scholarly journals Immune Mediator Profile in Aqueous Humor Differs in Patients with Primary Acquired Ocular Toxoplasmosis and Recurrent Acute Ocular Toxoplasmosis

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Claudia Thieme ◽  
Stephan Schlickeiser ◽  
Sylvia Metzner ◽  
Claudia Dames ◽  
Uwe Pleyer
Keyword(s):  
Inflammatory Response ◽  
Aqueous Humor ◽  
Clinical Characteristics ◽  
Multiplex Assay ◽  
Ocular Toxoplasmosis ◽  
Immune Mediator ◽  
Gm Csf ◽  
Immune Mediators ◽  
First Time ◽  
Type Response

Purpose. To compare the intraocular cytokine and chemokine profiles in patients with acute primary acquired ocular toxoplasmosis (pOT) or recurrent ocular toxoplasmosis (rOT) and to correlate them with their clinical characteristics.Methods. Aqueous humor samples were collected from 62 consecutive patients (21 pOT, 30 rOT, and 11 noninfected controls) and analyzed by multiplex assay. Correlations were assessed between cytokine/chemokine levels, type of inflammatory response (Th1, Th2, and Th17), and clinical characteristics. In all OT patients, the clinical diagnosis of either pOT or rOT was confirmed by positive intraocular Goldmann/Witmer-Desmonts coefficient. Correlations were assessed between a preselected panel of immune mediators and the clinical characteristics of OT.Results. In pOT patients, increased levels of IL-2, IFN-γ, TNF-α, IL-15, IL-4, IL-5, IL-9, IL-13, IL-17, IL-1Rα, IL-6, IL-1β, and chemokines MIP-1α, MIP-1β, IP-10, Eotaxin, IL-8, RANTES, PDGF-bb, GM-CSF, G-CSF, and MCP-1 were found in comparison to those in controls (p<0.05). Patients with rOT showed elevated levels of IL-2, IFN-γ, TNF-α, IL-15, IL-4, IL-5, IL-9, IL-17, IL-1Rα, IL-6, IL-1β, and chemokines MIP-1α, IP-10, Eotaxin, IL-8, RANTES, PDGF-bb, G-CSF, and MCP-1 compared to controls (p<0.05). In addition, IL-7 (p=0.028) differed between pOT and rOT; IL-9 (p=0.054) and IL-13 (p=0.051) showed a tendency of higher concentration in pOT than in rOT. A negative correlation was found between IL-7 (p=0.017) as well as IL-9 (p=0.008) and the number of recurrences. Cytokine ratios showed no difference between pOT and rOT, indicating a dominant Th1-type response in both infectious groups. Moreover, a positive correlation was detected between IL-7, VEGF, IL-13 and age at aqueous humor sampling (p<0.05).Conclusions. This study for the first time shows subtle differences between the intraocular cytokine profiles in patients with either acute pOT or rOT.

scholarly journals A Novel Role for the Thyroid Hormone-Activating Enzyme Type 2 Deiodinase in the Inflammatory Response of Macrophages

Endocrinology ◽  
2014 ◽  
Vol 155 (7) ◽  
pp. 2725-2734 ◽  
Author(s):  
J. Kwakkel ◽  
O.V. Surovtseva ◽  
E.M. de Vries ◽  
J. Stap ◽  
E. Fliers ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Inflammatory Response ◽  
Thyroid Hormone Receptor ◽  
Close Correlation ◽  
Monocarboxylate Transporter ◽  
Gm Csf ◽  
Serum T3 ◽  
Acute And Chronic Inflammation ◽  
First Time

Deiodinase type 2 (D2) is a thyroid hormone-activating enzyme converting the prohormone T4 into the active hormone T3. In the present study, we show for the first time that D2 is up-regulated in the mouse liver during acute and chronic inflammation, in close correlation with the proinflammatory cytokine IL-1β and independently of serum T3. Inflammation-induced D2 expression was confirmed in macrophages, in conjunction with selective thyroid hormone transporter (monocarboxylate transporter 10) and thyroid hormone receptor (TR)α1 stimulation, and was absent in hepatocytes. Moreover, D2 knockdown in macrophages resulted in a clear attenuation of the lipopolysaccharide (LPS)-induced IL-1β and GM-CSF expression, in addition to aberrant phagocytosis. Locally produced T3, acting via the TRα, may be instrumental in this novel inflammatory response, because LPS-treated TRα0/0 mice showed a markedly decreased LPS-induced GM-CSF mRNA expression. We now propose that hepatic D2 favors the innate immune response by specifically regulating cellular thyroid hormone levels in macrophages.

scholarly journals Proteomic Analysis of Synovial Fibroblasts and Articular Chondrocytes Co-Cultures Reveals Valuable VIP-Modulated Inflammatory and Degradative Proteins in Osteoarthritis

