scholarly journals Outcome of Surgical Treatment in Late-Onset Capsular Block Syndrome

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Yang Huang ◽  
Zi Ye ◽  
Hang Li ◽  
Zhaohui Li
Keyword(s):  
Surgical Treatment ◽  
Inflammatory Cytokines ◽  
Aqueous Humor ◽  
Late Onset ◽  
Anterior Chamber Depth ◽  
Human Lens ◽  
Necrosis Factor Alpha ◽  
Before And After ◽  
Factor Alpha ◽  
Capsular Block Syndrome

Purpose. To further investigate the pathogenesis of late-onset capsular block syndrome (CBS) and to evaluate the safety of surgical treatment.Methods. Seven patients diagnosed with late-onset CBS were retrospectively analyzed. Anterior chamber depth (ACD), intraocular pressure (IOP), refractive diopter, and best-corrected visual acuity (BCVA) before and after surgery were recorded. The opaque substance was tested with Western blot, and a flow cytometer multiple array assay system was utilized to evaluate the levels of inflammatory cytokines from opaque substance and aqueous humor, respectively.Results. Patients who had undergone surgical treatment showed a significant BCVA and spherical equivalent refractive error improvement (P=0.002,P=0.021, resp.). Nevertheless, ACD and IOP before and after surgery were in normal range with no difference (P=0.165,P=0.749, resp.).αB-crystallin andβB-crystallin were detected in all opaque substances. Tumor necrosis factor-alpha (TNF-α) and interlukin-1β(IL-1β) levels in opaque substance were significantly higher than those in aqueous humor (P=0.038,P=0.007, resp.), while IL-2 and IL-6 were not detected in any samples.Conclusions. Opaque substance is derived from human lens epithelial cells. Inflammatory cytokines may be involved in the pathogenesis of late-onset CBS. In addition, surgical treatment is an effective approach. This trial is registered withChiCTR-IOR-17011287.

scholarly journals Patulin, Deoxynivalenol, Zearalenone and T-2 Toxin Affect Viability and Modulate Cytokine Secretion in J774A.1 Murine Macrophages

2016 ◽  
Vol 8 (2) ◽  
pp. 22 ◽  
Author(s):  
Jonathan H. Loftus ◽  
Gregor S. Kijanka ◽  
Richard O’Kennedy ◽  
Christine E. Loscher
Keyword(s):  
Inflammatory Cytokines ◽  
Inflammatory Cytokine ◽  
Cytokine Secretion ◽  
Low Doses ◽  
Necrosis Factor Alpha ◽  
Before And After ◽  
Food And Feed ◽  
Factor Alpha ◽  
Anti Inflammatory ◽  
High Doses

<p>Mycotoxins are secondary fungal metabolites, which occur in food and feed. They have detrimental effects on the health of humans and animals, and they are known to cause immunosuppression. In this study the effect of patulin, deoxynivalenol (DON), zearalenone (ZEN) and T-2 toxin exposure on the viability and the secretion of key pro- and anti-inflammatory cytokines from the murine macrophage cell line, J774A.1, was investigated.  Exposure of macrophages to high doses of ZEN (100,000 pg/mL) and T-2 toxin (10,000 and 100,000 pg/mL) resulted in a significant decrease (P &lt; 0.05 and P &lt; 0.01) in cell viability. Exposure of macrophages to these mycotoxins resulted in a dose-dependent modulation of cytokine secretion. Specifically, exposure to low doses of patulin (0.001, 0.1 and 1 pg/mL) resulted in a statistically significant decrease in the secretion of the pro-inflammatory cytokines interleukin (IL) 6 (IL-6) and tumor necrosis factor alpha (TNF-α), following stimulation with lipopolysaccharide (LPS), a component of Gram-negative bacterial cell walls. Treatment with low doses of DON (0.001 pg/mL) and ZEN (0.001 and 0.01 pg/mL) significantly decreased (P &lt; 0.01) the secretion of the pro-inflammatory cytokine IL-12p40, while several doses of T-2 toxin (0.001, 0.01, 0.1, 1 and 100 pg/mL) caused a significant decrease the expression of IL-6. Each of the mycotoxins also significantly increased the production of the anti-inflammatory cytokine IL-10, both before and after LPS stimulation. This data provides further insight into the mechanisms by which mycotoxins modulate the host immune response to exert their immunosuppressive activity.</p>

