin and cytokines are necessary to understand the interactions between tumor and immune tumor microenvironment, which could be helpful in the development of new targeted therapy.

Download Full-text

Synthesis of Eicosapentaenoic acid-enriched Phosphatidylcholine and Its Effect on Pro-inflammatory Cytokine Expression

Combinatorial Chemistry & High Throughput Screening ◽

10.2174/1386207324666210118100049 ◽

2021 ◽

Vol 24 ◽

Author(s):

Jae Yeul Baek ◽

Eun Na ◽

Sun Young Lim

Keyword(s):

Eicosapentaenoic Acid ◽

Inflammatory Cytokines ◽

Immunosorbent Assay ◽

Inflammatory Cytokine ◽

Cytokine Expression ◽

Enzyme Linked Immunosorbent Assay ◽

Murine Splenocytes ◽

Ifn Γ ◽

Culture Supernatants ◽

Pro Inflammatory Cytokines

Aim and Objective: We synthesized eicosapentaenoic acid-enriched phosphatidylcholine (EPA-PC) and investigated its effect on the production of lipopolysaccharide (LPS)-induced cytokines in murine splenocytes. Material and Methods: The culture supernatants of splenocytes, which was exposed to EPA-PC along with LPS, was harvested to determine the production of cytokines [interleukin (IL)-4 , IL-5, IL-6, interferon (IFN)-γ, IL-2 and IL-12/IL-23(p40)]. Cytokines were measured using enzyme-linked immunosorbent assay (ELISA). Results: The co-administration of EPA-PC with LPS resulted in a significantly lower IFN-γ expression than that observed with LPS alone (p < 0.01). Moreover, treatment with EPA-PC and LPS significantly decreased IL-2, IL-6 and IL-12/IL-23(p40) expression (p < 0.01). Co-administration of EPA-PC at a concentration of 0.3 μg/mL with LPS resulted in a higher IL-5 expression after 24 hr of treatment when compared to LPS alone (p < 0.05). Conclusion: These results suggest that EPA-PC is more effective in decreasing the expression of pro-inflammatory cytokines [IL-2, IFN-γ, IL-6 and IL-12/IL-23(p40)] upon induction of inflammation.

Download Full-text

Abstract 116: Detrimental Role of Toll-Like Receptor 4 in Cardiovirus-Induced Myocarditis

Circulation Research ◽

10.1161/res.111.suppl_1.a116 ◽

2012 ◽

Vol 111 (suppl_1) ◽

Author(s):

Fumitaka Sato ◽

Seiichi Omura ◽

Nicholas E Martinez ◽

Eiichiro Kawai ◽

Ganta V Chaitanya ◽

...

Keyword(s):

