scholarly journals Traumatic Reticuloperitonitis in Water Buffalo (Bubalus bubalis): Clinical Findings and the Associated Inflammatory Response

2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Maged El-Ashker ◽  
Mohamed Salama ◽  
Mohamed El-Boshy
Keyword(s):  
Inflammatory Response ◽  
Water Buffalo ◽  
Bubalus Bubalis ◽  
Clinical Findings ◽  
Necrosis Factor Alpha ◽  
Reactive Protein ◽  
Amyloid A ◽  
Diagnostic Usefulness ◽  
Factor Alpha ◽  
Traumatic Reticuloperitonitis

The present study was carried out to describe the clinical picture of traumatic reticuloperitonitis (TRP) in water buffalo (Bubalus bubalis) and to evaluate the inflammatory and immunologic responses for this clinical condition. Twenty-two buffalo with acute local TRP were monitored in our study. Additionally, 10 clinically healthy buffalo were randomly selected and served as controls. Acute local TRP was initially diagnosed by clinical examination and confirmed by ultrasonographic (USG) examination and/or necropsy findings. Blood samples were collected from all examined buffalo to measure the respective levels of tumor necrosis factor alpha (TNF-α), interleukin (IL)-1β, IL-6, IL-10 and interferon gamma (INF)-γ, serum amyloid A (SAA), C-reactive protein (CRP), haptoglobin (Hp), fibrinogen (Fb), and serum sialic acid (SSA). It was found that TNF-α, IL-1β, IL-6, IL-10, SAA, CRP, Hp, Fb, and SSA were significantly higher in buffalo with TRP than the controls. Our findings suggest that the examined immunologic variables were helpful in documenting the inflammatory response in buffalo with TRP. However, their diagnostic usefulness only becomes apparent when considered in tandem with the clinical findings for any given animal, its anamnesis, and a subsequent USG assessment. Due to the frequent complications of TRP, more accurate indicators of its occurrence and severity would be useful.

scholarly journals The use of inflammatory markers as a prognostic aid for traumatic reticuloperitonitis in water buffalo (Bubalus bubalis)

2014 ◽  
Vol 59 (No. 5) ◽  
pp. 239-246 ◽  
Author(s):  
M. El-Ashker ◽  
M. Salama ◽  
A. Rizk ◽  
M. El-Boshy
Keyword(s):  
Inflammatory Markers ◽  
Water Buffalo ◽  
Inflammatory Responses ◽  
Prognostic Significance ◽  
Bubalus Bubalis ◽  
Cytokine Network ◽  
Necrosis Factor Alpha ◽  
Inflammatory Reactions ◽  
Amyloid A ◽  
Traumatic Reticuloperitonitis

The present study was conducted to evaluate the prognostic significance of selected inflammatory markers for prediction of clinical outcomes of traumatic reticuloperitonitis (TRP) in water buffalo (Bubalus bubalis). Acute local TRP was initially diagnosed in 32 buffalo by clinical examination and confirmed by ultrasonography (USG), laparo-rumenotomy and/or necropsy findings in non-surviving cases. Ten clinically healthy buffalo were randomly selected and served as controls. Blood was drawn from all examined buffalo to measure the respective levels of tumor necrosis factor alpha (TNF-α), interleukin (IL)-1β, IL-6, IL-10 interferon gamma (INF)-γ, serum amyloid A (SAA), haptoglobin (Hp), fibrinogen (Fb), C-reactive protein (CRP) and serum sialic acid (SSA). Clinically, the heart rates, but neither respiratory rate nor rectal temperature, were significantly higher in non-survivors compared with survivors (P < 0.05). In addition, the non-surviving buffalo were more likely to have anorexia and weakness compared with survivors. However, rumen stasis, recurrent ruminal tympany, lacrimation, lordosis, bruxism, and decreased milk production were commonly observed in all diseased animals. Biochemically, TNF-α, IL-1β, IL-6, IL-10, SAA, Hp, Fb, CRP, and SSA levels were significantly higher in diseased buffalo compared with controls, and were higher in non-survivors than survivors (P < 0.05). The data herein indicate an ongoing cascade of systemic inflammatory responses in buffalo with TRP with concomitant compensatory anti-inflammatory reactions and the overall degree of cytokine network disruption may be an important prognostic indicator. Medical strategies to modulate inflammation must take into account the complex of cytokine biology in buffalo with TRP.  

scholarly journals Neutrophils Are Essential for Rapid Clearance of Enterococcus faecium in Mice

2008 ◽  
Vol 77 (1) ◽  
pp. 485-491 ◽  
Author(s):  
Masja Leendertse ◽  
Rob J. L. Willems ◽  
Ida A. J. Giebelen ◽  
Joris J. T. H. Roelofs ◽  
Marc J. M. Bonten ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Enterococcus Faecium ◽  
Acute Phase Proteins ◽  
Progressive Increase ◽  
Necrosis Factor Alpha ◽  
Amyloid A ◽  
Neutropenic Patients ◽  
Rapid Clearance ◽  
Factor Alpha

