scholarly journals Human eosinophils can express the cytokines tumor necrosis factor-alpha and macrophage inflammatory protein-1 alpha.

1993 ◽  
Vol 91 (6) ◽  
pp. 2673-2684 ◽  
Author(s):  
J J Costa ◽  
K Matossian ◽  
M B Resnick ◽  
W J Beil ◽  
D T Wong ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Necrosis Factor Alpha ◽  
Inflammatory Protein ◽  
Factor Alpha ◽  
Macrophage Inflammatory Protein ◽  
Necrosis Factor

scholarly journals CCL20/Macrophage Inflammatory Protein 3α and Tumor Necrosis Factor Alpha Production by Primary Uterine Epithelial Cells in Response to Treatment with Lipopolysaccharide or Pam3Cys

2005 ◽  
Vol 73 (1) ◽  
pp. 476-484 ◽  
Author(s):  
Mardi A. Crane-Godreau ◽  
Charles R. Wira
Keyword(s):  
Tumor Necrosis Factor ◽  
Epithelial Cells ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Necrosis Factor Alpha ◽  
Inflammatory Protein ◽  
Tnf Α ◽  
Factor Alpha ◽  
Macrophage Inflammatory Protein ◽  
Necrosis Factor

ABSTRACT Having previously shown that CCL20/macrophage inflammatory protein 3α and tumor necrosis factor alpha (TNF-α) are released by polarized primary rat uterine epithelial cells (UEC) in response to Escherichia coli but not to Lactobacillus rhamnosus, we sought to determine if epithelial cells are responsive to pathogen-associated molecular patterns (PAMP), including lipopolysaccharide (LPS), lipoteichoic acid (LTA), and Pam3Cys, a bacterial lipoprotein analog. Epithelial cells were grown to confluence on Nunc cell culture inserts prior to apical treatment with PAMPs. In response to LPS, LTA, and Pam3Cys (EMC Microcollection GmbH, Tübingen, Germany), CCL20 levels increased (4- to 10-fold) while PAMPs caused increased TNF-α (1- to 4-fold) in the medium collected after 24 h of incubation. Both apical and basolateral secretion of CCL20 and TNF-α increased in response to PAMPs, but treatments had no effect on cell viability and integrity, as measured by transepithelial resistance. Time course studies of CCL20 and TNF-α release in response to Pam3Cys and LPS indicated that CCL20 release peaked between 2 and 4 h after treatment, whereas TNF-α release was gradual over the length of the incubation. Freeze-thaw and cell lysis experiments, along with actinomycin D studies, suggested that CCL20 and TNF-α are synthesized in response to PAMP stimulation. Taken together, these studies demonstrate that E. coli and selected PAMPs have direct effects on the production of CCL20 and TNF-α without affecting cell integrity. Since CCL20 is known to be both chemotactic and antimicrobial, the increase in apical and basolateral release by UEC in response to PAMPs suggests a new mechanism of innate immune protection in the female reproductive tract.

scholarly journals Activation by 9-(R)-[2-(Phosphonomethoxy)Propyl]Adenine of Chemokine (RANTES, Macrophage Inflammatory Protein 1α) and Cytokine (Tumor Necrosis Factor Alpha, Interleukin-10 [IL-10], IL-1β) Production

2001 ◽  
Vol 45 (12) ◽  
pp. 3381-3386 ◽  
Author(s):  
Zdenĕk Zı́dek ◽  
Daniela Franková ◽  
Antonı́n Holý
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Test System ◽  
In Vitro Test ◽  
Necrosis Factor Alpha ◽  
Inflammatory Protein ◽  
Factor Alpha ◽  
Macrophage Inflammatory Protein ◽  
Necrosis Factor

