scholarly journals Acinetobacter baumannii LOS Regulate the Expression of Inflammatory Cytokine Genes and Proteins in Human Mast Cells

Pathogens ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 290
Author(s):  
Takane Kikuchi-Ueda ◽  
Tsuneyuki Ubagai ◽  
Go Kamoshida ◽  
Ryuichi Nakano ◽  
Akiyo Nakano ◽  
...  
Keyword(s):  
Mast Cells ◽  
Acinetobacter Baumannii ◽  
Bacterial Infections ◽  
Inflammatory Responses ◽  
Critical Role ◽  
Bacterial Invasion ◽  
Inflammatory Genes ◽  
Human Mast Cells ◽  
Expression Of Genes ◽  
Tnf Α

Herein, we investigated the effect of bacterial lipooligosaccharides (LOS), from Acinetobacter baumannii, on the expression of pro-inflammatory genes that play an essential role in bacterial clearance. LAD2 human mast cells were stimulated with LOS derived from two strains of A. baumannii—ATCC 19606 and MDRA T14. LOS exposure induced the expression of genes for pro-inflammatory mediators, including TNF-α, IL-8, LTC4S, CCL4, and TLR4. The mRNA expression levels of a majority of the pro-inflammatory genes, except TLR4, in A. baumannii-LOS stimulated mast cells were increased. Moreover, co-culture of neutrophils with the supernatant obtained from LOS (ATCC 19606 and MDRA T14)-induced LAD2 cells increased the transmigration of neutrophils, which plays a critical role in the early protection against bacterial infections. The results of the present study suggest that LOS could be involved in the pathogenicity of A. baumannii by inducing inflammatory responses via mast cells and that IL-8 is involved in recruiting neutrophils in response to bacterial invasion.

The TNF-α of mast cells induces pro-inflammatory responses during infection with Acinetobacter baumannii

Immunobiology ◽  
2017 ◽  
Vol 222 (11) ◽  
pp. 1025-1034 ◽  
Author(s):  
Takane Kikuchi-Ueda ◽  
Go Kamoshida ◽  
Tsuneyuki Ubagai ◽  
Ryuichi Nakano ◽  
Akiyo Nakano ◽  
...  
Keyword(s):  
Mast Cells ◽  
Acinetobacter Baumannii ◽  
Inflammatory Responses ◽  
Tnf Α

scholarly journals IL-4–Stat6 Signaling Induces Tristetraprolin Expression and Inhibits TNF-α Production in Mast Cells

2003 ◽  
Vol 198 (11) ◽  
pp. 1717-1727 ◽  
Author(s):  
Kotaro Suzuki ◽  
Hiroshi Nakajima ◽  
Kei Ikeda ◽  
Yuko Maezawa ◽  
Akira Suto ◽  
...  
Keyword(s):  
Mast Cells ◽  
Rna Binding ◽  
Inflammatory Responses ◽  
Immunoglobulin E ◽  
Critical Role ◽  
Interleukin 4 ◽  
Dependent Manner ◽  
Tnf Α ◽  
Factor Α ◽  
Dependent Mechanism

Increasing evidence has revealed that mast cell–derived tumor necrosis factor α (TNF-α) plays a critical role in a number of inflammatory responses by recruiting inflammatory leukocytes. In this paper, we investigated the regulatory role of interleukin 4 (IL-4) in TNF-α production in mast cells. IL-4 inhibited immunoglobulin E–induced TNF-α production and neutrophil recruitment in the peritoneal cavity in wild-type mice but not in signal transducers and activators of transcription 6 (Stat6)–deficient mice. IL-4 also inhibited TNF-α production in cultured mast cells by a Stat6-dependent mechanism. IL-4–Stat6 signaling induced TNF-α mRNA destabilization in an AU-rich element (ARE)–dependent manner, but did not affect TNF-α promoter activity. Furthermore, IL-4 induced the expression of tristetraprolin (TTP), an RNA-binding protein that promotes decay of ARE-containing mRNA, in mast cells by a Stat6-dependent mechanism, and the depletion of TTP expression by RNA interference prevented IL-4–induced down-regulation of TNF-α production in mast cells. These results suggest that IL-4–Stat6 signaling induces TTP expression and, thus, destabilizes TNF-α mRNA in an ARE-dependent manner.

scholarly journals Human Mast Cells Release Metalloproteinase-9 on Contact with Activated T Cells: Juxtacrine Regulation by TNF-α

2001 ◽  
Vol 167 (7) ◽  
pp. 4008-4016 ◽  
Author(s):  
Dana Baram ◽  
Gayle G. Vaday ◽  
Pazit Salamon ◽  
Ilana Drucker ◽  
Rami Hershkoviz ◽  
...  
Keyword(s):  
T Cells ◽  
Mast Cells ◽  
Activated T Cells ◽  
Human Mast Cells ◽  
Tnf Α ◽  
Metalloproteinase 9

Adenoviral E3-14.7K protein in LPS-induced lung inflammation

2000 ◽  
Vol 278 (4) ◽  
pp. L631-L639 ◽  
Author(s):  
Kevin S. Harrod ◽  
Amber D. Mounday ◽  
Jeffrey A. Whitsett
Keyword(s):  
Transgenic Mice ◽  
Lung Inflammation ◽  
Cell Injury ◽  
Inflammatory Responses ◽  
Critical Role ◽  
Respiratory Epithelium ◽  
Wild Type ◽  
Intracellular Staining ◽  
Intratracheal Administration ◽  
Tnf Α

