scholarly journals Chronic Stress-Induced Changes in Pro-Inflammatory Cytokines and Spinal Glia Markers in the Rat: A Time Course Study

2012 ◽  
Vol 19 (6) ◽  
pp. 367-376 ◽  
Author(s):  
Viktoriya Golovatscka ◽  
Helena Ennes ◽  
Emeran A. Mayer ◽  
Sylvie Bradesi
Keyword(s):  
Chronic Stress ◽  
Inflammatory Cytokines ◽  
Time Course ◽  
Time Course Study ◽  
Induced Changes ◽  
Pro Inflammatory Cytokines

893 PRO-Inflammatory Cytokines and Spinal Glia Markers in the Model of Chronic Water Avoidance Stress: A Time Course Study

2012 ◽  
Vol 142 (5) ◽  
pp. S-156
Author(s):  
Sylvie Bradesi ◽  
Viktoriya Golovatscka ◽  
Helena S. Ennes ◽  
Emeran A. Mayer
Keyword(s):  
Inflammatory Cytokines ◽  
Time Course ◽  
Time Course Study ◽  
Pro Inflammatory Cytokines

scholarly journals MORPHOLOGY OF NASAL POLYPS IN PATIENTS WITH ALTERED IMMUNOLOGICAL REACTIVITY

2017 ◽  
Vol 25 (4) ◽  
pp. 22-26
Author(s):  
P. A. Sukhachev ◽  
O. S. Sergeev ◽  
I. O. Prokhorenko ◽  
M. I. Panina
Keyword(s):  
Mast Cells ◽  
Chronic Stress ◽  
Inflammatory Cytokines ◽  
Final Stage ◽  
Nasal Polyps ◽  
Early Stage ◽  
Ciliated Epithelium ◽  
Immunological Reactivity ◽  
Typical Picture ◽  
Pro Inflammatory Cytokines

Morphological-functional characteristics of nasal polyps were studied in 88 patients with rhinosinusitis polyps. The tissue of a polyp had typical picture, multi-rows ciliated epithelium with a large number of goblet celts. Different stages of polyp maturation were observed: from edematous to perivascular and diffuse cellular infiltrates consisting of eosinophils, lymphocytes and mast cells. Their presence proves allergic nature of rhinosinusitis, which as any pathology process by stress is accompanied. At the early stage, chronic stress downregulate pro-inflammatory cytokines, while upregulating the anti-inflammatory cytokines. All the steps induced continued increased pro-inflammatory cytokines and finally inflammation, which induce various diseases. The final stage of polyp maturation was characterized by fibrous induration of its stroma with cirrhosis signs.

The time course of particle-induced cell migration correlates with up-regulation of pro-inflammatory cytokines and chemokines

2015 ◽  
Vol 238 (2) ◽  
pp. S180-S181
Author(s):  
G. Westphal ◽  
I. Schremmer ◽  
A. Bryk ◽  
N. Rosenkranz ◽  
D. Weber ◽  
...  
Keyword(s):  
Cell Migration ◽  
Inflammatory Cytokines ◽  
Time Course ◽  
Cytokines And Chemokines ◽  
Pro Inflammatory Cytokines

scholarly journals Oxidative modification of the intestinal mucus layer is a critical but unrecognized component of trauma hemorrhagic shock-induced gut barrier failure

2013 ◽  
Vol 304 (1) ◽  
pp. G57-G63 ◽  
Author(s):  
Jordan E. Fishman ◽  
Gal Levy ◽  
Vamsi Alli ◽  
Sharvil Sheth ◽  
Qu Lu ◽  
...  
Keyword(s):  
Free Radical ◽  
Hemorrhagic Shock ◽  
Antioxidant Capacity ◽  
Total Antioxidant Capacity ◽  
Time Course ◽  
Mucus Layer ◽  
Gut Barrier ◽  
Total Antioxidant ◽  
Time Course Study ◽  
Induced Changes

