scholarly journals The use of inflammatory markers as a diagnostic and prognostic approach in neonatal calves with septicaemia

2019 ◽  
Vol 67 (3) ◽  
pp. 360-376
Author(s):  
Akın Kirbas ◽  
Fatih Mehmet Kandemir ◽  
Demet Celebi ◽  
Basak Hanedan ◽  
Mehmet Ozkan Timurkan
Keyword(s):  
Blood Cell ◽  
Inflammatory Markers ◽  
Necrosis Factor Alpha ◽  
E Coli ◽  
Diagnosis And Prognosis ◽  
Tnf Α ◽  
Faecal Samples ◽  
Factor Alpha ◽  
Neonatal Calves ◽  
Biochemical Analyses

The objective of this study was to evaluate the usefulness of inflammatory markers as a diagnostic and prognostic approach in neonatal calves with septicaemia. The study material consisted of 13 neonatal calves with septicaemia (septicaemic calves, SC) and ten healthy neonatal calves (control calves, CC). Blood samples were collected for biochemical, haematological and microbiological analyses. In addition, faecal samples were collected for microbiological and virological analyses. Three of neonatal calves with septicaemia were positive for E. coli (E. coli O157 serotype) by microbiological examination, but all neonatal calves with septicaemia were negative for rota- and coronaviruses. By haematological examination, there were no significant differences between SC and CC for white blood cell (WBC) and neutrophil (NEU) counts (P > 0.05). NEU counts were higher on day 0 than on day 15 in SC (P < 0.05). Red blood cell (RBC) counts and packed cell volume (PCV) values were higher on day 0 in the SC than in the CC (P < 0.05). By biochemical analyses, tumour necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), procalcitonin (PCT), haptoglobin (Hp), and fibrinogen (Fb) concentrations were higher on day 0 in the SC than in the CC (P < 0.05). After treatment (on day 15), the serum IL-6, PCT, Hp, and Fb concentrations were significantly decreased in the SC compared to the CC (P < 0.05). The serum iron (Fe) concentrations were lower on day 0 in the SC than in the CC (P < 0.05), and were higher on day 15 than on day 0 in the SC (P < 0.05). The study revealed that inflammatory markers could be used for determining the diagnosis and prognosis in neonatal calves with septicaemia.

scholarly journals DNA from Protozoan Parasites Babesia bovis, Trypanosoma cruzi, and T. brucei Is Mitogenic for B Lymphocytes and Stimulates Macrophage Expression of Interleukin-12, Tumor Necrosis Factor Alpha, and Nitric Oxide

2001 ◽  
Vol 69 (4) ◽  
pp. 2162-2171 ◽  
Author(s):  
Lisl K. M. Shoda ◽  
Kimberly A. Kegerreis ◽  
Carlos E. Suarez ◽  
Isabel Roditi ◽  
Ricardo S. Corral ◽  
...  
Keyword(s):  
B Lymphocytes ◽  
Tumor Necrosis ◽  
Babesia Bovis ◽  
Interleukin 12 ◽  
Protozoan Parasites ◽  
Necrosis Factor Alpha ◽  
E Coli ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT The activation of innate immune responses by genomic DNA from bacteria and several nonvertebrate organisms represents a novel mechanism of pathogen recognition. We recently demonstrated the CpG-dependent mitogenic activity of DNA from the protozoan parasiteBabesia bovis for bovine B lymphocytes (W. C. Brown, D. M. Estes, S. E. Chantler, K. A. Kegerreis, and C. E. Suarez, Infect. Immun. 66:5423–5432, 1998). However, activation of macrophages by DNA from protozoan parasites has not been demonstrated. The present study was therefore conducted to determine whether DNA from the protozan parasites B. bovis, Trypanosoma cruzi, and T. brucei activates macrophages to secrete inflammatory mediators associated with protective immunity. DNA fromEscherichia coli and all three parasites stimulated B-lymphocyte proliferation and increased macrophage production of interleukin-12 (IL-12), tumor necrosis factor alpha (TNF-α), and nitric oxide (NO). Regulation of IL-12 and NO production occurred at the level of transcription. The amounts of IL-12, TNF-α, and NO induced by E. coli and protozoal DNA were strongly correlated (r 2 > 0.9) with the frequency of CG dinucleotides in the genome, and immunostimulation by DNA occurred in the order E. coli ≥ T. cruzi > T. brucei > B. bovis. Induction of inflammatory mediators by E. coli, T. brucei, and B. bovis DNA was dependent on the presence of unmethylated CpG dinucleotides. However, at high concentrations,E. coli and T. cruzi DNA-mediated macrophage activation was not inhibited following methylation. The recognition of protozoal DNA by B lymphocytes and macrophages may provide an important innate defense mechanism to control parasite replication and promote persistent infection.

