2008
DOI: 10.1186/1743-422x-5-17
|View full text |Cite
|
Sign up to set email alerts
|

Human adenovirus type 19 infection of corneal cells induces p38 MAPK-dependent interleukin-8 expression

Abstract: Background: Human adenovirus type 19 (HAdV-19) is a major cause of epidemic keratoconjunctivitis, the only ocular adenoviral infection associated with prolonged corneal inflammation. In this study, we investigated the role of p38 mitogen-activated protein kinase (MAPK) in HAdV-19 infection, with particular attention to the role of p38 MAPK in the transcriptional control of interleukin-8 (IL-8), a chemokine previously shown to be central to the initiation of adenovirus keratitis.

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1
1

Citation Types

3
45
1

Year Published

2009
2009
2020
2020

Publication Types

Select...
8
1

Relationship

2
7

Authors

Journals

citations
Cited by 33 publications
(49 citation statements)
references
References 49 publications
3
45
1
Order By: Relevance
“…On the other hand, activation of the Erk1/2 pathway has been described in native and beta-hematin-fed murine macrophages (23,24) but not yet in humans. However, since large amounts of data from several models indicate a correlation between activation of p38 MAPK and higher levels of IL-8 and HSP27 (2,26,50), major investigations into the role of MAPK cascades in HZ-dependent enhancement of chemokine expression, induction of HSP27 expression, and prevention of apoptosis is certainly warranted.…”
Section: Discussionmentioning
confidence: 99%
“…On the other hand, activation of the Erk1/2 pathway has been described in native and beta-hematin-fed murine macrophages (23,24) but not yet in humans. However, since large amounts of data from several models indicate a correlation between activation of p38 MAPK and higher levels of IL-8 and HSP27 (2,26,50), major investigations into the role of MAPK cascades in HZ-dependent enhancement of chemokine expression, induction of HSP27 expression, and prevention of apoptosis is certainly warranted.…”
Section: Discussionmentioning
confidence: 99%
“…However, the mechanism by which E3 inhibits p38 phosphorylation is not known. Moreover, both PKR and p38 are known to regulate the cytokine response to virus infection (7,19,37), but it remains to be determined whether these proteins play a role in vaccinia virus-induced cytokine expression. Therefore, to study the signaling pathways which may regulate cytokine expression in vaccinia virus-infected cells, we investigated the roles of PKR and p38 activation, as measured by phosphorylation, following infection of HeLa cells with vv⌬E3L-Rev or vv⌬E3L.…”
Section: Vol 83 2009 Vaccinia Virus E3 Suppresses Cytokine Expressimentioning
confidence: 99%
“…PKR can activate signaling by both p38 and nuclear factor B (NF-B) (17), known mediators of the cytokine response. p38, a member of the mitogen-activated protein kinase (MAPK) family, can regulate IFN signaling and the cytokine response to adenovirus infection (30,33,37). Upon treatment of cells with pIC, PKR specifically interacts with MAPK kinase 6 (MKK6), resulting in MKK6 phosphorylation and downstream activation of p38 (44).…”
mentioning
confidence: 99%
“…Many DNA and RNA viruses subvert host MAPK signaling pathways to stimulate their productive replication, control cell proliferation, suppress apoptosis, or regulate latency (17, 25, 39, 50-52, 55, 56). MAPK activation is also associated with virus-induced cytokine production and inflammation (39,41). Importantly, in cells infected with herpes simplex virus 1 (HSV-1), all three major MAPK pathways are deregulated in response to virus infection (14,28,51,57).…”
mentioning
confidence: 99%