The adenoviral E3-14.7K protein is a cytoplasmic protein synthesized after adenoviral infection. To assess the contribution of E3-14.7K-sensitive pathways in the modulation of inflammation by the respiratory epithelium, inflammatory responses to intratracheal lipopolysaccharide (LPS) and tumor necrosis factor (TNF)-α were assessed in transgenic mice bearing the adenoviral E3-14.7K gene under the direction of the surfactant protein (SP) C promoter. When E3-14.7K transgenic mice were administered LPS intratracheally, lung inflammation as indicated by macrophage and neutrophil accumulation in bronchoalveolar lavage fluid was decreased compared with wild-type control mice. Lung inflammation and epithelial cell injury were decreased in E3-14.7K mice 24 and 48 h after LPS administration. Intracellular staining for surfactant proprotein (proSP) B, proSP-C, and SP-B was decreased and extracellular staining was markedly increased in wild-type mice after LPS administration, consistent with LPS-induced lung injury. In contrast, intense intracellular staining of proSP-B, proSP-C, and SP-B persisted in type II cells of E3-14.7K mice, whereas extracellular staining of proSP-B and proSP-C was absent. Inhibitory effects of intratracheal LPS on SP-C mRNA were ameliorated by expression of the E3-14.7Kgene. Similar to the response to LPS, lung inflammation after intratracheal administration of TNF-α was decreased in E3-14.7K transgenic mice. Levels of TNF-α after LPS administration were similar in wild-type and E3-14.7K-bearing mice. Cell-selective expression of E3-14.7K in the respiratory epithelium inhibited LPS- and TNF-α-mediated lung inflammation, demonstrating the critical role of respiratory epithelial cells in LPS- and TNF-α-induced lung inflammation.

scholarly journals Immunization with 3-oxododecanoyl-l-homoserine lactone–protein conjugate protects mice from lethal Pseudomonas aeruginosa lung infection

2006 ◽  
Vol 55 (10) ◽  
pp. 1381-1387 ◽  
Author(s):  
Shinichi Miyairi ◽  
Kazuhiro Tateda ◽  
Etsu T. Fuse ◽  
Chihiro Ueda ◽  
Hiroaki Saito ◽  
...  
Keyword(s):  
Quorum Sensing ◽  
Specific Antibody ◽  
Bacterial Infections ◽  
Inflammatory Responses ◽  
Critical Role ◽  
Lung Infection ◽  
Homoserine Lactone ◽  
Vaccine Strategy ◽  
Protein Conjugate

Quorum-sensing systems have been reported to play a critical role in the pathogenesis of several bacterial infections. Recent data have demonstrated that Pseudomonas N-3-oxododecanoyl-l-homoserine lactone (3-oxo-C12-homoserine lactone, 3-oxo-C12-HSL), but not N-butanoyl-l-homoserine lactone (C4-HSL), induces apoptosis in macrophages and neutrophils. In the present study, the effects of active immunization with 3-oxo-C12-HSL–carrier protein conjugate on acute P. aeruginosa lung infection in mice were investigated. Immunization with 3-oxo-C12-HSL–BSA conjugate (subcutaneous, four times, at 2-week intervals) elaborated significant amounts of specific antibody in serum. Control and immunized mice were intranasally challenged with approximately 3×106 c.f.u. P. aeruginosa PAO1, and survival was then compared. All control mice died by day 2 post bacterial challenge, while 36 % of immunized mice survived to day 4 (P<0.05). Interestingly, bacterial numbers in the lungs did not differ between control and immunized groups, whereas the levels of pulmonary tumour necrosis factor (TNF)-α in the immunized mice were significantly lower than those of control mice (P<0.05). Furthermore, the extractable 3-oxo-C12-HSL levels in serum and lung homogenate were also significantly diminished in the immunized mice. Immune serum completely rescued reduction of cell viability by 3-oxo-C12-HSL-mediated apoptosis in macrophages in vitro. These results demonstrated that specific antibody to 3-oxo-C12-HSL plays a protective role in acute P. aeruginosa infection, probably through blocking of host inflammatory responses, without altering lung bacterial burden. The present data identify a promising potential vaccine strategy targeting bacterial quorum-sensing molecules, including autoinducers.

Transforming growth factor-β-regulated expression of genes in macrophages implicated in the control of cholesterol homoeostasis

2006 ◽  
Vol 34 (6) ◽  
pp. 1141-1144 ◽  
Author(s):  
D.P. Ramji ◽  
N.N. Singh ◽  
P. Foka ◽  
S.A. Irvine ◽  
K. Arnaoutakis
Keyword(s):  
Growth Factor ◽  
Molecular Mechanisms ◽  
Transforming Growth Factor ◽  
Inflammatory Responses ◽  
Critical Role ◽  
Transforming Growth Factor Β ◽  
Crucial Importance ◽  
Expression Of Genes ◽  
Regulated Expression ◽  
Key Genes

The regulation of macrophage cholesterol homoeostasis is of crucial importance in the pathogenesis of atherosclerosis, an underlying cause of heart attack and stroke. Several recent studies have revealed a critical role for the cytokine TGF-β (transforming growth factor-β), a key regulator of the immune and inflammatory responses, in atherogenesis. We discuss here the TGF-β signalling pathway and its role in this disease along with the outcome of our recent studies on the action of the cytokine on the expression of key genes implicated in the uptake or efflux of cholesterol by macrophages and the molecular mechanisms underlying such regulation.

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