scholarly journals Synergistic Induction of Macrophage Inflammatory Protein-3α/CCL20 Production by Interleukin-17A and Tumor Necrosis Factor-αin Nasal Polyp Fibroblasts

2009 ◽  
Vol 2 (10) ◽  
pp. 218-223 ◽  
Author(s):  
Manabu Nonaka ◽  
Nozomu Ogihara ◽  
Akira Fukumoto ◽  
Atsuko Sakanushi ◽  
Kaoru Kusama ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Nasal Polyp ◽  
Tumor Necrosis ◽  
Inflammatory Protein ◽  
Interleukin 17A ◽  
Synergistic Induction ◽  
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 Divergent Roles of Tumor Necrosis Factor and Platelet-Activating Factor in Endotoxin-Induced Release of Monocyte Chemoattractant Protein 1 and Macrophage Inflammatory Protein 1β in Chimpanzees

1999 ◽  
Vol 67 (10) ◽  
pp. 5480-5482 ◽  
Author(s):  
Pascale E. P. Dekkers ◽  
Marcel Levi ◽  
Sander J. H. van Deventer ◽  
Tom van der Poll
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Platelet Activating Factor ◽  
Necrosis Factor Alpha ◽  
Monocyte Chemoattractant Protein 1 ◽  
Monocyte Chemoattractant ◽  
Monocyte Chemoattractant Protein ◽  
Inflammatory Protein ◽  
Macrophage Inflammatory Protein ◽  
Necrosis Factor

ABSTRACT A platelet-activating factor receptor antagonist reduced the release of macrophage inflammatory protein 1β (MIP-1β) during endotoxemia in chimpanzees but did not influence the secretion of monocyte chemoattractant protein 1 (MCP-1). Anti-tumor necrosis factor alpha monoclonal antibody completely prevented MCP-1 release and simultaneously enhanced the secretion of MIP-1β. Levels of MIP-1β and MCP-1 release were differentially regulated during endotoxemia.

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 Anti-Tumor Necrosis Factor Therapies Reduce Serum Macrophage Inflammatory Protein-1α in Ankylosing Spondylitis: Table 1.

2010 ◽  
Vol 37 (5) ◽  
pp. 1073-1074 ◽  
Author(s):  
HANDAN AKBULUT ◽  
SULEYMAN S. KOCA ◽  
METIN OZGEN ◽  
AHMET ISIK
Keyword(s):  
Ankylosing Spondylitis ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Inflammatory Protein ◽  
Macrophage Inflammatory Protein ◽  
Necrosis Factor
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