scholarly journals Differential Tumor Necrosis Factor Alpha Expression and Release from Peritoneal Mouse Macrophages In Vitro in Response to Proliferating Gram-Positive versus Gram-Negative Bacteria

2000 ◽  
Vol 68 (8) ◽  
pp. 4422-4429 ◽  
Author(s):  
Wei Cui ◽  
David C. Morrison ◽  
Richard Silverstein
Keyword(s):  
Tumor Necrosis ◽  
Necrosis Factor Alpha ◽  
Gram Negative ◽  
E Coli ◽  
Tnf Α ◽  
Mouse Macrophages ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT Viable Escherichia coli and Staphylococcus aureus bacteria elicited markedly different in vitro tumor necrosis factor alpha (TNF-α) responses when placed in coculture with peritoneal murine macrophages. These include quantitative differences in TNF-α mRNA expression and corresponding protein product secretion as well as kinetic differences in the profiles of the TNF-α responses. Further, lipopolysaccharide (from E. coli) is a major contributing factor to these differences, as revealed by comparative experiments with endotoxin-responsive (C3Heb/FeJ) and endotoxin-hyporesponsive (C3H/HeJ) macrophages. Nevertheless, the eventual overall magnitude of the TNF-α secretion of macrophages in response to S. aureus was at least equivalent to that observed with E. coli, while appearing at time periods hours later than the E. coli-elicited TNF-α response. Both the magnitude and kinetic profile of the TNF-α responses were found to be relatively independent of the rate of bacterial proliferation, at least to the extent that similar results were observed with both viable and paraformaldehyde-killed microbes. Nevertheless, S. aureus treated in culture with the carbapenem antibiotic imipenem manifests markedly altered profiles of TNF-α response, with the appearance of an early TNF-α peak not seen with viable organisms, a finding strikingly similar to that recently reported by our laboratory from in vivo studies (R. Silverstein, J. G. Wood, Q. Xue, M. Norimatsu, D. L. Horn, and D. C. Morrison, Infect. Immun. 68:2301–2308, 2000). In contrast, imipenem treatment of E. coli-cocultured macrophages does not significantly alter the observed TNF-α response either in vitro or in vivo. In conclusion, our data support the concept that the host inflammatory response of cultured mouse macrophages in response to viable gram-positive versus gram-negative microbes exhibits distinctive characteristics and that these distinctions are, under some conditions, altered on subsequent bacterial killing, depending on the mode of killing. Of potential importance, these distinctive in vitro TNF-α profiles faithfully reflect circulating levels of TNF-α in infected mice. These results suggest that coculture of peritoneal macrophages with viable versus antibiotic-killed bacteria and subsequent assessment of cytokine response (TNF-α) may be of value in clarifying, and ultimately controlling, related host inflammatory responses in septic patients.

scholarly journals Comparative Kinetics ofEscherichia coli- andStaphylococcus aureus-Specific Activation of Key Immune Pathways in Mammary Epithelial Cells Demonstrates ThatS. aureusElicits a Delayed Response Dominated by Interleukin-6 (IL-6) but Not by IL-1A or Tumor Necrosis Factor Alpha