Immune Responses ◽

Acute Phase ◽

Viral Entry ◽

Viral Myocarditis ◽

Chronic Phase ◽

Enzyme Linked Immunosorbent Assay ◽

Tlr4 Ligand ◽

Ifn Γ ◽

Deficient Mice

Picornavirus infections have been known as a leading cause of viral myocarditis in humans. Theiler’s murine encephalomyelitis virus (TMEV) belongs to the genus Cardiovirus, the family Picornaviridae and was reported to cause inflammation in the heart in one manuscript, while its pathomechanism is unclear. In viral myocarditis, viral replication in the heart and/or immune responses against virus as well as heart-antigen (autoimmunity) can contribute to the pathogenesis. Toll-like receptors (TLRs) are pattern recognition receptors (PRRs) that are important for recognizing pathogens as well as triggering innate immunity. Among TLRs, TLR4 has been demonstrated to play important roles in virus-mediated pathology: 1) TLR4 can contribute to viral entry in some viruses, 2) TLR4 may mediate tissue damage by anti-virus immune responses (immunopathology), 3) high levels of TLR4 expression were observed in the heart of patients with dilated cardiomyopathy following acute viral myocarditis, and 4) some viruses can bind to lipopolysaccharide (LPS), which is a TLR4 ligand. To determine the role of TLR4 in TMEV-induced myocarditis, we infected male C3H/HeJ (TLR4-deficient) and C3H/HeNtac (control TLR4+) mice with the DA strain of TMEV. We harvested the hearts and spleens on days 6 and 7 (acute phase) or days 63 and 64 (chronic phase) post-infection. Cardiac pathology was evaluated by hematoxylin and eosin staining and production of pro-inflammatory cytokines, interleukin (IL)-17A and interferon (IFN)-γ, from spleen cells was measured by an enzyme-linked immunosorbent assay (ELISA). In both mice, mild myocarditis was observed during the acute phase of TMEV infection. During the chronic phase, both mice developed severe pathology in the heart, including basophilic degeneration and calcification. However, the incidence of myocarditis was higher in control mice than TLR4-deficient mice. IL-17A and IFN-γ production was higher in control mice than in TLR4-deficient mice (control vs. TLR4-deficient mice, acute phase: IL-17A, 196 vs. 146 pg/ml; IFN-γ, 72 vs. 39 ng/ml; chronic phase: IL-17A, 290 vs. 229 pg/ml; IFN- γ, 142 vs. 88 ng/ml). These results suggest that TLR4 may be detrimental in TMEV-induced myocarditis by increasing pro-inflammatory cytokine production.

Download Full-text

TheBDKRB2 +9/-9 Polymorphisms Influence Pro-Inflammatory Cytokine Levels in Knee Osteoarthritis by Altering TLR-2 Expression: Clinical and in Vitro Studies

Cellular Physiology and Biochemistry ◽

10.1159/000443072 ◽

2016 ◽

Vol 38 (3) ◽

pp. 1245-1256 ◽

Cited By ~ 2

Author(s):

Shuo Chen ◽

Lei Zhang ◽

Ruonan Xu ◽

Yunfan Ti ◽

Yunlong Zhao ◽

...

Keyword(s):

Knee Osteoarthritis ◽

Inflammatory Cytokine ◽

Molecular Mechanisms ◽

Enzyme Linked Immunosorbent Assay ◽

Mrna Levels ◽

Knee Oa ◽

Tnf Α ◽

Cytokine Levels ◽

Underlying Mechanisms

Background/Aims: The bradykinin B2 receptor (BDKRB2) +9/-9 gene polymorphisms have been shown to be associated with the susceptibility and severity of osteoarthritis (OA); however, the underlying mechanisms are unclear. In this study, we investigated the correlation between the BDKRB2 +9/-9 polymorphisms and pro-inflammatory cytokine levels in OA and the molecular mechanisms involved. Methods: A total of 156 patients with primary knee OA and 121 healthy controls were enrolled. The BDKRB2 +9/-9 polymorphisms were genotyped. The tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, and IL-8 levels were determined using Enzyme-linked immunosorbent assay (ELISA). The toll-like receptor (TLR)-2 and TLR-4 mRNA levels were determined by quantitative real-time PCR. The basal and bradykinin-stimulated pro-inflammatory cytokine secretion in human OA synoviocytes and the involvement of TLR-2 and mitogen-activated protein kinases (MAPKs) were investigated. Results: The presence of -9 bp genotype is associated with higher TNF-α, IL-6, and IL-8 levels and higher TLR-2 expression in OA patients. The basal and bradykinin-induced TLR-2 expressions in human OA synoviocytes were significantly reduced by specific inhibitors of p38, JNK1/2, and ERK1/2. Both the B2 receptor antagonist MEN16132 and TLR-2 silencing inhibited IL-6 and IL-8 secretion in human OA synoviocytes. Conclusion: The data suggested that the BDKRB2 +9/-9 polymorphisms influence pro-inflammatory cytokine levels in knee osteoarthritis by altering TLR-2 expression.