ABSTRACT A progressive increase in infections with multiresistant Enterococcus faecium has been reported, especially in cancer patients and neutropenic patients. Despite its increasing importance as a nosocomial pathogen, knowledge of the pathogenesis of E. faecium infections is highly limited. In this study, we investigated the role of neutrophils during peritonitis with subsequent bacteremia caused by E. faecium. Therefore, we depleted neutrophils by intraperitoneal injections of monoclonal antibody RB6-8C5. Mice were followed for 5 days, and the enterococcal outgrowth and inflammatory response were compared between neutropenic mice and immunoglobulin G-injected control mice. Neutropenic mice demonstrated a severe delay in enterococcal clearance from all cultured organs (peritoneal fluid, blood, and lung and liver tissue). In particular, neutropenic mice remained bacteremic for up to 3 days, whereas all nonneutropenic mice had cleared the bacteria from circulation by 2 days. Furthermore, neutropenic mice displayed elevated peritoneal cytokine and chemokine levels 1 day after the infection and attracted fewer macrophages into the peritoneal cavity. In the circulation, a prolonged elevation of tumor necrosis factor alpha, interleukin-6, and the acute-phase proteins serum amyloid A and complement 3 were measured in neutropenic mice. In conclusion, attraction of neutrophils to the primary site of E. faecium infection is important for a rapid clearance of this bacterium, thereby attenuating a systemic inflammatory response.

Effects of recombinant human interleukin-6 in cancer patients: a phase I-II study

Blood ◽  
1994 ◽  
Vol 84 (5) ◽  
pp. 1434-1441 ◽  
Author(s):  
MM van Gameren ◽  
PH Willemse ◽  
NH Mulder ◽  
PC Limburg ◽  
HJ Groen ◽  
...  
Keyword(s):  
Side Effects ◽  
Phase I ◽  
Interleukin 6 ◽  
Nonsmall Cell Lung Cancer ◽  
Outpatient Basis ◽  
Necrosis Factor Alpha ◽  
Reactive Protein ◽  
Amyloid A ◽  
Cholesterol Levels ◽  
Factor Alpha

To define the toxicity profile of recombinant human interleukin-6 (rhIL- 6) and to study its effect on hematopoiesis, biochemical parameters and other cytokines, rhIL-6 was administered in a phase I-II study to 20 patients with breast carcinoma or nonsmall cell lung cancer. RhIL-6 doses were 0.5, 1.0, 2.5, 5.0, 10, and 20 micrograms/kg/d, with at least three patients per dose level. RhIL-6 was administered 24 hours by continuous intravenous infusion followed by subcutaneous (SC) administration for 6 days, partly on an outpatient basis. RhIL-6- related side effects were fever, headache, myalgia, and local erythema. Starting at 2.5 micrograms/kg/d, these side effects were compounded by nausea, reversible increase in liver enzymes, and anemia. Flu-like symptoms were controllable up to and including 10 micrograms rhIL- 6/kg/d with acetaminophen. RhIL-6 increased platelet counts with a decrease in mean platelet volume and increased leukocytes caused by neutrophil, monocyte, and lymphocyte increase, with an increase in T cells and natural killer cells at 1.0 and 2.5 micrograms rhIL-6/kg/d. The reversible anemia was characterized by a decrease in serum iron, and an increase in ferritin and erythropoietin without reticulocytosis. RhIL-6 reduced total cholesterol levels and a dose-related increase of C-reactive protein and serum amyloid A plasma levels was observed. Serum IL-6 levels were increased, especially at 10 and 20 micrograms/kg/d, whereas no change in IL-1 beta and tumor necrosis factor alpha levels was observed. RhIL-6 can be administered with controllable side effects in this setting, up to and including a SC dose of 10 micrograms/kg/d on an outpatient basis, and has a promising stimulating effect on leukopoiesis and thrombopoiesis.

scholarly journals Effects of recombinant human interleukin-6 in cancer patients: a phase I-II study

Blood ◽  
1994 ◽  
Vol 84 (5) ◽  
pp. 1434-1441 ◽  
Author(s):  
MM van Gameren ◽  
PH Willemse ◽  
NH Mulder ◽  
PC Limburg ◽  
HJ Groen ◽  
...  
Keyword(s):  
Side Effects ◽  
Phase I ◽  
Interleukin 6 ◽  
Nonsmall Cell Lung Cancer ◽  
Outpatient Basis ◽  
Necrosis Factor Alpha ◽  
Reactive Protein ◽  
Amyloid A ◽  
Cholesterol Levels ◽  
Factor Alpha