2010 ◽  
Vol 79 (2) ◽  
pp. 695-707 ◽  
Author(s):  
Juliane Günther ◽  
Kathrin Esch ◽  
Norbert Poschadel ◽  
Wolfram Petzl ◽  
Holm Zerbe ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Necrosis Factor Alpha ◽  
E Coli ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACTInfections of the udder byEscherichia colivery often elicit acute inflammation, whileStaphylococcus aureusinfections tend to cause mild, subclinical inflammation and persistent infections. The molecular causes underlying the different disease patterns are poorly understood. We therefore profiled the kinetics and extents of global changes in the transcriptome of primary bovine mammary epithelial cells (MEC) after challenging them with heat-inactivated preparations ofE. coliorS. aureuspathogens.E. coliswiftly and strongly induced an expression of cytokines and bactericidal factors.S. aureuselicited a retarded response and failed to quickly induce an expression of bactericidal factors. Both pathogens induced similar patterns of chemokines for cell recruitment into the udder, butE. colistimulated their synthesis much faster and stronger. The genes that are exclusively and most strongly upregulated byE. colimay be clustered into a regulatory network with tumor necrosis factor alpha (TNF-α) and interleukin-1 (IL-1) in a central position. In contrast, the expression of these master cytokines is barely regulated byS. aureus. Both pathogens quickly trigger an enhanced expression of IL-6. This is still possible after completely abrogating MyD88-dependent Toll-like receptor (TLR) signaling in MEC. TheE. coli-specific strong induction of TNF-α and IL-1 expression may be causative for the severe inflammatory symptoms of animals suffering fromE. colimastitis, while the avoidance to quickly induce the synthesis of bactericidal factors may support the persistent survival ofS. aureuswithin the udder. We suggest thatS. aureussubverts the MyD88-dependent activation of immune gene expression in MEC.

scholarly journals Effect of Resin Acid and Zinc Oxide on Immune Status of Weaned Piglets Challenged With E. coli Lipopolysaccharide

2021 ◽  
Vol 8 ◽  
Author(s):  
Xiaonan Guan ◽  
Regiane R. Santos ◽  
Hannele Kettunen ◽  
Juhani Vuorenmaa ◽  
Francesc Molist
Keyword(s):  
Zinc Oxide ◽  
Resin Acid ◽  
Serum Levels ◽  
Immune Defence ◽  
Weaned Piglets ◽  
Necrosis Factor Alpha ◽  
E Coli ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

With the ban of zinc oxide (ZnO) at high dosages in piglet diets in Europe by 2022, alternative nutritional solutions are being tested to support piglet immune defence during their weaning, the most critical and stressful moment of pig production. The present study evaluated the effect of zinc oxide (ZnO; 2,500 mg/kg diet) and resin acid concentrate (RAC; 200 mg/kg diet) on the immune defence of weaned piglets challenged with lipopolysaccharide (LPS). Piglets were challenged at days 7 and 21 post-weaning, and blood was sampled 1.5 and 3.0 h after each challenge to determine serum levels of pro- and anti-inflammatory cytokines. The levels of serum tumour necrosis factor alpha (TNF-α) and interleukin 8 (IL-8) increased at days 7 and 21, and those of IL-6 at day 21 when challenged piglets were fed a diet supplemented with ZnO. In challenged piglets fed with RAC, the serum levels of IL-1β, IL-6, IL-8, IL-10 and TNF-α were increased at days 7 and 21, except for that of IL-1β, which was not affected at day 21. The increased levels of these cytokines indicate the successful immune-modulatory effect of ZnO and RAC, which appears as a candidate to replace ZnO in weaned piglets' diets.