Experimental autoimmune encephalomyelitis-induced upregulation of tumor necrosis factor-alpha in the dorsal root ganglia

2009 ◽  
Vol 15 (10) ◽  
pp. 1135-1145 ◽  
Author(s):  
M. Melanson ◽  
P. Miao ◽  
D. Eisenstat ◽  
Y. Gong ◽  
X. Gu ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Tumor Necrosis Factor ◽  
Inflammatory Cytokines ◽  
Dorsal Root ◽  
Tumor Necrosis ◽  
Autoimmune Encephalomyelitis ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Necrosis Factor ◽  
Experimental Autoimmune

Background: Multiple sclerosis (MS) is a chronic, neurological disease characterized by targeted destruction of central nervous system (CNS) myelin. The autoimmune theory is the most widely accepted explanation of disease pathology. Circulating Th1 cells become activated by exposure to CNS-specific antigens such as myelin basic protein. The activated Th1 cells secrete inflammatory cytokines, which are pivotal for inflammatory responses. We hypothesize that enhanced production of inflammatory cytokines triggers cellular events within the dorsal root ganglia (DRG) and/or spinal cord, facilitating the development of neuropathic pain (NPP) in MS. NPP, the second worst disease-induced symptom suffered by patients with MS, is normally regulated by DRG and/or spinal cord. Objective: To determine gene and protein expression levels of tumor necrosis factor-alpha (TNFα) within DRG and/or spinal cord in an animal model of MS. Methods: Experimental autoimmune encephalomyelitis (EAE) was induced in adolescent female Lewis rats. Animals were sacrificed every 3 days post-disease induction. DRG and spinal cords were harvested for protein and gene expression analysis. Results: We show significant increases in TNFα expression in the DRG and of EAE animals at peak disease stage, as assessed by clinical symptoms. Conclusion: Antigen-induced production of inflammatory cytokines such as TNFα within the DRG identifies a potential novel mechanism for MS-induced NPP.

scholarly journals Profiling of inflammatory cytokines in patients with caustic gastrointestinal tract injury

PLoS ONE ◽  
2021 ◽  
Vol 16 (11) ◽  
pp. e0260012
Author(s):  
Hao-Tsai Cheng ◽  
Chen-June Seak ◽  
Chien-Cheng Cheng ◽  
Tsung-Hsing Chen ◽  
Chang-Mu Sung ◽  
...  
Keyword(s):  
Gastrointestinal Tract ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Inflammatory Cytokines ◽  
Tumor Necrosis ◽  
Necrosis Factor Alpha ◽  
Gastrointestinal Complications ◽  
Severe Group ◽  
Factor Alpha ◽  
Necrosis Factor

Introduction Study of inflammatory cytokines in patients with caustic gastrointestinal tract injury is sketchy. This study investigated the cytokine profiling of patients with caustic substance ingestion, and analyzed the differences between patients with severe and mild injury. Methods This prospective, cross-sectional study enrolled 22 patients admitted to Chang Gung Memorial Hospital between March and October 2018. All patients underwent esophagogastroduodenoscopy in 24 hours. Patients were categorized into two subgroups, as mild (<2b, n = 11) or severe (≥2b, n = 11) group. Results The neutrophil count was higher in severe than mild group (P = 0.032). Patients in mild and severe groups exhibited significantly higher circulating inflammatory cytokines than healthy control, including interleukin (IL)-2, IL-5, IL-8, IL-9, IL-12, IL-13, interferon-gamma inducible protein-10, macrophage inflammatory protein-1 beta, regulated upon activation, normal T cell expressed and presumably secreted and tumor necrosis factor-alpha. Furthermore, the levels of IL-2 and tumor necrosis factor-alpha were significantly higher in patients with severe group than mild group. Although there was no difference in cumulative survival between both groups (P = 0.147), the severe group received more operations (P = 0.035) and suffered more gastrointestinal complications (P = 0.035) than mild group. Conclusion Caustic substance ingestion produces mucosal damages and leads to excessive neutrophils and inflammatory cytokines in peripheral blood.