Recent studies demonstrate that mechanisms underlying gut barrier failure include systemic processes and less studied luminal processes. We thus tested the hypothesis that mucus layer oxidation is a component of trauma/hemorrhagic shock-induced gut injury and dysfunction. Male Sprague-Dawley rats underwent trauma/hemorrhagic shock. Controls underwent trauma only. Mucus from the terminal 30 cm of the ileum was collected, processed, and analyzed for reactive nitrogen intermediates (RNI)-mediated damage, reactive oxygen species (ROS)-induced damage, and total antioxidant capacity. The distal ileum was stained to quantify the mucus layer; gut permeability was assessed physiologically. A time course study was conducted to determine the temporal sequence of mucus layer damage. The role of free radical-mediated damage to the gut barrier was investigated by the effect of the free radical scavenger dimethyl sulfoxide on trauma/hemorrhagic shock-induced changes on the mucus and on gut permeability. Trauma/hemorrhagic shock increased intestinal permeability, which was associated with evidence of loss of the unstirred mucus layer. These changes correlated with increased ROS- and RNI-mediated mucus damage and loss of mucus total antioxidant capacity. Based on the time course study, ROS-mediated mucus damage and loss of total antioxidant capacity were present immediately following shock, whereas RNI-mediated damage was delayed for 3 h. Dimethyl sulfoxide ameliorated gut barrier loss, ROS-mediated changes to the mucus layer, and loss of total antioxidant capacity. There was no change in RNI-induced changes to the mucus layer. These results support the hypothesis that trauma/hemorrhagic shock leads to mucus damage and gut dysfunction through the generation of free radical species.

scholarly journals Simultaneous proteomics and three PTMomics characterization of pro-inflammatory cytokines stimulated INS-1E cells using TiO2enrichment strategy

2019 ◽  
Author(s):  
Honggang Huang ◽  
Lylia Drici ◽  
Pernille S. Lassen ◽  
Giuseppe Palmisano ◽  
Martin R. Larsen
Keyword(s):  
Signaling Pathways ◽  
Inflammatory Cytokines ◽  
Cellular Localization ◽  
Time Course ◽  
Fine Tuning ◽  
Β Cell ◽  
Form Complex ◽  
Post Translational Modifications ◽  
Pro Inflammatory Cytokines

AbstractDiverse protein post-translational modifications (PTMs) in proteins form complex combinatorial patterns to regulate the protein function and biological processes in a fine-tuning manner. Reversible phosphorylation, cysteines (Cys) modification, and N-linked glycosylation are essentially involved in cellular signaling pathways of pro-inflammatory cytokines, which can induce beta cell death and diabetes. Here we developed a novel mass spectrometry–based proteomic strategy (termed TiCPG) for the simultaneous comprehensive characterization of the proteome and three post-translational modifications (PTMomes) by applying TiO2enrichment of peptides with reversibly modified Cysteine (rmCys), Phosphorylation, and sialylated N-linked (SAN-) Glycosylation from low amount of sample material with largely minimized sample loss. We applied this TiCPG strategy to quantitatively study the change of the three PTMs in β-cell-like INS-1E cells subject to pro-inflammatory cytokines stimulation. It enabled efficient enrichment and quantitative analysis of 8346 rmCys sites, 10321 phosphosites and 1906 SAN-glycosylation sites from 5853 proteins. Significant regulation was found on 100 proteins at the total protein level, while much higher degree of regulation was identified on 3025 peptides with PTMs from 1490 proteins. The three PTMs were co-regulated in proteins, but demonstrated differential spatial and temporal patterns related to protein cellular localization and function in the time course of cytokines stimulation, and they were extensively involved in essential signaling pathways related to pro-inflammatory cytokine mediated β-cell apoptosis, such as the inducible NO synthase (NOS2) signaling pathway, Overall, the TiCPG strategy is proved as a straight forward and powerful tool for multiple PTMomics studies.

Pregnancy- and lactation-induced changes in active intestinal calcium transport in rats

1992 ◽  
Vol 263 (1) ◽  
pp. G127-G134 ◽  
Author(s):  
A. Boass ◽  
J. A. Lovdal ◽  
S. U. Toverud
Keyword(s):  
Time Course ◽  
Late Pregnancy ◽  
Serum Prolactin ◽  
Marked Rise ◽  
Pregnant Rats ◽  
Ca Transport ◽  
Everted Gut Sac ◽  
Pregnancy And Lactation ◽  
Time Course Study ◽  
Induced Changes

A time course study of active Ca transport in the duodenum and the terminal ileum was conducted using the everted gut sac technique during the last week of pregnancy and throughout lactation. A triphasic pattern was revealed in the proximal duodenum: a marked rise between 18 and 20 days of pregnancy, a plateau maintained during the last 3 days of pregnancy and the first 2-3 days of lactation, and a fall by day 4 of lactation. The late-pregnancy rise was significant also when expressed as milligrams Ca transported relative to tissue weight, indicating that intestinal hypertrophy was not the cause of the increase. The ratio of serosal to mucosal Ca concentration remained low until approximately day 11 of lactation, when it rose toward a new peak. There was no active Ca transport in the ileum until the third week of lactation. Serum prolactin levels increased 10-fold between 18 and 20 days of pregnancy and remained high until at least day 7 of lactation, but did not correlate significantly with duodenal Ca transport. Injected rat prolactin did not result in a precocious rise in Ca transport in pregnant rats. The fluctuations in duodenal Ca transport during lactation were reflected by a small, but statistically significant, decrease in net fractional Ca absorption at 6-9 days compared with either 2-4 days or 13-16 days. We suggest that duodenal active Ca transport plays only a small role in total intestinal Ca absorption in the lactating rat except when dietary Ca is greatly restricted.

A New Model of Acute Sickle Cell Vaso-Occlusion Elicited by IgGMediated Hemolytic Transfusion Reactions

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 122-122
Author(s):  
Jung-Eun Jang ◽  
Paul S. Frenette
Keyword(s):  
Inflammatory Cytokines ◽  
Sickle Cell ◽  
Murine Model ◽  
Time Course ◽  
White Blood Cells ◽  
Single Amino Acid ◽  
Rank Test ◽  
Transfusion Therapy ◽  
Pro Inflammatory Cytokines

Abstract Sickle cell disease (SCD) is caused by a single amino acid substitution in the β-globin chain of hemoglobin. Acute vaso-occlusive crisis (VOC) is an important complication of SCD and is a major cause of morbidity and mortality for these patients. Red blood cell (RBC) transfusion therapy is widely used to manage SCD. However, IgG-mediated delayed hemolytic transfusion reaction (HTR) represent a serious side effect of transfusion therapy, and HTR can frequently trigger VOC in SCD patients. To understand HTR pathophysiology in SCD, we established a model of alloimmune IgG-mediated HTRs using a well-characterized humanized murine model of SCD (Paszty et al., Science 1997). We previously showed that VOC in this murine model of SCD is caused by interactions in the microvasculature between sickle RBCs and adherent white blood cells (WBCs) (Turhan et al, P.N.A.S. 2002). In addition, because IgG-mediated HTRs in wild-type (WT) mice are associated with a cytokine storm (Hod et al., Blood 2008), we hypothesized that the circulating pro-inflammatory cytokines induced by HTRs would lead to VOC in the murine model of SCD. To this end, fluorescently labeled RBCs from human glycophorin A transgenic (hGPA-Tg) or WT mice were transfused into SCD mice that had been passively immunized with an IgG monoclonal anti-hGPA antibody. Serial flow cytometry analyses revealed that the survival of incompatible hGPA-Tg RBCs in passively immunized SCD mice was 42 ± 10% 2 hours after transfusion, whereas the survival of compatible WT RBCs was 98 ± 2%. Using intravital microscopy, we examined leukocyte recruitment in post-capillary and collecting venules, and evaluated the interactions between RBCs and WBCs in passively immunized mice that were not previously treated with inflammatory cytokines. As compared to the transfusion of compatible WT RBCs, transfusion of incompatible hGPA-Tg RBCs significantly increased leukocyte adhesion to the endothelium by 1.6 fold (2,669 ± 186 vs 1,717 ± 107 adherent WBCs per mm2; p<0.001) and sickle RBC-leukocyte interactions by 3.9 fold between 91 and 120 minutes (1.1 ± 0.2 vs 0.3 ± 0.2 RBC-WBC interactions per minute; p=0.01), leading to acute VOC in post-capillary venules by the 2 hour time point. Moreover, the survival of SCD mice transfused with incompatible RBCs was significantly shorter (by 3 hours) than control mice transfused with compatible RBCs (p=0.04, Log rank test). The time course of these complications correlated with increased levels of circulating pro-inflammatory cytokines (e.g. MCP-1, MIP-1β, KC) at 2 hours following incompatible transfusion, suggesting that endogenously produced cytokines may play an important role in the pathophysiology of VOC in this model. In conclusion, these in vivo results indicate that this IgG-mediated HTR model in SCD mice reproduces the VOC seen in SCD patients experiencing delayed HTRs. This model will be useful to identify the key inflammatory cytokine(s) that can trigger VOC and design novel therapies to alleviate this major manisfestation of the disease.

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