scholarly journals Clindamycin Suppresses Endotoxin Released by Ceftazidime-TreatedEscherichia coli O55:B5 and Subsequent Production of Tumor Necrosis Factor Alpha and Interleukin-1β

1999 ◽  
Vol 43 (3) ◽  
pp. 616-622 ◽  
Author(s):  
Kenji Kishi ◽  
Kazuhiro Hirai ◽  
Kazufumi Hiramatsu ◽  
Tohru Yamasaki ◽  
Masaru Nasu
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Culture Supernatant ◽  
Interleukin 1Β ◽  
Necrosis Factor Alpha ◽  
E Coli ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

Treatment of septicemia caused by Escherichia coli with ceftazidime (CAZ) may be associated with the development of septic shock due to the release of bacterial lipopolysaccharide. We examined the suppressive effect of clindamycin (CLDM) on CAZ-induced release of endotoxin by cultured E. coli and the subsequent production of inflammatory cytokines (tumor necrosis factor alpha [TNF-α] and interleukin-1β [IL-1β]). E. coli ATCC 12014 was incubated in inactivated horse serum with or without CLDM for 1, 4, or 18 h, followed by the addition of CAZ and collection of the culture supernatant at 0, 1, and 2 h. The concentration of endotoxin in each sample was measured by a chromogenicLimulus test. Another portion of the culture supernatant was added to THP-1 cell culture and incubated for 4 h, and the concentrations of TNF-α and IL-1β in the supernatant were measured by an enzyme-linked immunosorbent assay. In the control group (no CLDM), CAZ administration resulted in significant increases in endotoxin, TNF-α, and IL-1β concentrations. Pretreatment of E. coli with CLDM for 4 or 18 h before the addition of CAZ significantly suppressed the concentrations of endotoxin, TNF-α, and IL-1β in a time-dependent manner. In addition, CAZ treatment transformed E. coli from rod-shaped bacteria to filament-like structures, as determined by electron microscopy, while pretreatment with CLDM prevented these morphological changes. Our in vitro studies showed that CAZ-induced release of large quantities of endotoxin by E. colicould be suppressed by prior administration of CLDM.

scholarly journals Effect of Escherichia coli and Lactobacillus rhamnosus on Macrophage Inflammatory Protein 3α, Tumor Necrosis Factor Alpha, and Transforming Growth Factor β Release by Polarized Rat Uterine Epithelial Cells in Culture

2004 ◽  
Vol 72 (4) ◽  
pp. 1866-1873 ◽  
Author(s):  
Mardi A. Crane-Godreau ◽  
Charles R. Wira
Keyword(s):  
Epithelial Cell ◽  
Transforming Growth Factor ◽  
Lactobacillus Rhamnosus ◽  
Transforming Growth Factor Β ◽  
Necrosis Factor Alpha ◽  
E Coli ◽  
Inflammatory Protein ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT Entry of bacteria from the vagina into the uterus raises the question of uterine epithelial cell (UEC) signaling in response to the presence of bacteria. Our model system helps to define microbially elicited UEC basolateral cytokine release, important in regulating underlying stromal immune cell protection. UECs from adult rats were grown in cell culture inserts to establish a confluent polarized monolayer as was determined by transepithelial resistance (TER). Polarized epithelial cell cultures were treated apically with live or heat-killed Escherichia coli or Lactobacillus rhamnosus prior to collection of basolateral media after 24 h of incubation. Coculture of polarized UECs with live E. coli had no effect on epithelial cell TER. In response to exposure to live E. coli, epithelial cell basolateral release of macrophage inflammatory protein 3α (MIP3α) and tumor necrosis factor alpha (TNF-α) increased at a time when basolateral release of biologically active transforming growth factor β (TGF-β) decreased. Incubation of UECs with heat-killed E. coli resulted in an increased basolateral release of MIP3α and TNF-α, without affecting TER or TGF-β. In contrast to E. coli, live or heat-killed L. rhamnosus had no effect on TER or cytokine release. These studies indicate that polarized rat UECs respond to gram-negative E. coli by releasing the cytokines MIP3α and TNF-α, signals important to both the innate and adaptive immune systems. These findings suggest that UEC responses to bacteria are selective and important in initiating and regulating immune protection in the female reproductive tract.

