The Role of Interleukin 8 and NF(nuclear factor)-κB in Rhinovirus-Induced Airway Inflammation

2003 ◽  
Vol 54 (1) ◽  
pp. 104
Author(s):  
Ho Joo Yoon ◽  
Mi Ok Kim ◽  
Jang Won Sohn ◽  
Jung Mogg Kim ◽  
Dong Ho Shin ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Nuclear Factor Κb ◽  
Interleukin 8 ◽  
Nuclear Factor

scholarly journals Essential Role of Transcription Factor Nuclear Factor-κB in Regulation of Interleukin-8 Gene Expression by Nitrite Reductase from Pseudomonas aeruginosa in Respiratory Epithelial Cells

1999 ◽  
Vol 67 (8) ◽  
pp. 3872-3878 ◽  
Author(s):  
Naoki Mori ◽  
Kazunori Oishi ◽  
Borann Sar ◽  
Naofumi Mukaida ◽  
Tsuyoshi Nagatake ◽  
...  
Keyword(s):  
Gene Expression ◽  
Pseudomonas Aeruginosa ◽  
Epithelial Cells ◽  
Nitrite Reductase ◽  
Critical Role ◽  
Nuclear Factor Κb ◽  
Interleukin 8 ◽  
Nuclear Factor ◽  
Respiratory Cells

ABSTRACT Persistent infection with Pseudomonas aeruginosaincreases interleukin-8 (IL-8) levels and causes dense neutrophil infiltrations in the airways of patients with chronic airway diseases. Recently, we have reported that nitrite reductase from P. aeruginosa induces the production of IL-8 in respiratory cells, including bronchial epithelial cells. To determine the molecular mechanism(s) of nitrite reductase-induced IL-8 expression in respiratory cells, A549 epithelial cells were transfected with plasmids containing serial deletions of the 5′-flanking region of the IL-8 gene and then exposed to nitrite reductase. Nitrite reductase significantly enhanced IL-8 gene promoter-driven reporter activity. This increased IL-8 gene expression was inhibited by mutating the nuclear factor-κB (NF-κB) binding element. Nitrite reductase enhanced nuclear localization of the NF-κB binding complex. Furthermore, nitrite reductase induced the degradation of IκBα, the major cytoplasmic inhibitor of NF-κB, and the expression of IκBα mRNA. These data support the critical role of the activation of NF-κB in nitrite reductase-induced IL-8 gene expression in airway epithelium.

ROLE OF NUCLEAR FACTOR κB IN MELANOMA PROGRESSION.

2007 ◽  
Vol 55 (1) ◽  
pp. S158
Author(s):  
A. M. DeLuca ◽  
B. Ryu ◽  
R. Alani
Keyword(s):  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Melanoma Progression

Role of nuclear factor-κB in gastric ulcer healing in rats

2001 ◽  
Vol 280 (6) ◽  
pp. G1296-G1304 ◽  
Author(s):  
Satoru Takahashi ◽  
Takuya Fujita ◽  
Akira Yamamoto
Keyword(s):  
Gastric Ulcer ◽  
Mrna Expression ◽  
Ulcer Healing ◽  
Nuclear Factor Κb ◽  
Normal Mucosa ◽  
Cyclooxygenase 2 ◽  
Interleukin 1Β ◽  
Nuclear Factor ◽  
Gastric Ulcer Healing

We investigated the role of nuclear factor-κB (NF-κB) in gastric ulcer healing in rats. NF-κB was activated in ulcerated tissue but not in normal mucosa, and the level of the activation was decreased with ulcer healing. NF-κB activation was observed in fibroblasts, monocytes/macrophages, and neutrophils. Treatment of gastric fibroblasts, isolated from the ulcer base, with interleukin-1β activated NF-κB and the subsequently induced cyclooxygenase-2 and cytokine-induced neutrophil chemoattractant-1 (CINC-1) mRNA expression. Inhibition of activated NF-κB action resulted in suppression of both their mRNA expression and increases in PGE2 and CINC-1 levels induced by interleukin-1β. Persistent prevention of NF-κB activation caused an impairment of ulcer healing in rats. Gene expression of interleukin-1β, CINC-1, cyclooxygenase-2, and inducible nitric oxide synthase in ulcerated tissue had been inhibited before the delay in ulcer healing became manifest. The increased levels of cyclooxygenase-2 protein and PGE2 production were also reduced. These results demonstrate that NF-κB, activated in ulcerated tissue, might upregulate the expression of healing-promoting factors responsible for gastric ulcer healing in rats.

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