| pubmed-article:19120971 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19120971 | lifeskim:mentions | umls-concept:C0206679 | lld:lifeskim |
| pubmed-article:19120971 | lifeskim:mentions | umls-concept:C0754728 | lld:lifeskim |
| pubmed-article:19120971 | lifeskim:mentions | umls-concept:C1155075 | lld:lifeskim |
| pubmed-article:19120971 | lifeskim:mentions | umls-concept:C1880266 | lld:lifeskim |
| pubmed-article:19120971 | lifeskim:mentions | umls-concept:C0718566 | lld:lifeskim |
| pubmed-article:19120971 | lifeskim:mentions | umls-concept:C1292733 | lld:lifeskim |
| pubmed-article:19120971 | pubmed:issue | 12 | lld:pubmed |
| pubmed-article:19120971 | pubmed:dateCreated | 2009-1-5 | lld:pubmed |
| pubmed-article:19120971 | pubmed:abstractText | We investigated the interplay occurring between pathogens in the course of dual infections, using an in vitro model in which the THP-1 monocytic cell line is first infected with HSV-1 and then exposed to Ca or Cn. These three pathogens share some pathogenic features: they cause opportunistic infections, target macrophages and are neurotropic. Here, we show that HSV-1-infected THP-1 cells exhibited augmented phagocytosis against the two opportunistic fungi but reduced capability to counteract fungal infection: the better ingestion by monocytes was followed by facilitated fungal survival and replication. Reduced IL-12 production was also observed. Cytofluorimetric analysis showed that HSV-1-infected monocytes exhibit: (i) downregulated TLR-2 and TLR-4, critical structures in fungal recognition; (ii) reduced expression of CD38 and CD69, known to be important markers of monocyte activation; and (iii) enhanced expression of apoptosis and necrosis markers, in the absence of altered cell proliferation. Overall, these findings imply that HSV-1 infection prevents monocyte activation, thus leading to a significant dysfunction of the monocyte-mediated anti-Candida response; HSV-1 induced apoptosis and necrosis of monocytes further contribute to this impairment. | lld:pubmed |
| pubmed-article:19120971 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19120971 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19120971 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:19120971 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19120971 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19120971 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19120971 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19120971 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:19120971 | pubmed:issn | 0385-5600 | lld:pubmed |
| pubmed-article:19120971 | pubmed:author | pubmed-author:CossarizzaAnd... | lld:pubmed |
| pubmed-article:19120971 | pubmed:author | pubmed-author:BlasiElisabet... | lld:pubmed |
| pubmed-article:19120971 | pubmed:author | pubmed-author:CermelliClaud... | lld:pubmed |
| pubmed-article:19120971 | pubmed:author | pubmed-author:ArdizzoniAndr... | lld:pubmed |
| pubmed-article:19120971 | pubmed:author | pubmed-author:LugliEnricoE | lld:pubmed |
| pubmed-article:19120971 | pubmed:author | pubmed-author:OrsiCarlotta... | lld:pubmed |
| pubmed-article:19120971 | pubmed:author | pubmed-author:CenacchiValer... | lld:pubmed |
| pubmed-article:19120971 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:19120971 | pubmed:volume | 52 | lld:pubmed |
| pubmed-article:19120971 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19120971 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19120971 | pubmed:pagination | 575-84 | lld:pubmed |
| pubmed-article:19120971 | pubmed:meshHeading | pubmed-meshheading:19120971... | lld:pubmed |
| pubmed-article:19120971 | pubmed:meshHeading | pubmed-meshheading:19120971... | lld:pubmed |
| pubmed-article:19120971 | pubmed:meshHeading | pubmed-meshheading:19120971... | lld:pubmed |
| pubmed-article:19120971 | pubmed:meshHeading | pubmed-meshheading:19120971... | lld:pubmed |
| pubmed-article:19120971 | pubmed:meshHeading | pubmed-meshheading:19120971... | lld:pubmed |
| pubmed-article:19120971 | pubmed:meshHeading | pubmed-meshheading:19120971... | lld:pubmed |
| pubmed-article:19120971 | pubmed:meshHeading | pubmed-meshheading:19120971... | lld:pubmed |
| pubmed-article:19120971 | pubmed:meshHeading | pubmed-meshheading:19120971... | lld:pubmed |
| pubmed-article:19120971 | pubmed:meshHeading | pubmed-meshheading:19120971... | lld:pubmed |
| pubmed-article:19120971 | pubmed:meshHeading | pubmed-meshheading:19120971... | lld:pubmed |
| pubmed-article:19120971 | pubmed:meshHeading | pubmed-meshheading:19120971... | lld:pubmed |
| pubmed-article:19120971 | pubmed:meshHeading | pubmed-meshheading:19120971... | lld:pubmed |
| pubmed-article:19120971 | pubmed:year | 2008 | lld:pubmed |
| pubmed-article:19120971 | pubmed:articleTitle | Herpes simplex virus type 1 dysregulates anti-fungal defenses preventing monocyte activation and downregulating toll-like receptor-2. | lld:pubmed |
| pubmed-article:19120971 | pubmed:affiliation | Department of Public Health Sciences, University of Modena and Reggio Emilia, Modena, Italy. claudio.cermelli@unimore.it | lld:pubmed |
| pubmed-article:19120971 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:19120971 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| entrez-gene:7097 | entrezgene:pubmed | pubmed-article:19120971 | lld:entrezgene |
| http://linkedlifedata.com/r... | entrezgene:pubmed | pubmed-article:19120971 | lld:entrezgene |