Download Full-text

GPR110 (ADGRF1) mediates anti-inflammatory effects of N-docosahexaenoylethanolamine

Journal of Neuroinflammation ◽

10.1186/s12974-019-1621-2 ◽

2019 ◽

Vol 16 (1) ◽

Cited By ~ 8

Author(s):

Taeyeop Park ◽

Huazhen Chen ◽

Hee-Yong Kim

Keyword(s):

Inflammatory Cytokine ◽

Inflammatory Responses ◽

Cytokine Expression ◽

Regulatory Function ◽

Enzyme Linked Immunosorbent Assay ◽

Inflammatory Condition ◽

Wild Type ◽

Knock Out ◽

The Brain

Abstract Background Neuroinflammation is a widely accepted underlying condition for various pathological processes in the brain. In a recent study, synaptamide, an endogenous metabolite derived from docosahexaenoic acid (DHA, 22:6n-3), was identified as a specific ligand to orphan adhesion G-protein-coupled receptor 110 (GPR110, ADGRF1). Synaptamide has been shown to suppress lipopolysaccharide (LPS)-induced neuroinflammation in mice, but involvement of GPR110 in this process has not been established. In this study, we investigated the possible immune regulatory role of GPR110 in mediating the anti-neuroinflammatory effects of synaptamide under a systemic inflammatory condition. Methods For in vitro studies, we assessed the role of GPR110 in synaptamide effects on LPS-induced inflammatory responses in adult primary mouse microglia, immortalized murine microglial cells (BV2), primary neutrophil, and peritoneal macrophage by using quantitative PCR (qPCR) and enzyme-linked immunosorbent assay (ELISA) as well as neutrophil migration and ROS production assays. To evaluate in vivo effects, wild-type (WT) and GPR110 knock-out (KO) mice were injected with LPS intraperitoneally (i.p.) or TNF intravenously (i.v.) followed by synaptamide (i.p.), and expression of proinflammatory mediators was measured by qPCR, ELISA, and western blot analysis. Activated microglia in the brain and NF-kB activation in cells were examined microscopically after immunostaining for Iba-1 and RelA, respectively. Results Intraperitoneal (i.p.) administration of LPS increased TNF and IL-1β in the blood and induced pro-inflammatory cytokine expression in the brain. Subsequent i.p. injection of the GPR110 ligand synaptamide significantly reduced LPS-induced inflammatory responses in wild-type (WT) but not in GPR110 knock-out (KO) mice. In cultured microglia, synaptamide increased cAMP and inhibited LPS-induced proinflammatory cytokine expression by inhibiting the translocation of NF-κB subunit RelA into the nucleus. These effects were abolished by blocking synaptamide binding to GPR110 using an N-terminal targeting antibody. GPR110 expression was found to be high in neutrophils and macrophages where synaptamide also caused a GPR110-dependent increase in cAMP and inhibition of LPS-induced pro-inflammatory mediator expression. Intravenous injection of TNF, a pro-inflammatory cytokine that increases in the circulation after LPS treatment, elicited inflammatory responses in the brain which were dampened by the subsequent injection (i.p.) of synaptamide in a GPR110-dependent manner. Conclusion Our study demonstrates the immune-regulatory function of GPR110 in both brain and periphery, collectively contributing to the anti-neuroinflammatory effects of synaptamide under a systemic inflammatory condition. We suggest GPR110 activation as a novel therapeutic strategy to ameliorate inflammation in the brain as well as periphery.

Download Full-text

Bee pollen and propolis improve neuroinflammation and dysbiosis induced by propionic acid, a short chain fatty acid in a rodent model of autism

Lipids in Health and Disease ◽

10.1186/s12944-019-1150-0 ◽

2019 ◽

Vol 18 (1) ◽

Cited By ~ 4

Author(s):

Kawther Aabed ◽

Ramesa Shafi Bhat ◽

Abeer Al-Dbass ◽

Nadine Moubayed ◽

Norah Algahtani ◽

...