ABSTRACT Development of a novel group of antiviral agents, acyclic nucleoside phosphonates, has provided a new perspective for treating human immunodeficiency virus (HIV) infection. One of the compounds, 9-(R)-[2-(phosphonomethoxy)propyl]adenine (PMPA) (tenofovir), has been shown to confer complete protection against AIDS in a simian model of the infection. The aim of our study was to investigate whether the antiviral efficacy of PMPA, which depends mainly on inhibition of virus-induced DNA polymerase or of reverse transcriptase, could be contributed by immunomodulatory potential of this drug. We screened for its ability to activate production of cytokines and chemokines that are known to interfere with the replication and/or the entry of HIV in cells. Using the in vitro test system of mouse macrophages and lymphocytes, it has been found that PMPA stimulates macrophage secretion of interleukin-1β (IL-1β), IL-10, and tumor necrosis factor alpha. Production of the chemokines RANTES and macrophage inflammatory protein 1α was activated in both macrophages and lymphocytes, and also in human cell line U937. Other cytokines—i.e., IL-2, IL-12, IL-13, and gamma interferon—remained uninfluenced by PMPA. The cytokines were stimulated in a dose-dependent fashion, with rapid onset, and peak concentrations were achieved within 5 to 24 h. The findings contribute to a more complex understanding of mechanisms of antiviral effectiveness of PMPA and support the view that this drug could become a promising candidate for therapeutic exploitation in anti-HIV preventive medicine.

scholarly journals Effects of Estradiol on Lipopolysaccharide and Pam3Cys Stimulation of CCL20/Macrophage Inflammatory Protein 3 Alpha and Tumor Necrosis Factor Alpha Production by Uterine Epithelial Cells in Culture

2005 ◽  
Vol 73 (7) ◽  
pp. 4231-4237 ◽  
Author(s):  
Mardi A. Crane-Godreau ◽  
Charles R. Wira
Keyword(s):  
Tumor Necrosis Factor ◽  
Epithelial Cells ◽  
Tumor Necrosis ◽  
Necrosis Factor Alpha ◽  
Ici 182,780 ◽  
Inflammatory Protein ◽  
Tnf Α ◽  
Factor Alpha ◽  
Macrophage Inflammatory Protein ◽  
Necrosis Factor

ABSTRACT We have previously demonstrated that rat uterine epithelial cells (UEC) produce CCL20/macrophage inflammatory protein 3 alpha (MIP3α) and tumor necrosis factor alpha (TNF-α) in response to live and heat-killed Escherichia coli and to the pathogen-associated molecular patterns (PAMP) lipopolysaccharide (LPS) and Pam3Cys. To determine whether estradiol (E2) modulates PAMP-induced CCL20/MIP3α and TNF-α secretion, primary cultures of rat UEC were incubated with E2 for 24 h and then treated with LPS or Pam3Cys or not treated for an additional 12 h. E2 inhibited the constitutive secretion of TNF-α and CCL20/MIP3α into culture media. Interestingly, E2 pretreatment enhanced CCL20/MIP3α secretion due to LPS and Pam3Cys administration. In contrast, and at the same time, E2 lowered the TNF-α response to both PAMP. To determine whether estrogen receptors (ER) mediated the effects of E2, epithelial cells were incubated with E2 and/or ICI 182,780, a known ER antagonist. ICI 182,780 had no effect on E2 inhibition of constitutive TNF-α and CCL20/MIP3α secretion. In contrast, ICI 182,780 reversed the stimulatory effect of E2 on LPS- and/or Pam3Cys-induced CCL20/MIP3α secretion as well as partially reversed the inhibitory effect of E2 on TNF-α production by epithelial cells. Overall, these results indicate that E2 regulates the production of TNF-α and CCL20/MIP3α by UEC in the absence as well as presence of PAMP. Since CCL20/MIP3α has antimicrobial activity and is chemotactic for immune cells, these studies suggest that regulation of CCL20/MIP3α and TNF-α by E2 and PAMP may have profound effects on innate and adaptive immune responses to microbial challenge in the female reproductive tract.

scholarly journals Role of inflammation and iron exchange disorders in progression of liver cirrosis

2021 ◽  
Vol 38 (1) ◽  
pp. 38-45
Author(s):  
I. A. Bulatova ◽  
A. P. Shchekotova ◽  
S. V. Paducheva
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Clinical Manifestations ◽  
Control Group ◽  
Necrosis Factor Alpha ◽  
Inflammatory Protein ◽  
Factor Alpha ◽  
Necrosis Factor

