| pubmed-article:19043549 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19043549 | lifeskim:mentions | umls-concept:C0332307 | lld:lifeskim |
| pubmed-article:19043549 | lifeskim:mentions | umls-concept:C0023238 | lld:lifeskim |
| pubmed-article:19043549 | lifeskim:mentions | umls-concept:C1167395 | lld:lifeskim |
| pubmed-article:19043549 | lifeskim:mentions | umls-concept:C0079189 | lld:lifeskim |
| pubmed-article:19043549 | lifeskim:mentions | umls-concept:C0752312 | lld:lifeskim |
| pubmed-article:19043549 | lifeskim:mentions | umls-concept:C1704632 | lld:lifeskim |
| pubmed-article:19043549 | lifeskim:mentions | umls-concept:C0871261 | lld:lifeskim |
| pubmed-article:19043549 | lifeskim:mentions | umls-concept:C0205217 | lld:lifeskim |
| pubmed-article:19043549 | lifeskim:mentions | umls-concept:C2911692 | lld:lifeskim |
| pubmed-article:19043549 | lifeskim:mentions | umls-concept:C1706817 | lld:lifeskim |
| pubmed-article:19043549 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:19043549 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:19043549 | pubmed:issue | 11 | lld:pubmed |
| pubmed-article:19043549 | pubmed:dateCreated | 2008-12-1 | lld:pubmed |
| pubmed-article:19043549 | pubmed:abstractText | The immune system must discriminate between pathogenic and nonpathogenic microbes in order to initiate an appropriate response. Toll-like receptors (TLRs) detect microbial components common to both pathogenic and nonpathogenic bacteria, whereas Nod-like receptors (NLRs) sense microbial components introduced into the host cytosol by the specialized secretion systems or pore-forming toxins of bacterial pathogens. The host signaling pathways that respond to bacterial secretion systems remain poorly understood. Infection with the pathogen Legionella pneumophila, which utilizes a type IV secretion system (T4SS), induced an increased proinflammatory cytokine response compared to avirulent bacteria in which the T4SS was inactivated. This enhanced response involved NF-kappaB activation by TLR signaling as well as Nod1 and Nod2 detection of type IV secretion. Furthermore, a TLR- and RIP2-independent pathway leading to p38 and SAPK/JNK MAPK activation was found to play an equally important role in the host response to virulent L. pneumophila. Activation of this MAPK pathway was T4SS-dependent and coordinated with TLR signaling to mount a robust proinflammatory cytokine response to virulent L. pneumophila. These findings define a previously uncharacterized host response to bacterial type IV secretion that activates MAPK signaling and demonstrate that coincident detection of multiple bacterial components enables immune discrimination between virulent and avirulent bacteria. | lld:pubmed |
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| pubmed-article:19043549 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:19043549 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:19043549 | pubmed:status | MEDLINE | lld:pubmed |