Abstract To define the toxicity profile of recombinant human interleukin-6 (rhIL- 6) and to study its effect on hematopoiesis, biochemical parameters and other cytokines, rhIL-6 was administered in a phase I-II study to 20 patients with breast carcinoma or nonsmall cell lung cancer. RhIL-6 doses were 0.5, 1.0, 2.5, 5.0, 10, and 20 micrograms/kg/d, with at least three patients per dose level. RhIL-6 was administered 24 hours by continuous intravenous infusion followed by subcutaneous (SC) administration for 6 days, partly on an outpatient basis. RhIL-6- related side effects were fever, headache, myalgia, and local erythema. Starting at 2.5 micrograms/kg/d, these side effects were compounded by nausea, reversible increase in liver enzymes, and anemia. Flu-like symptoms were controllable up to and including 10 micrograms rhIL- 6/kg/d with acetaminophen. RhIL-6 increased platelet counts with a decrease in mean platelet volume and increased leukocytes caused by neutrophil, monocyte, and lymphocyte increase, with an increase in T cells and natural killer cells at 1.0 and 2.5 micrograms rhIL-6/kg/d. The reversible anemia was characterized by a decrease in serum iron, and an increase in ferritin and erythropoietin without reticulocytosis. RhIL-6 reduced total cholesterol levels and a dose-related increase of C-reactive protein and serum amyloid A plasma levels was observed. Serum IL-6 levels were increased, especially at 10 and 20 micrograms/kg/d, whereas no change in IL-1 beta and tumor necrosis factor alpha levels was observed. RhIL-6 can be administered with controllable side effects in this setting, up to and including a SC dose of 10 micrograms/kg/d on an outpatient basis, and has a promising stimulating effect on leukopoiesis and thrombopoiesis.

scholarly journals The Inflammatory Response to Alcohol Consumption and Its Role in the Pathology of Alcohol Hangover

2020 ◽  
Vol 9 (7) ◽  
pp. 2081 ◽  
Author(s):  
Aurora J.A.E. van de Loo ◽  
Marlou Mackus ◽  
Oran Kwon ◽  
Illathu Madhavamenon Krishnakumar ◽  
Johan Garssen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alcohol Consumption ◽  
Inflammatory Response ◽  
Necrosis Factor Alpha ◽  
Blood Concentrations ◽  
Reactive Protein ◽  
Tnf Α ◽  
Factor Alpha ◽  
Alcohol Hangover ◽  
The Relationship

An increasing number of studies are focusing on the inflammatory response to alcohol as a potentially important determinant of hangover severity. In this article, data from two studies were re-evaluated to investigate the relationship between hangover severity and relevant biomarkers of alcohol metabolism, oxidative stress and the inflammatory response to alcohol. Hangover severity was significantly and positively correlated with blood concentrations of biomarkers of the inflammatory response to alcohol, in particular, Interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α) and C-reactive protein (CRP). At 4 h after alcohol consumption, blood ethanol concentration (but not acetaldehyde) was significantly and positively associated with elevated levels of IL-6, suggesting a direct inflammatory effect of ethanol. In addition, biomarkers of oxidative stress, i.e., malondialdehyde and 8-isoprostrane, were significantly correlated with hangover severity, suggesting that oxidative stress also contributes to the inflammatory response. The timing of the assessments suggests initial slow elimination of ethanol in the first hours after alcohol consumption. As a consequence, more ethanol is present in the second half of the night and the next morning, which will elicit more oxidative stress and a more profound inflammatory response. Together, these processes result in more severe hangovers.

scholarly journals The Inflammatory Response Induced by Aspartic Proteases of Candida albicans Is Independent of Proteolytic Activity

2010 ◽  
Vol 78 (11) ◽  
pp. 4754-4762 ◽  
Author(s):  
Donatella Pietrella ◽  
Anna Rachini ◽  
Neelam Pandey ◽  
Lydia Schild ◽  
Mihai Netea ◽  
...  
Keyword(s):  
Candida Albicans ◽  
Inflammatory Response ◽  
Proteolytic Activity ◽  
Necrosis Factor Alpha ◽  
Pathogenic Yeast ◽  
Aspartic Proteases ◽  
Akt Activation ◽  
Tnf Α ◽  
Factor Alpha ◽  
Pepstatin A

ABSTRACT The secretion of aspartic proteases (Saps) has long been recognized as a virulence-associated trait of the pathogenic yeast Candida albicans. In this study, we report that different recombinant Saps, including Sap1, Sap2, Sap3, and Sap6, have differing abilities to induce secretion of proinflammatory cytokines by human monocytes. In particular Sap1, Sap2, and Sap6 significantly induced interleukin-1β (IL-1β), tumor necrosis factor alpha (TNF-α), and IL-6 production. Sap3 was able to stimulate the secretion of IL-1β and TNF-α. All Saps tested were able to induce Ca2+ influx in monocytes. Treatment of these Saps with pepstatin A did not have any effect on cytokine secretion, indicating that their stimulatory potential was independent from their proteolytic activity. The capacity of Saps to induce inflammatory cytokine production was also independent from protease-activated receptor (PAR) activation and from the optimal pH for individual Sap activity. The interaction of Saps with monocytes induced Akt activation and phosphorylation of IκBα, which mediates translocation of NF-κB into the nucleus. Overall, these results suggest that individual Sap proteins can induce an inflammatory response and that this phenomenon is independent from the pH of a specific host niche and from Sap enzymatic activity. The inflammatory response is partially dependent on Sap denaturation and is triggered by the Akt/NF-κB activation pathway. Our data suggest a novel, activity-independent aspect of Saps during interactions of C. albicans with the host.

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