scholarly journals Limited Role for Interleukin-18 in the Host Protection Response to Pulmonary Infection with Pseudomonas aeruginosa in Mice

2004 ◽  
Vol 72 (10) ◽  
pp. 6176-6180 ◽  
Author(s):  
Chikara Nakasone ◽  
Kazuyoshi Kawakami ◽  
Tomoaki Hoshino ◽  
Yusuke Kawase ◽  
Koichi Yokota ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Pulmonary Infection ◽  
Interleukin 18 ◽  
Necrosis Factor Alpha ◽  
Host Protection ◽  
Limited Role ◽  
Inflammatory Protein ◽  
Factor Alpha ◽  
Macrophage Inflammatory Protein ◽  
Necrosis Factor

ABSTRACT We report that clearance of Pseudomonas aeruginosa, accumulation of neutrophils, and synthesis of tumor necrosis factor alpha and macrophage inflammatory protein 2 in the infected lung were not largely different in interleukin-18 (IL-18) knockout or transgenic mice compared with control mice. Our results suggest a limited role for IL-18 in the host defense against P. aeruginosa.

scholarly journals Haemophilus influenzae Porin Contributes to Signaling of the Inflammatory Cascade in Rat Brain

2001 ◽  
Vol 69 (1) ◽  
pp. 221-227 ◽  
Author(s):  
Massimiliano Galdiero ◽  
Michele D'Amico ◽  
Fernanda Gorga ◽  
Clara Di Filippo ◽  
Marina D'Isanto ◽  
...  
Keyword(s):  
Haemophilus Influenzae ◽  
Serum Proteins ◽  
Necrosis Factor Alpha ◽  
Inflammatory Protein ◽  
Tnf Α ◽  
Factor Alpha ◽  
Interleukin 1Α ◽  
Macrophage Inflammatory Protein ◽  
Brain Water ◽  
Necrosis Factor

ABSTRACT In the present study we observed that the Haemophilus influenzae type b (Hib) porin, among the different surface bacterial components, is involved in the pathophysiology of bacterial meningitis. This study demonstrates that inoculation of Hib porin into the fourth cerebral ventricle causes the simultaneous expression of interleukin-1α (IL-1α), tumor necrosis factor alpha (TNF-α), and macrophage inflammatory protein 2 (MIP-2) at 6 h after inoculation. At 24 h, the expression of MIP-2 decreases while the expression of IL-1α and TNF-α increases. The mRNA expression of IL-1α, TNF-α, and MIP-2 is correlated with injury to the blood-brain barrier as demonstrated by the appearance of serum proteins and leukocytes in cerebrospinal fluid and by the increase in brain water content.

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 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 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

Role of tumor necrosis factor alpha in innate resistance to mouse pulmonary infection with Pseudomonas aeruginosa.

1995 ◽  
Vol 63 (9) ◽  
pp. 3272-3278 ◽  
Author(s):  
D Gosselin ◽  
J DeSanctis ◽  
M Boulé ◽  
E Skamene ◽  
C Matouk ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Pulmonary Infection ◽  
Necrosis Factor Alpha ◽  
Innate Resistance ◽  
Factor Alpha ◽  
Necrosis Factor

scholarly journals Interleukin-18 Impairs the Pulmonary Host Response to Pseudomonas aeruginosa

2003 ◽  
Vol 71 (4) ◽  
pp. 1630-1634 ◽  
Author(s):  
Marc J. Schultz ◽  
Sylvia Knapp ◽  
Sandrine Florquin ◽  
Jennie Pater ◽  
Kiyoshi Takeda ◽  
...  
Keyword(s):  
Inflammatory Responses ◽  
Pulmonary Inflammation ◽  
Wild Type ◽  
Interleukin 18 ◽  
Necrosis Factor Alpha ◽  
Fusion Construct ◽  
Inflammatory Protein ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT Interleukin-18 (IL-18) is a potent cytokine with many different proinflammatory activities. To study the role of IL-18 in the pathogenesis of Pseudomonas pneumonia, IL-18-deficient (IL-18 −/−) and wild-type mice were intranasally inoculated with Pseudomonas aeruginosa. IL-18 deficiency was associated with reduced outgrowth of Pseudomonas in the lungs and diminished dissemination of the infection. In addition, pulmonary inflammation (histopathology) and levels of tumor necrosis factor alpha, IL-6, and macrophage inflammatory protein-2 in lungs and plasma were lower in IL-18 −/− mice. Consistent with results obtained for IL-18 −/− mice, treatment of wild-type mice with a neutralizing IL-18 binding protein-immunoglobulin G Fc fusion construct also attenuated outgrowth of Pseudomonas compared with that for mice treated with a control protein. These results demonstrate that the presence of endogenous IL-18 activity facilitates inflammatory responses in the lung during Pseudomonas pneumonia, concurrently impairing bacterial clearance.

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