Keyword(s):

Propionic Acid ◽

Inflammatory Cytokine ◽

Interleukin 1 ◽

Rodent Model ◽

Control Group ◽

Bee Pollen ◽

Group I ◽

Cytokine Levels ◽

Neurotoxic Effects ◽

Ifn Γ

Abstract Background Neuroinflammation plays a major role in the pathogenesis of autism because the cytokine levels are typically disturbed in the brain in autistic patients. Prebiotics-rich diet maintains the healthy gut microbiota and hence can regulate the neuroinflammation indirectly. The study aimed to investigate the role of bee pollen and propolis in ameliorating neuroinflammation, including cytokine levels, in an animal model of autism. Methods Hamsters were classified as four groups: Group I, control; Group II, autistic model/animals treated with 250 mg propionic acid (PPA)/kg body weight (BW)/day for 3 days; Group III, animals treated with bee pollen at a dose of 250 mg/kg BW/day for 4 weeks; and Group IV, animals treated with propolis at a dose of 250 mg/kg BW/day for 4 weeks. Neuroinflammatory responses were evaluated using the levels of interferon γ (IFN-γ), interleukin 1 alpha (IL-1α), IL-6, IL-10, IL-12 (p70), vascular endothelial growth factor (VEGF), and tumor necrosis factor α (TNFα). Results Significant decrease of IL-10 (P<0.026), VEGF (P<0.005), and TNFα(P<0.005) levels and increased IL-1α (P<0.032), IL-6(P<0.028), and IFN-γ (P<0.013) levels were observed between the four studied groups. The neurotoxic effects of PPA was clearly presented as much higher IL-6, as pro-inflammatory cytokine (P<0.05), concomitant with much lower IL-10, as anti-inflammatory cytokine(P<0.015) compared to controls. Both bee pollen and propolis were effective in ameliorating the neurotoxic effects of PPA demonstrating non-significant changes of IL-6 and IL-10 when compared to control healthy hamsters. Conclusions Our findings indicate that both bee pollen and propolis protect against neuroinflammation in the rodent model of autism. However, further studies are needed to investigate the clinical benefits of prebiotics-rich diet in neurodevelopmental disorders, such as autism.

Download Full-text

SEX-DIMORPHISM IN THE GENOMIC REGULATION OF AGING

Innovation in Aging ◽

10.1093/geroni/igz038.2825 ◽

2019 ◽

Vol 3 (Supplement_1) ◽

pp. S768-S769

Author(s):

Bérénice A Benayoun ◽

Ryan A Lu ◽

Nirmal K Sampathkumar

Keyword(s):

Inflammatory Cytokines ◽

Rna Seq ◽

Male Mice ◽

Sex Dimorphism ◽

Exceptional Longevity ◽

Cytokine Levels ◽

Genomic Regulation ◽

Pro Inflammatory Cytokines

Abstract The current cohort of human supercentenarians reveals a surprising predictor for achieving such an exceptional longevity: being female. Indeed, out of 34 living supercentenarians, 33 are women. We obtained samples from 4 and 20 months old female and male mice. Our data indicates that cytokine levels are differentially regulated with age in males vs. females, with pro-inflammatory cytokines specifically upregulated in the serum of old males, but not females. Because of the central role of macrophages in inflammation and their infiltration in tissues with age, we have generated RNA-seq from purified macrophages of aging animals. Female macrophages displayed ~7-20-fold more transcriptional remodeling with aging than males. Pathways specifically downregulated in females with aging included lysosome, inflammation and phagolysosome. Consistently, our data shows that aged female, but not male macrophages, display decreased phagocytic efficiency. Our results support the notion that there are differences in aging trajectories in female vs. male mice.

Download Full-text

Role of Interferon-Gamma (Ifn-γ) in Immune Response Regulation in Hiv-1 and Hiv-1 + Mycobacterium Tuberculosis (Tb) Infected Patients / Interferona-gamma (Ifn-γ) Loma Imūnās Atbildes Regulēšanā Pacientiem Ar HIV-1 un HIV-1 + mycobacterium Tuberculosis

Proceedings of the Latvian Academy of Sciences Section B Natural Exact and Applied Sciences ◽

10.1515/prolas-2016-0033 ◽

2016 ◽

Vol 70 (4) ◽

pp. 211-214

Author(s):

Inga Januškevica ◽

Baiba Rozentāle ◽

Elvīra Hagina ◽

Jeīena Eglīte ◽

Tatjana Kolupajeva ◽

...