2021 ◽  
Vol 22 (12) ◽  
pp. 6441
Author(s):  
Selene Pérez-García ◽  
Valentina Calamia ◽  
Tamara Hermida-Gómez ◽  
Irene Gutiérrez-Cañas ◽  
Mar Carrión ◽  
...  
Keyword(s):  
Isotope Labeling ◽  
Articular Chondrocytes ◽  
Synovial Fibroblasts ◽  
Immune Mediators ◽  
Cartilage Extracellular Matrix ◽  
Fibronectin Fragments ◽  
Ecm Degradation ◽  
Key Events ◽  
First Time

Osteoarthritis (OA) is the most common musculoskeletal disorder causing a great disability and a reduction in the quality of life. In OA, articular chondrocytes (AC) and synovial fibroblasts (SF) release innate-derived immune mediators that initiate and perpetuate inflammation, inducing cartilage extracellular matrix (ECM) degradation. Given the lack of therapies for the treatment of OA, in this study, we explore biomarkers that enable the development of new therapeutical approaches. We analyze the set of secreted proteins in AC and SF co-cultures by stable isotope labeling with amino acids (SILAC). We describe, for the first time, 115 proteins detected in SF-AC co-cultures stimulated by fibronectin fragments (Fn-fs). We also study the role of the vasoactive intestinal peptide (VIP) in this secretome, providing new proteins involved in the main events of OA, confirmed by ELISA and multiplex analyses. VIP decreases proteins involved in the inflammatory process (CHI3L1, PTX3), complement activation (C1r, C3), and cartilage ECM degradation (DCN, CTSB and MMP2), key events in the initiation and progression of OA. Our results support the anti-inflammatory and anti-catabolic properties of VIP in rheumatic diseases and provide potential new targets for OA treatment.

Abstract 110: Adiponectin Inhibits TNF-a-Induced Vascular Inflammatory Response via Caveolin-Mediated Ceramidase Recruitment and Activation

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Yajing Wang ◽  
Wayne Lau ◽  
Erhe Gao ◽  
Walter Koch ◽  
Xin Ma
Keyword(s):  
Inflammatory Response ◽  
Protective Action ◽  
Receptor Subtype ◽  
Protective Actions ◽  
Nitrative Stress ◽  
S1p Receptor ◽  
Anti Inflammatory ◽  
Or Gene ◽  
First Time

Anti-inflammatory and vascular protective actions of adiponectin (APN) are well-recognized. However, many fundamental questions remain unanswered. The current study attempted to identify the APN receptor subtype responsible for APN’s vascular protective action, and investigate the role of ceramidase activation in APN anti-inflammatory signaling. Wild type (WT) or gene manipulated HUVEC were treated with TNFα in the presence and absence of APN. The effect of APN on TNFα-induced inflammatory and oxidative/nitrative stress was determined. In WT HUVEC, APN significantly reduced TNFα-induced ICAM-1 expression and attenuated TNFα-induced superoxide and peroxynitrite formation (P<0.01). These anti-inflammatory actions were virtually abolished by AdipoR1-, but not AdipoR2-, knockdown (KD). Treatment with APN significantly increased neutral ceramidase (nCDase) activity (3.7-fold, P<0.01). AdipoR1-KD markedly (P0.05), reduced APN-induced nCDase activation. More importantly, siRNA mediated nCDase-KD markedly blocked the effect of APN upon TNFα-induced ICAM-1 expression (P0.05), and modestly inhibited APN anti-inflammatory effect (P87% of APN-induced nCDase activation was lost. Whereas APN treatment failed to inhibit TNFα-induced ICAM-1 expression, treatment with S1P or SEW (S1P receptor agonist) remained effective in Cav1-KD cells in reducing TNFα-induced ICAM-1 expression (P<0.01). AdipoR1 and Cav1 co-localized and co-precipitated in HUVECs. APN treatment did not affect this interaction. Moreover, re-expression of WT Cav1 in Cav1-KD cells restored nCDase activation in response to APN (P<0.01 vs. vehicle), whereas re-expression of a mutated Cav1 blocking AdipoR1/Cav1 interaction failed to restore APN-mediated nCDase activation. Finally, there is weak basal Cav1/nCDase interaction, which significantly increased following APN treatment. These results demonstrate for the first time that APN inhibits TNFα-induced inflammatory response via Cav1-mediated ceramidase recruitment and activation in an AdipoR1- dependent fashion.

scholarly journals MiR-155-Mediated Deregulation of GPER1 Plays an Important Role in the Gender Differences Related to Inflammatory Bowel Disease

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Xiaojuan Shao ◽  
Jintao Li ◽  
Fumin Xu ◽  
Dongfeng Chen ◽  
Kaijun Liu
Keyword(s):  
Gender Differences ◽  
Inflammatory Bowel Disease ◽  
Estrogen Receptor ◽  
Inflammatory Response ◽  
Proinflammatory Cytokines ◽  
Bowel Disease ◽  
Clinical Characteristics ◽  
Intestinal Flora ◽  
Inflammatory Bowel ◽  
Proinflammatory Activity