scholarly journals Association of Prenatal Famine Exposure With Inflammatory Markers and Its Impact on Adulthood Liver Function Across Consecutive Generations

2022 ◽  
Vol 8 ◽  
Author(s):  
Shiwei Yan ◽  
Jingqi Ruan ◽  
Yu Wang ◽  
Jiaxu Xu ◽  
Changhao Sun ◽  
...  
Keyword(s):  
Liver Function ◽  
Inflammatory Markers ◽  
Necrosis Factor Alpha ◽  
Mixed Effect ◽  
Reactive Protein ◽  
Mixed Effect Models ◽  
Tnf Α ◽  
Factor Alpha ◽  
Famine Exposure ◽  
Prenatal Famine

Although there has been increasing recognition that famine exposure in the fetal stage damages liver function in adulthood, this deteriorated effect could be extended to the next generation remains vague. This study aimed to explore whether famine exposure was associated with liver function in the two consecutive generations, and its association with the mediation role of inflammatory markers. We analyzed the data of 2,681 participants from Suihua rural area, Heilongjiang Province, China. According to the date of birth, the participants were classified as fetal exposed and nonexposed. The F2 subjects were classified as having no parents exposed to famine, maternal famine exposure, paternal famine exposure, or parental famine exposure. In the mixed-effect models, prenatal exposure to famine was associated with the elevation of Δ aspartate aminotransferase (ΔAST) (β: 0.22, 95% CI: 0.01, 0.43) and Δ alanine aminotransferase (ΔALT) (β: 0.42, 95% CI: 0.19, 0.66) levels in F1 adults. The mediation analysis showed that the inflammatory markers including serum C-reactive protein (CRP) and tumor necrosis factor-alpha (TNF-α) might mediate the famine-liver function association. This longitudinal data were consistent with the hypothesis that the inflammatory markers explained part of the influence of prenatal famine exposure on liver function injury, and the natal mechanism was needed to be elucidated in the future study.

Regulation of microRNAs in Inflammation-Associated Colorectal Cancer: A Mechanistic Approach

2020 ◽  
Vol 20 ◽  
Author(s):  
Sridhar Muthusami ◽  
Ilangovan Ramachandran ◽  
Sneha Krishnamoorthy ◽  
Yuvaraj Sambandam ◽  
Satish Ramalingam ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Molecular Mechanisms ◽  
Colorectal Carcinogenesis ◽  
Model Systems ◽  
Necrosis Factor Alpha ◽  
Multi Stage ◽  
Mechanistic Approach ◽  
Tnf Α ◽  
Factor Alpha

: The development of colorectal cancer (CRC) is a multi-stage process. The inflammation of the colon as in inflammatory bowel disease (IBD) such as ulcerative colitis (UC) or Crohn’s disease (CD) is often regarded as the initial trigger for the development of CRC. Many cytokines such as tumor necrosis factor alpha (TNF-α) and several interleukins (ILs) are known to exert proinflammatory actions, and inflammation initiates or promotes tumorigenesis of various cancers, including CRC through differential regulation of microRNAs (miRNAs/miRs). miRNAs can be oncogenic miRNAs (oncomiRs) or anti-oncomiRs/tumor suppressor miRNAs, and they play key roles during colorectal carcinogenesis. However, the functions and molecular mechanisms of regulation of miRNAs involved in inflammation-associated CRC are still anecdotal and largely unknown. Consolidating the published results and offering perspective solutions to circumvent CRC, the current review is focused on the role of miRNAs and their regulation in the development of CRC. We have also discussed the model systems adapted by researchers to delineate the role of miRNAs in inflammation-associated CRC.

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