Keyword(s):

Mycobacterium Tuberculosis ◽

Viral Load ◽

University Hospital ◽

Enzyme Linked Immunosorbent Assay ◽

Cell Counts ◽

Cd4 Cell Counts ◽

Ifn Γ ◽

Cd4 Cell ◽

Hiv 1

Abstract The aim of this research was to investigate the role of IFN-γ in interaction between IL-10, IL-18, IL-1b, CD4 cell counts and HIV-1 RNA viral load in the development of HIV-1 in patients co-infected with Mycobacterium tuberculosis (TB). The study was conducted by Rīga East Clinical University Hospital with data from the HIV-1 register, in collaboration with the RSU Joint Laboratory of Clinical Immunology and Immunogenetics. 200 HIV-1 infected patients and 184 HIV-1 with TB co-infection patients divided in four groups were included in the study. IFN-γ, IL-10, IL-18, IL-1b levels were measured in serum with commercially enzyme-linked immunosorbent assay (ELISA Vector-Best Corporation, Novosibirsk, Russia). CD4 cell counts were measured by flow Partec IVD cytometry (USA). HIV-1 RNA quantification was performed using the COBAS AmpliPrep/COBAS Taqman HIV-1 Test (Germany). All groups were compared with each another. IFN-γ production was significantly lower, and IL-10 and CD4 cell counts were significantly higher, in HIV-1 patients without TB compared with the other groups. The group with HIV-1 and TB had significantly elevated IL-18 production. HIV patients with primary TB had significantly elevated IFN-γ production and HIV-1 RNA viral load and significantly lower IL-10 production.

Download Full-text

Association of pro-inflammatory cytokines with PTSd severity in patients treated with omega-3 supplementation – a pilot study

European Psychiatry ◽

10.1016/j.eurpsy.2016.01.519 ◽

2016 ◽

Vol 33 (S1) ◽

pp. S214-S214

Author(s):

D. Kalinić ◽

N. Mimica ◽

A. Jeroncic ◽

M. Lalovac ◽

I. Delaš

Keyword(s):

Inflammatory Cytokines ◽

Assay Method ◽

Enzyme Linked Immunosorbent Assay ◽

Hamilton Depression Scale ◽

Ptsd Symptoms ◽

Omega 3 ◽

Cytokine Levels ◽

Ptsd Symptomatology ◽

Pro Inflammatory Cytokines ◽

Ptsd Severity

IntroductionAssociation of pro-inflammatory cytokines with severity of various psychiatric disorders is shown. Evidence suggests omega-3 fatty acids reduce psychiatric symptoms due to anti-inflammatory properties.ObjectivesTo evaluate if serum levels of pro-inflammatory cytokines correlate with the intensity of PTSD symptoms, and the observed change in symptoms’ severity induced by omega-3 supplementation.MethodsWe included 26 Croatian Homeland war veterans (aged 39–60) with chronic PTSD and no major comorbidity, who were on stable therapeutic sertraline dose at least three months before recruitment. Levels of pro-inflammatory cytokines (TNF-α, IL-6, and IL-1β) were determined by the enzyme-linked immunosorbent assay method. Intensity of PTSD symptomatology was assessed by Clinician-Administered PTSD Scale (CAPS), Hamilton Anxiety Scale (HAM-A) and 17-item Hamilton Depression Scale (17-HAM-D). During 12 weeks, participants took omega-3 capsules (600 mg/day) while continuing sertraline therapy.ResultsMost participants presented with moderate PTSD evaluated by CAPS. At baseline, cytokine levels were not associated with the severity of PTSD symptoms, as measured by all three scales (P ≥ 0.209). After 12 weeks of omega-3 supplementation the severity of PTSD symptoms significantly decreased, on average by 8 to 13% on the psychometric scales per person (P < 0.001 for all). However, no association was found between the change in cytokine levels and the change in scores, induced by omega-3, on the assessed scales (P ≥ 0.730).SummaryCytokine levels are not associated with PTSD severity or with improvement in PTSD symptomatology. At the same time, sertraline therapy supplemented with omega-3 seemed to reduce the severity of PTSD symptoms.Disclosure of interestThe authors have not supplied their declaration of competing interest.

