nfkb activation by nontypeable hemophilus influenzae
| PAG Title | nfkb activation by nontypeable hemophilus influenzae |
| PAG ID | WAG000416 |
| Type | P |
| Source Link |  BioCarta |
| Publication Reference | NA |
| PAG Description | The role of Hemophilus influenzae in ear infections and chronic obstructive pulmory disease includes the induction of an inflammatory response through activation of the transcription factor NF-kB. In addition to activation of inflammatory cytokine genes like IL-1 and TNF, H. influenzae activates TLR2 expression and genes involved in mucus production. Hemophilus influenzae activates NF-kB by multiple mechanisms, starting with activation of the Toll-like receptor 2 (TLR2) by the p16 protein in the H. influenzae outer membrane. TLR2 plays a key role in inte immune responses and is expressed in high levels in lymphoid cells as well as low levels in epithelial cells. The role of TLR2 was supported by blocking NF-kB activation with a domint negative TLR2 and increasing it with transfection of a normal TLR2 gene. TLR2 in turn activates TAK1, which activates two divergent sigling pathways. One of these pathways leads to IkB kise activation, IkB phosphorylation and degradation, releasing the NF-kB heterodimer to translocate into the nucleus and activate transcription of target genes. In the alterte pathway, TAK1 also activates NF-kB through a Map kise pathway, activating p38 and NF-kB in a nuclear translocation independent manner. Investigation of the mechanisms of H. influenzae sigling involved in NF-kB activation may provide the information needed to develop better treatments for inflammatory conditions caused by this pathogen. |
| Species | Homo sapiens |
| Quality Metric Scores | nCoCo Score: 1,320 |
| Information Content | Rich |
| Other IDs | |
| Base PAG ID | WAG000416 |
| Human Phenotyte Annotation | |
| Curator | PAGER curation team |
| Curator Contact | PAGER-contact@googlegroups.com |
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