Angiography significantly decreased serum levels of IL-8 independent of artery stenosis

2020 ◽  
Author(s):  
Lida Zare ◽  
Akram Eidi ◽  
Mohammad Safarian ◽  
Mohammad Kazemi Arababadi
Keyword(s):  
Protective Factor ◽  
Serum Levels ◽  
Artery Stenosis ◽  
Enzyme Linked Immunosorbent Assay ◽  
Dependent Manner ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Before And After ◽  
Elisa Technique ◽  
Factor Alpha

Abstract Background Angiography is a safe cardiovascular technique for the diagnosis and treatment of the cardiovascular disorders. The potential effects of angiography on the cytokines are yet to be clarified completely. Interleukin-8 (IL-8) and tumor necrosis factor-alpha (TNF-α) are the important pro-inflammatory cytokines that participate in the pathogenesis of artery stenosis. The aim of his project was to study the angiography effects on the serum levels of IL-8 and TNF-α. Methods Fifty-five participants in three groups, without, with one and with more than one artery stenosis, were explored in this project. Serum levels of IL-8 and TNF-α were measured in the participants before and after angiography using enzyme linked immunosorbent assay (ELISA) technique. Results Serum levels of IL-8, but not TNF-α, were significantly decreased following angiography. X-ray doses had moderate positive correlation with serum levels of TNF-α in the patients with more than one artery stenosis. Serum levels of IL-8 and TNF-α were not different among male and female participants in all groups. Discussion Angiography may be a protective factor for inflammation in IL-8 dependent manner. Using angiography in the patients with more than one artery stenosis needs to be executed cautiously.

scholarly journals Babesia bovis-Stimulated Macrophages Express Interleukin-1β, Interleukin-12, Tumor Necrosis Factor Alpha, and Nitric Oxide and Inhibit Parasite Replication In Vitro

2000 ◽  
Vol 68 (9) ◽  
pp. 5139-5145 ◽  
Author(s):  
Lisl K. M. Shoda ◽  
Guy H. Palmer ◽  
Jorge Florin-Christensen ◽  
Monica Florin-Christensen ◽  
Dale L. Godson ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Inflammatory Cytokines ◽  
Tumor Necrosis ◽  
Acute Infection ◽  
Babesia Bovis ◽  
Necrosis Factor Alpha ◽  
Parasite Replication ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT The tick-transmitted hemoparasite Babesia bovis causes an acute infection that results in persistence and immunity against challenge infection in cattle that control the initial parasitemia. Resolution of acute infection with this protozoal pathogen is believed to be dependent on products of activated macrophages (Mφ), including inflammatory cytokines and nitric oxide (NO) and its derivatives.B. bovis stimulates inducible nitric oxide synthase (iNOS) and production of NO in bovine Mφ, and chemical donors of NO inhibit the growth of B. bovis in vitro. However, the induction of inflammatory cytokines in Mφ by babesial parasites has not been described, and the antiparasitic activity of NO produced by B. bovis-stimulated Mφ has not been definitively demonstrated. We report that monocyte-derived Mφ activated by B. bovisexpressed enhanced levels of inflammatory cytokines interleukin-1β (IL-1β), IL-12, and tumor necrosis factor alpha that are important for stimulating innate and acquired immunity against protozoal pathogens. Furthermore, a lipid fraction of B. bovis-infected erythrocytes stimulated iNOS expression and NO production by Mφ. Cocultures of Mφ and B. bovis-infected erythrocytes either in contact or physically separated resulted in reduced parasite viability. However, NO produced by bovine Mφ in response to B. bovis-infected erythrocytes was only partially responsible for parasite growth inhibition, suggesting that additional factors contribute to the inhibition of B. bovis replication. These findings demonstrate that B. bovis induces an innate immune response that is capable of controlling parasite replication and that could potentially result in host survival and parasite persistence.

