PMID- 9781806
OWN - NLM
STAT- MEDLINE
DCOM- 19981230
LR  - 20071114
IS  - 1079-9907 (Print)
IS  - 1079-9907 (Linking)
VI  - 18
IP  - 9
DP  - 1998 Sep
TI  - Herpes simplex virus replication-induced expression of chemokines and 
      proinflammatory cytokines in the eye: implications in herpetic stromal keratitis.
PG  - 681-90
AB  - On infection of the cornea with herpes simplex virus (HSV), an immunopathologic 
      response termed herpetic stromal keratitis (HSK) ensues. This response is 
      mediated primarily by CD4+ T cells and only occurs if mice are infected with 
      replication-competent virus, although replication-defective mutants induce 
      cellular immune responses following infection. To determine the consequences of 
      HSV replication in the cornea, which is crucial for HSK manifestation, corneas 
      infected with productive virus and replication-defective mutants were analyzed 
      for chemokines and proinflammatory cytokine mRNA expression by RT-PCR at various 
      times. While productive infection resulted in rapid upregulation and sustained 
      expression of such chemokines as N51/KC, macrophage inflammatory protein-1beta 
      (MIP-1beta), MIP-2, and monocyte chemotactic protein-1 (MCP-1) and such cytokines 
      as interleukin-1 (IL-1), IL-6, IL-12, and tumor necrosis factor-alpha 
      (TNF-alpha), expression of such inflammatory mediators was minimal and transient 
      after unproductive infection. Expression of MIP-1alpha and lymphotactin along 
      with a biphasic expression of IL-6 and MIP-2 were seen only with productive 
      infection. Initial PMN recruitment into the cornea was approximately 50-fold 
      greater with productive infection than with unproductive infection. These data 
      suggest that a replication-induced proinflammatory milieu in the cornea is 
      crucial for the subsequent progression of HSK possibly because of enhancement of 
      the expression of corneal agonists that drive HSK manifestation.
FAU - Thomas, J
AU  - Thomas J
AD  - Department of Microbiology, University of Tennessee, Knoxville 37996, USA.
FAU - Kanangat, S
AU  - Kanangat S
FAU - Rouse, B T
AU  - Rouse BT
LA  - eng
GR  - EY05093/EY/NEI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Interferon Cytokine Res
JT  - Journal of interferon & cytokine research : the official journal of the 
      International Society for Interferon and Cytokine Research
JID - 9507088
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokines)
RN  - 0 (Chemokines, C)
RN  - 0 (Cytokines)
RN  - 0 (Interleukins)
RN  - 0 (Lymphokines)
RN  - 0 (Macrophage Inflammatory Proteins)
RN  - 0 (Sialoglycoproteins)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (Xcl1 protein, mouse)
RN  - 0 (lymphotactin)
SB  - IM
MH  - Animals
MH  - Chemokine CCL2/biosynthesis
MH  - Chemokines/*biosynthesis
MH  - *Chemokines, C
MH  - Cytokines/*biosynthesis
MH  - Eye/*metabolism
MH  - Interleukins/biosynthesis
MH  - Keratitis, Herpetic/*metabolism/virology
MH  - Lymphokines/biosynthesis
MH  - Macrophage Inflammatory Proteins/biosynthesis
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Sialoglycoproteins/biosynthesis
MH  - Simplexvirus/*growth & development
MH  - Stromal Cells/metabolism/virology
MH  - Tumor Necrosis Factor-alpha/biosynthesis
MH  - *Virus Replication
EDAT- 1998/10/22 00:00
MHDA- 1998/10/22 00:01
CRDT- 1998/10/22 00:00
PHST- 1998/10/22 00:00 [pubmed]
PHST- 1998/10/22 00:01 [medline]
PHST- 1998/10/22 00:00 [entrez]
AID - 10.1089/jir.1998.18.681 [doi]
PST - ppublish
SO  - J Interferon Cytokine Res. 1998 Sep;18(9):681-90. doi: 10.1089/jir.1998.18.681.