PMID- 12874304
OWN - NLM
STAT- MEDLINE
DCOM- 20030826
LR  - 20231105
IS  - 0019-9567 (Print)
IS  - 1098-5522 (Electronic)
IS  - 0019-9567 (Linking)
VI  - 71
IP  - 8
DP  - 2003 Aug
TI  - Expression of cytokine and chemokine genes by human middle ear epithelial cells 
      induced by influenza A virus and Streptococcus pneumoniae opacity variants.
PG  - 4289-96
AB  - Real-time PCR and enzyme-linked immunosorbent assay were used to evaluate the 
      ability of influenza A virus and Streptococcus pneumoniae opacity variants, 
      either alone or in combination, to induce cytokine and chemokine genes in primary 
      cultures of human middle ear epithelial (HMEE) cells. Following treatment with 
      influenza A virus, the induction of gene expression, which occurred in a dose- 
      and time-dependent manner, was strong for macrophage inflammatory protein 1 alpha 
      (MIP-1 alpha) and MIP-1 beta; moderate for tumor necrosis factor alpha 
      (TNF-alpha), interleukin-6 (IL-6), and IL-8; and weak for IL-1 beta and monocyte 
      chemotactic peptide 1 (MCP-1). Except for TNF-alpha, all the gene products were 
      detected in the cell culture supernatants. In contrast, infection of HMEE cells 
      with S. pneumoniae alone induced low levels of mRNA expression of MIP-1 alpha and 
      MIP-1 beta and did not significantly induce the transcription of the other 
      cytokines and chemokines examined. However, both S. pneumoniae opacity variants 
      increased mRNA expression of MIP-1 alpha, MIP-1 beta, IL-6, and MCP-1 in HMEE 
      cells activated by a prior influenza A virus infection compared to levels in 
      cells treated with either agent alone. Up-regulation of IL-6, IL-8, and MCP-1 
      mRNA expression and production by the virus in combination with opaque S. 
      pneumoniae was two- to threefold higher than that induced by the virus combined 
      with the transparent S. pneumoniae variant. These data indicate that the 
      activation of HMEE cells by influenza A virus enhances the induction of cytokine 
      and chemokine gene transcripts by S. pneumoniae and that this effect appears to 
      be most pronounced when S. pneumoniae is in the opaque phase.
FAU - Tong, H H
AU  - Tong HH
AD  - Division of Otologic Research, College of Medicine and Public Health, The Ohio 
      State University, Columbus, Ohio 43210, USA.
FAU - Long, J P
AU  - Long JP
FAU - Shannon, P A
AU  - Shannon PA
FAU - DeMaria, T F
AU  - DeMaria TF
LA  - eng
GR  - R01 DC003105/DC/NIDCD NIH HHS/United States
GR  - R01 DC3105-06/DC/NIDCD NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Infect Immun
JT  - Infection and immunity
JID - 0246127
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokine CCL3)
RN  - 0 (Chemokine CCL4)
RN  - 0 (Chemokines)
RN  - 0 (Cytokines)
RN  - 0 (Interleukin-1)
RN  - 0 (Interleukin-6)
RN  - 0 (Interleukin-8)
RN  - 0 (Macrophage Inflammatory Proteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Cells, Cultured
MH  - Chemokine CCL2/genetics
MH  - Chemokine CCL3
MH  - Chemokine CCL4
MH  - Chemokines/*genetics
MH  - Cytokines/*genetics
MH  - Ear, Middle/cytology/immunology/virology
MH  - Epithelial Cells/immunology/virology
MH  - Gene Expression
MH  - Genetic Variation
MH  - Humans
MH  - Immunity, Innate
MH  - Influenza A virus/*pathogenicity
MH  - Interleukin-1/genetics
MH  - Interleukin-6/genetics
MH  - Interleukin-8/genetics
MH  - Macrophage Inflammatory Proteins/genetics
MH  - Otitis Media/etiology
MH  - RNA, Messenger/genetics/metabolism
MH  - Streptococcus pneumoniae/*genetics/*pathogenicity
MH  - Tumor Necrosis Factor-alpha/genetics
PMC - PMC166016
EDAT- 2003/07/23 05:00
MHDA- 2003/08/27 05:00
PMCR- 2003/08/01
CRDT- 2003/07/23 05:00
PHST- 2003/07/23 05:00 [pubmed]
PHST- 2003/08/27 05:00 [medline]
PHST- 2003/07/23 05:00 [entrez]
PHST- 2003/08/01 00:00 [pmc-release]
AID - 0330 [pii]
AID - 10.1128/IAI.71.8.4289-4296.2003 [doi]
PST - ppublish
SO  - Infect Immun. 2003 Aug;71(8):4289-96. doi: 10.1128/IAI.71.8.4289-4296.2003.