scholarly journals Human serum IgA downregulates the release of inflammatory cytokines (tumor necrosis factor-alpha, interleukin-6) in human monocytes

Blood ◽  
1994 ◽  
Vol 83 (5) ◽  
pp. 1278-1288 ◽  
Author(s):  
HM Wolf ◽  
MB Fischer ◽  
H Puhringer ◽  
A Samstag ◽  
E Vogel ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Inflammatory Cytokines ◽  
Tumor Necrosis ◽  
Tnf Alpha ◽  
Human Monocytes ◽  
Necrosis Factor Alpha ◽  
Serum Iga ◽  
Iga Antibodies ◽  
Factor Alpha ◽  
Necrosis Factor

Abstract While the protective effect of IgA antibodies against infection of the mucosal surfaces is well documented, the mechanisms involved are not entirely clear. The aim of the current study is to investigate the effect of human serum IgA on the release of inflammatory cytokines in human monocytes activated with a particulate stimulus, Haemophilus influenzae type b (Hib), or soluble lipopolysaccharide (LPS) purified from Escherichia coli. Our results show that IgA downregulates tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) production, whereas IgG examined in parallel had no effect. IgA had no inhibitory effect on Hib-induced granulocyte-macrophage colony-stimulating factor release. TNF-alpha and IL-6 release were downmodulated if IgA was present during cytokine induction, and IgA was also inhibitory if added to Hib-pretreated monocytes during the phase of cytokine release. These findings indicate that there are at least two mechanisms whereby IgA antibodies can downregulate TNF-alpha and IL-6 release in human monocytes: by a mechanism acting during the time of monocyte activation, and a mechanism that downregulates the production and/or the release of these cytokines in activated monocytes. Regulation of TNF-alpha and IL-6 release by IgA may be among the antiinflammatory mechanisms preventing an uncontrolled release of potentially noxious levels of inflammatory cytokines during acute and/or chronic inflammation.

scholarly journals Human serum IgA downregulates the release of inflammatory cytokines (tumor necrosis factor-alpha, interleukin-6) in human monocytes

Blood ◽  
1994 ◽  
Vol 83 (5) ◽  
pp. 1278-1288 ◽  
Author(s):  
HM Wolf ◽  
MB Fischer ◽  
H Puhringer ◽  
A Samstag ◽  
E Vogel ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Inflammatory Cytokines ◽  
Tumor Necrosis ◽  
Tnf Alpha ◽  
Human Monocytes ◽  
Necrosis Factor Alpha ◽  
Serum Iga ◽  
Iga Antibodies ◽  
Factor Alpha ◽  
Necrosis Factor

While the protective effect of IgA antibodies against infection of the mucosal surfaces is well documented, the mechanisms involved are not entirely clear. The aim of the current study is to investigate the effect of human serum IgA on the release of inflammatory cytokines in human monocytes activated with a particulate stimulus, Haemophilus influenzae type b (Hib), or soluble lipopolysaccharide (LPS) purified from Escherichia coli. Our results show that IgA downregulates tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) production, whereas IgG examined in parallel had no effect. IgA had no inhibitory effect on Hib-induced granulocyte-macrophage colony-stimulating factor release. TNF-alpha and IL-6 release were downmodulated if IgA was present during cytokine induction, and IgA was also inhibitory if added to Hib-pretreated monocytes during the phase of cytokine release. These findings indicate that there are at least two mechanisms whereby IgA antibodies can downregulate TNF-alpha and IL-6 release in human monocytes: by a mechanism acting during the time of monocyte activation, and a mechanism that downregulates the production and/or the release of these cytokines in activated monocytes. Regulation of TNF-alpha and IL-6 release by IgA may be among the antiinflammatory mechanisms preventing an uncontrolled release of potentially noxious levels of inflammatory cytokines during acute and/or chronic inflammation.

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