Download Full-text

Role of Interleukin-6 and Interleukin-8 Cytokines as Early Diagnostic Markers of Sepsis

Bangladesh Journal of Infectious Diseases ◽

10.3329/bjid.v6i2.46102 ◽

2020 ◽

Vol 6 (2) ◽

pp. 34-38

Author(s):

Mohammad Moniruzzaman ◽

Ashesh Kumar Chowdhury ◽

ASM Areef Ahsan ◽

Md Zakiur Rahman ◽

Saimun Nahar Rumana ◽

...

Keyword(s):

Metabolic Disorders ◽

Serum Levels ◽

Clinicopathological Parameters ◽

Enzyme Linked Immunosorbent Assay ◽

Significant Difference ◽

Relationship Of ◽

The Relationship ◽

Culture Positive ◽

Control Study

Background: Rapid diagnosis is essential for effective therapy among the patients with sepsis. Objectives: The purpose of the present study was to determine the relationship of serum levels of IL-6, IL-8 in patients with various stages of sepsis. Methodology: This case control study was conducted in the Department of Immunology at Bangladesh Institute of Research and Rehabilitation in Diabetes, Endocrine and Metabolic Disorders (BIRDEM), Dhaka from January 2015 to December 2015 for a period of one (01) year. All patients had been selected from the ICU of BIRDEM General Hospital with known clinicopathological parameters of sepsis. Serum levels of IL-6 and IL-8 were assessed using Enzyme Linked Immunosorbent Assay (ELISA) method. Results: In this study, a total of 80 subjects was enrolled of which 60 patients were with at least 2 SIRS criteria and 20 healthy age matched controls without SIRS. Significant difference was found in IL-6 and IL-8 values in the patients with bacteriological culture positive and negative group (p<0.05). AUC for IL-6 was 0.710 (95% CI 0.580-0.840), sensitivity 54.16%, specificity 59.09%, PPV 74.28% and NPV 52% with cutoff value >177pg/ml. Conclusion: Elevated levels of serum IL-6 and IL-8 is found in the patients with sepsis Bangladesh Journal of Infectious Diseases 2019;6(2):34-38

Download Full-text

Interleukin-35 inhibited production of histamine and pro-inflammatory cytokines through suppression MAPKs pathway in HMC-1 cells

10.21203/rs.3.rs-41258/v1 ◽

2020 ◽

Author(s):

Tao Chen ◽

Lixin Fu ◽

Qiaomei Sun ◽

Peimei Zhou ◽

Zai-pei Guo

Keyword(s):

Immune Response ◽

Inflammatory Cytokine ◽

Human Mast Cell ◽

Rt Pcr ◽

Effector Cells ◽

Response System ◽

Mast Cell Line ◽

Anti Inflammatory Cytokine ◽

Pro Inflammatory Cytokines

Abstract Background: IL-35 is a newly anti-inflammatory cytokine which belong to the IL-12 family. Mast cells, as one of the major effector cells in the immune response system, play important roles in the pathogenesis of chronic spontaneous urticarial (CSU). The aim of our study is to explore the inhibited role of IL-35 in HMC-1. Methods: The effects of IL-35 on cell proliferation, cytokine expression and histamine release in human mast cell line (HMC1) were investigated by CCK8, ELISA or RT-PCR. The phosphorylation of ERK1/2, p38 and JNK1/2, in PMA and A23187 induced HMC-1 cells were detected by Western Blot.Results: We found that IL-35 significantly inhibited the proliferation of HMC-1 cells stimulated by PMA and A23187. IL-35 also down-regulates the released of histamine and the mRNA expression of IL-6 and IL-17 in activated HMC-1. Furthermore, IL-35 markedly inhibited the phosphorylation of ERK1/2, p38 and JNK1/2, in PMA and A23187 induced HMC-1 cells. Conclusions: This study provides first observations on the inhibitory and anti-inflammtory effect of IL-35 on activated HMC-1 cells. We suggest that IL35 may play an inhibited role in the pathogenesis of CSU.

Download Full-text