Objective. To assess the role of the main pathogenetically significant molecules, including tumor necrosis factor alpha (TNF-) and transferrin, as an inflammatory protein, in the progression of chronic diffuse liver diseases (CDLD). Material and methods. The study involved 86 patients with cirrhosis of the liver (LC) of viral, alcoholic and mixed etiology. Inflammatory parameters were studied, including tumor necrosis factor alpha (TNF-), indicators of iron metabolism, -fetoprotein (AFP), vasculoendothelial growth factor (VEGF), and functional liver biochemical tests. The control group consisted of 70 persons. Results. It was revealed that the LC severity class is interrelated with the clinical manifestations of the disease, the severity of biochemical syndromes as well as a significant increase in the concentration of -globulins, CRP, the amount of TNF- up to 3.5 (2.64.7) pg/ ml (p 0.001) and ferritin up to 325.8 (209; 401) ng / ml (p 0.001) compared to the control group. An increase in TNF- and ferritin as inflammatory protein in LC confirms the growth of the activity of inflammation in the liver and correlates with other parameters involved in the pathogenesis of LC: with VEGF, as a marker of endothelial dysfunction, which is involved in the activation of fibrosis and neoangiogenesis, and AFP, reflecting regeneration processes in the liver. Conclusions. The progression of liver damage in cirrhosis is based primarily on the secondary inflammation caused by portal hypertension with the entry of intestinal antigens and toxins into the central bloodstream. At the same time, the perverse circle of the development of the disease is closed.

Statistical Prediction of the Type of Gastric Aspiration Lung Injury Based on Early Cytokine/Chemokine Profiles

2006 ◽  
Vol 104 (1) ◽  
pp. 73-79 ◽  
Author(s):  
Alan D. Hutson ◽  
Bruce A. Davidson ◽  
Krishnan Raghavendran ◽  
Patricia R. Chess ◽  
Alan R. Tait ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Lung Injury ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Wild Type ◽  
Necrosis Factor Alpha ◽  
Inflammatory Protein ◽  
Gastric Aspiration ◽  
Factor Alpha ◽  
Necrosis Factor

Background Unwitnessed gastric aspiration can be a diagnostic dilemma, and early discrimination of different forms may help to identify individuals with increased risk of development of severe clinical acute lung injury or acute respiratory distress syndrome. The authors hypothesized that inflammatory mediator profiles could be used to help diagnose different types of gastric aspiration. Methods Diagnostic modeling using a newly modified receiver operator characteristic approach was applied to recently published data from our laboratory on lavaged inflammatory mediators from rodents given intratracheal normal saline, hydrochloric acid, small nonacidified gastric particles, or a combination of acid and small gastric particles. Multiple animal groups and postaspiration times of injury were analyzed to gauge the applicability of the predictive approach: rats (6 and 24 h), C57/BL6 wild-type mice (5 and 24 h), and transgenic mice on the same background deficient in the gene for monocyte chemoattractant protein 1 (MCP-1 [-/-] mice; 5 and 24 h). Results Overall, the four types of aspiration were correctly discriminated in 85 of 96 rats (89%), 72 of 78 wild-type mice (92%), and 59 of 73 MCP-1 (-/-) mice (81%) by models that used a maximum of only two mediators. The severe "two-hit" aspirate of the combination of acid and small gastric particles was correctly predicted in 21 of 24 rats, 23 of 23 wild-type mice, and 21 of 21 MCP-1 (-/-) mice. Specific best-fit mediators or mediator pairs varied with aspirate type, animal type, and time of injury. Cytokines and chemokines that best predicted the combination of acid and small gastric particles were cytokine-induced neutrophil chemoattractant 1 (6 h) and MCP-1 (24 h) in rats, tumor necrosis factor alpha/macrophage inflammatory protein 2 (5 h) and tumor necrosis factor alpha/MCP-1 (24 h) in wild-type mice, and tumor necrosis factor alpha/macrophage inflammatory protein 2 (5 h) and tumor necrosis factor alpha/keratinocyte-derived cytokine (24 h) in MCP-1 (-/-) mice. Conclusions These results support the potential feasibility of developing predictive models that use focused measurements of inflammatory mediators to help diagnose severe clinical forms of unwitnessed gastric aspiration, such as the combination of acid and small gastric particles, that may have a high risk of progression to acute lung injury/acute respiratory distress syndrome.

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