PMID- 11846225
OWN - NLM
STAT- MEDLINE
DCOM- 20020726
LR  - 20061115
IS  - 0171-2985 (Print)
IS  - 0171-2985 (Linking)
VI  - 204
IP  - 5
DP  - 2001 Dec
TI  - Defense against influenza A virus infection: essential role of the chemokine 
      system.
PG  - 603-13
AB  - Monocytes/macrophages are highly susceptible to an infection with influenza A 
      virus. After infection, de novo virus protein synthesis is detectable but rapidly 
      interrupted before completion of the first viral replication cycle. Within 24-48 
      hours the infected monocytes die by apoptosis. Before cell death, infected 
      monocytes initiate a cell-specific immune response. This includes the 
      transcription and subsequent release of TNF-alpha (tumor necrosis factor alpha), 
      IL-1beta (Interleukin 1beta), IL-6, type I inferferons and CC chemokines. 
      Enhanced cytokine mRNA expression is due to a prolonged mRNA stability and an 
      augmented gene transcription. Activation of transcription factors such as 
      NF-kappaB (nuclear factor kappaB) and AP-1 are involved in activation of cytokine 
      mRNA transcription. Infection of monocytes with influenza A virus induces the 
      selective expression of mononuclear leukocyte attracting chemokines, such as 
      MCP-1 (monocyte chemotactic protein 1), MIP-1alpha (macrophage inflammatory 
      protein 1alpha) and RANTES (regulated upon activation, normal T cell expressed 
      and secreted). In striking contrast, the release of the neutrophil-specific 
      chemokines IL-8 (interleukin 8) and GRO-alpha (growth stimulatory activity alpha) 
      is entirely suppressed. This differentially regulated chemokine expression may 
      explain the mononuclear cell infiltrate characteristic for virus-infected tissue. 
      Thus, infection of monocytes/macrophages with influenza A virus primes for a 
      rapid proinflammatory reaction and induces an enhanced immigration of mononuclear 
      cells into infected tissue. Taken together, these mechanisms may prepare the 
      infected host for a fast and virus-specific immune response.
FAU - Kaufmann, A
AU  - Kaufmann A
AD  - Institute of Immunology, Philipps-University, Marburg, Germany. 
      kaufmana@mailer.uni-marburg.de
FAU - Salentin, R
AU  - Salentin R
FAU - Meyer, R G
AU  - Meyer RG
FAU - Bussfeld, D
AU  - Bussfeld D
FAU - Pauligk, C
AU  - Pauligk C
FAU - Fesq, H
AU  - Fesq H
FAU - Hofmann, P
AU  - Hofmann P
FAU - Nain, M
AU  - Nain M
FAU - Gemsa, D
AU  - Gemsa D
FAU - Sprenger, H
AU  - Sprenger H
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - Netherlands
TA  - