Gut ischemia and mesenteric synthesis of inflammatory cytokines after hemorrhagic or endotoxic shock

1997 ◽  
Vol 273 (2) ◽  
pp. G314-G321 ◽  
Author(s):  
F. Tamion ◽  
V. Richard ◽  
S. Lyoumi ◽  
M. Daveau ◽  
G. Bonmarchand ◽  
...  
Keyword(s):  
Gene Expression ◽  
Intestinal Ischemia ◽  
Ischemia Reperfusion ◽  
Multiorgan Failure ◽  
Endotoxic Shock ◽  
Cytokine Gene Expression ◽  
Tnf Alpha ◽  
Cytokine Gene ◽  
Necrosis Factor Alpha ◽  
Intestinal Ischemia Reperfusion

The intestine plays a major role in the pathophysiology of multiorgan failure. Although the systemic inflammatory response might be induced by endotoxin released through bacterial translocation, other factors such as intestinal ischemia might be implicated. We investigated the relationship between intestinal ischemia-reperfusion and cytokine release in rat models of hemorrhagic or endotoxic shock. Plasma levels of tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), lactate, and endotoxin, as well as macrophage TNF-alpha and IL-6 mRNA expression, were assessed at the end of shock and resuscitation. Hemodynamic changes and lactate levels suggested the presence of intestinal ischemia in both models. Mesenteric levels of TNF-alpha and IL-6 were increased by hemorrhage and further increased after saline resuscitation. Similar results were obtained with mRNA cytokine gene expression in macrophages. Endotoxin was not detectable in the hemorrhagic group. Endotoxic shock also increased production of cytokines, which, in contrast to hemorrhage, was not further increased by resuscitation. These results suggest that intestinal ischemia-reperfusion upon hemorrhage and resuscitation may be a major trigger for cytokine gene expression in the absence of endotoxin.

scholarly journals Patterns of cytokine gene expression in infectious mononucleosis

Blood ◽  
1994 ◽  
Vol 83 (3) ◽  
pp. 707-712 ◽  
Author(s):  
HD Foss ◽  
H Herbst ◽  
M Hummel ◽  
I Araujo ◽  
U Latza ◽  
...  
Keyword(s):  
Gene Expression ◽  
Infectious Mononucleosis ◽  
Clinical Presentation ◽  
Gene Expression Pattern ◽  
Cytokine Gene Expression ◽  
Tnf Alpha ◽  
High Signal ◽  
Cytokine Gene ◽  
Necrosis Factor Alpha ◽  
Infected Cells

Abstract Primary infection with Epstein-Barr virus (EBV) may arise as infectious mononucleosis (IM) in adolescents and young adults. Morphologically, IM- affected lymphoid tissue is characterized by expanded interfollicular areas with formation of atypical lymphoid blasts. It is assumed that morphology and clinical presentation of IM are related to characteristic patterns of cytokine production by EBV-infected and reactive cells. We studied IM tonsils of eight patients and six normal tonsils with a double in situ hybridization procedure using [35S]- labeled RNA probes specific for various cytokines and digoxigenin- labeled probes for the detection of the nuclear EBV encoded RNA transcripts, EBER 1 and 2. All of the IM cases displayed the same distinct cytokine gene expression pattern. When compared with interfollicular areas of normal tonsils, expression of lymphotoxin (LT), tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), and IL-1 beta, but not IL-8 or IL-1 alpha was strongly enhanced in interfollicular areas in IM tonsils. LT was expressed predominantly by EBV-infected cells. TNF-alpha transcripts were also present in EBV- infected cells, although in smaller proportions. IL-6 specific signals were only found in few EBV-infected cells. IL-1 alpha-, IL-1 beta-, and IL-8-specific signals were not observed in EBV-infected cells, but were present at high signal intensity in many cells within and around foci of EBV-infected cells (IL-1 beta), next to areas of necrosis (IL-8, IL- 1 beta), or in epithelial cells (IL-1 alpha). These data suggest that EBV infection in form of IM results in induction of specific sets of cytokine genes in EBV-infected and in neighboring EBV-negative cells contributing to the characteristic morphology and cellular arrangement of the lesion as well as the clinical presentation.

scholarly journals Patterns of cytokine gene expression in infectious mononucleosis

Blood ◽  
1994 ◽  
Vol 83 (3) ◽  
pp. 707-712 ◽  
Author(s):  
HD Foss ◽  
H Herbst ◽  
M Hummel ◽  
I Araujo ◽  
U Latza ◽  
...  
Keyword(s):  
Gene Expression ◽  
Infectious Mononucleosis ◽  
Clinical Presentation ◽  
Gene Expression Pattern ◽  
Cytokine Gene Expression ◽  
Tnf Alpha ◽  
High Signal ◽  
Cytokine Gene ◽  
Necrosis Factor Alpha ◽  
Infected Cells

Primary infection with Epstein-Barr virus (EBV) may arise as infectious mononucleosis (IM) in adolescents and young adults. Morphologically, IM- affected lymphoid tissue is characterized by expanded interfollicular areas with formation of atypical lymphoid blasts. It is assumed that morphology and clinical presentation of IM are related to characteristic patterns of cytokine production by EBV-infected and reactive cells. We studied IM tonsils of eight patients and six normal tonsils with a double in situ hybridization procedure using [35S]- labeled RNA probes specific for various cytokines and digoxigenin- labeled probes for the detection of the nuclear EBV encoded RNA transcripts, EBER 1 and 2. All of the IM cases displayed the same distinct cytokine gene expression pattern. When compared with interfollicular areas of normal tonsils, expression of lymphotoxin (LT), tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), and IL-1 beta, but not IL-8 or IL-1 alpha was strongly enhanced in interfollicular areas in IM tonsils. LT was expressed predominantly by EBV-infected cells. TNF-alpha transcripts were also present in EBV- infected cells, although in smaller proportions. IL-6 specific signals were only found in few EBV-infected cells. IL-1 alpha-, IL-1 beta-, and IL-8-specific signals were not observed in EBV-infected cells, but were present at high signal intensity in many cells within and around foci of EBV-infected cells (IL-1 beta), next to areas of necrosis (IL-8, IL- 1 beta), or in epithelial cells (IL-1 alpha). These data suggest that EBV infection in form of IM results in induction of specific sets of cytokine genes in EBV-infected and in neighboring EBV-negative cells contributing to the characteristic morphology and cellular arrangement of the lesion as well as the clinical presentation.

scholarly journals Comparative Effects of Triflusal, S-Adenosylmethionine, and Dextromethorphan over Intestinal Ischemia/Reperfusion Injury

2011 ◽  
Vol 11 ◽  
pp. 1886-1892
Author(s):  
Carlos R. Cámara-Lemarroy ◽  
Francisco J. Guzmán-de la Garza ◽  
Paula Cordero-Pérez ◽  
Gabriela Alarcón-Galván ◽  
Liliana Torres-Gonzalez ◽  
...  
Keyword(s):  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Intestinal Morphology ◽  
Tnf Alpha ◽  
Necrosis Factor Alpha ◽  
Total Antioxidant ◽  
Factor Alpha ◽  
Endogenous Antioxidant ◽  
Intestinal Ischemia Reperfusion ◽  
Necrosis Factor

Ischemia/reperfusion (I/R) is a condition that stimulates an intense inflammatory response. No ideal treatment exists. Triflusal is an antiplatelet salicylate derivative with anti-inflammatory effects. S-adenosylmethionine is a metabolic precursor for glutathione, an endogenous antioxidant. Dextromethorphan is a low-affinity N-methyl-D-aspartate receptor inhibitor. There is evidence that these agents modulate some of the pathways involved in I/R physiopathology. Intestinal I/R was induced in rats by clamping the superior mesenteric artery for 60 minutes, followed by 60 minutes of reperfusion. Rats either received saline or the drugs studied. At the end of the procedure, serum concentrations of tumor necrosis factor-alpha (TNF-alpha), malonaldehyde (MDA), and total antioxidant capacity (TAC) were determined and intestinal morphology analyzed. I/R resulted in tissue damage, serum TNF-alpha and MDA elevations, and depletion of TAC. All drugs showed tissue protection. Only triflusal reduced TNF-alpha levels. All drugs lowered MDA levels, but only triflusal and S-adenosylmethionine maintained the serum TAC.

scholarly journals Intestinal ischemia/reperfusion induces bronchial hyperreactivity and increases serum TNF-alpha in rats

Clinics ◽  
2006 ◽  
Vol 61 (1) ◽  
pp. 21-28 ◽  
Author(s):  
Marcio Jose Cristiano de Arruda ◽  
Renato Sergio Poggetti ◽  
Belchor Fontes ◽  
Riad N. Younes ◽  
Almerindo Lourenço Souza Jr. ◽  
...  
Keyword(s):  
Intestinal Ischemia ◽  
Ischemia Reperfusion ◽  
Bronchial Hyperreactivity ◽  
Tnf Alpha ◽  
Intestinal Ischemia Reperfusion

Abstract P100: Gene Targeting of Npr1 Reveals Its Repressive Role in Cardiac Hypertrophy and Proinflammatory Cytokine Gene Expression

2011 ◽  
Vol 109 (suppl_1) ◽  
Author(s):  
Kailash N Pandey ◽  
Elangovan Vellaichamy
Keyword(s):  
Gene Expression ◽  
Guanylyl Cyclase ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Cytokine Gene Expression ◽  
Heart Weight ◽  
Cytokine Gene ◽  
Wild Type ◽  
Necrosis Factor Alpha ◽  
Natriuretic Peptide Receptor A

The objective of the present study was to examine whether genetically determined differences in the Npr1 gene (coding for guanylyl cyclase/natriuretic peptide receptor-A; GC-A/NPRA) affect the expression of cardiac pro-inflammatory cytokines and nuclear factor kappa-B (NF-kB) levels in Npr1 gene-targeted mice. The Npr1 gene-disrupted null mutant ( Npr1 −/− ; 0-copy) mice had 32-38 mmHg higher systolic blood pressure (SBP) and 60% greater heart weight to body weight (HW:BW) ratio, however, Npr1 gene-duplicated mice ( Npr1 ++/++ ; 4-copy) exhibited 10-15 mmHg lower SBP with no change in the HW:BW ratio compared with wild-type ( Npr1 +/+ ; 2-copy) mice. Significant up-regulation of interleukin-6 (IL-6; 2-fold tumor necrosis factor-alpha), TNF-α; 4-fold), and transforming growth factor-beta (TGF-β1; 4-fold), along with increases in NF-κB and activating protein-1 (AP-1) binding activities (170% and 130%, p < 0.01, respectively), were increased in the Npr1 −/− mice hearts. Conversely, a significant decrease in cytokine gene expression and NF-κB and AP-1 binding activities were found in gene-duplicated mice hearts compared with wild-type mice. The ventricular guanylyl cyclase (GC) activity and cGMP levels were reduced by almost 10-fold and 5-fold, respectively, in Npr1 -/- mice. However, GC activity and cGMP levels were increased, respectively, by almost 9-fold and 6-fold, respectively, in gene-duplicated mice. The present results provide direct evidence that duplication of Npr1 gene in mice represses the inflammatory cytokine gene expression via inhibition NF-κB- and AP-1-mediated signaling mechanisms, and is associated with cardiac protection.

scholarly journals A distinct pattern of cytokine gene expression by human CD83+ blood dendritic cells

Blood ◽  
1995 ◽  
Vol 86 (9) ◽  
pp. 3295-3301 ◽  
Author(s):  
LJ Zhou ◽  
TF Tedder
Keyword(s):  
Gene Expression ◽  
Dendritic Cells ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Distinct Pattern ◽  
Cytokine Gene Expression ◽  
Cytokine Gene ◽  
Tgf Beta ◽  
Necrosis Factor Alpha ◽  
Gm Csf

Dendritic cells are the most potent antigen-presenting cells of the immune system. Although dendritic cells are likely to secrete selective cytokines that facilitate antigen presentation, the difficulty in isolating pure dendritic cells in sufficient numbers has made assessment of this function imprecise. In this study, pure populations of CD83+ human blood dendritic cells were isolated by previously established enrichment procedures and subsequent cell sorting. Cytokine gene expression was assessed by reverse transcription-polymerase chain reaction (RT-PCR) amplification of mRNA. Resting CD83+ dendritic cells expressed interleukin-6 (IL-6), IL-8, IL-10, tumor necrosis factor- alpha (TNF-alpha), and transforming growth factor-beta 1 (TGF-beta 1) mRNA, while activation of cells with phorbol myristate acetate induced IL-1 alpha and beta, IL-9, TNF-beta, interferon-gamma, granulocyte- macrophage colony-stimulating factor (GM-CSF), M-CSF, and G-CSF mRNA expression. Resting CD83+ cells also expressed the Rantes, MCP-1, MIP-1 alpha, and MIP-1 beta chemokines, with 1–309 expression induced upon activation. Resting and activated CD83+ dendritic cells also expressed receptors for IL-2 (CD25), TGF-beta 1 and -beta 3, and GM-CSF as determined by indirect immunofluorescence staining. These results indicate that dendritic cells have the ability to produce a variety of soluble factors which are likely to contribute substantially to the potent allostimulatory activity of these cells.

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