Aim. The incidence and clinical manifestations of inflammatory bowel disease (IBD) are thought to have gender differences, which suggests that the estrogen signaling pathway and intestinal flora may play key roles in the pathogenesis of IBD. In IBD, microRNA-155 (miR-155) is upregulated and regulates G protein coupled estrogen receptor (GPER1), which affects the intestinal flora. The objective of this study was to investigate the role of the estrogen receptors and miR-155 in the pathogenesis of IBD. Methods. From July 2018 to July 2019, in the Department of Gastroenterology at Daping Hospital, Army Military Medical University, a total of 50 patients with IBD were included in this study, and 24 healthy examinees were randomly selected as the control group. Colonoscopies were performed, and clinical characteristics and blood samples were collected from all of the subjects. The serum cytokine levels in the patients with IBD and the health donors were detected by ELISA, and the estrogen receptor level measurements for all of the participants were assessed by immunohistochemistry (IHC) and quantitative real-time PCR (qPCR). The miR-155 levels were detected by qPCR in all of the participants, and miR-155−/− mice were used to investigate the mechanism of miR-155 in the pathogenesis of IBD. Results. The clinical characteristics and medications were different for the IBD patients when gender was considered. The male patients produced more proinflammatory cytokines, and while GPER1 expression was downregulated, miR-155 was upregulated in the patients with IBD. MiR-155 showed proinflammatory activity, while GPER1 showed an anti-inflammatory response during the pathogenesis of IBD. The miR-155−/− mice showed improvements in weight loss, survival, rectal bleeding, colon length, and histopathological changes compared with the wild-type mice. Furthermore, the male miR-155−/− mice showed increased inflammation compared to the female miR-155−/− mice in the above aspects. Conclusion. This study presents evidence indicating that miR-155 plays a key role in the pathogenesis of IBD for the different genders. MiR-155 was upregulated and showed proinflammatory activity, whereas GPER1 showed an anti-inflammatory response during the pathogenesis of IBD. The results demonstrated that more proinflammatory cytokines and reduced GPER1 levels were observed in the male IBD patients. Thus, miR-155 was involved in the regulation of GPER1 and induced gender differences in IBD patients. MiR-155 may be a potential marker for IBD-targeted therapy.

Co-administration of aqueous ginseng extract with tobramycin stimulates the pro-inflammatory response and promotes the killing of Pseudomonas aeruginosa in the lungs of infected rats

2013 ◽  
Vol 91 (11) ◽  
pp. 935-940 ◽  
Author(s):  
Misagh Alipour ◽  
Abdelwahab Omri ◽  
Edmund M.K. Lui ◽  
Zacharias E. Suntres
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Inflammatory Response ◽  
Body Mass ◽  
Intratracheal Instillation ◽  
Lung Infection ◽  
Male Rats ◽  
Control Group ◽  
Ginseng Extract ◽  
Gm Csf

North American ginseng is known to have immunomodulatory and antipseudomonal properties in vitro. In this study we investigated the effects of aqueous ginseng extract, either alone or in a combination with the antibiotic tobramycin, in an animal model of chronic Pseudomonas aeruginosa lung infection. The lungs of male rats (n = 5) were infected with P. aeruginosa (2 × 108 cfu/mL) in agar-beads by intratracheal instillation. Starting on day 7 post-infection, animals were treated daily for 3 consecutive days with saline, tobramycin (300 μg/kg body mass, intratracheal), and (or) ginseng (100 mg/kg body mass, subcutaneous); animals were sacrificed 24 h after the third drug treatment. Lung bacteria counts, cytokine levels in sera, and lung histopathology were examined. The treatment of infected animals with tobramycin [6.6 × 104 colony forming units (cfu)], ginseng (5.3 × 104 cfu), or tobramycin plus ginseng (2.0 × 103 cfu) lessened the lung infection compared with the control group (saline treated) (6.0 × 106 cfu). The levels of pro-inflammatory cytokines (IL-2, IL-4, IL-6, IL-12p70, IFN-γ, GM-CSF, TNF-α) in infected animals were significantly increased with co-treatment of ginseng plus tobramycin. These data suggest that co-administration of aqueous ginseng extract and tobramycin stimulated the pro-inflammatory response and promoted the killing of P. aeruginosa.

scholarly journals Identification of immunologic and clinical characteristics that predict inflammatory response to C. Novyi-NT bacteriolytic immunotherapy

2018 ◽  
Vol 14 (1) ◽  
Author(s):  
Amy E. DeClue ◽  
Sandra M. Axiak-Bechtel ◽  
Yan Zhang ◽  
Saurabh Saha ◽  
Linping Zhang ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Clinical Characteristics
Sign in / Sign up

Export Citation Format

Share Document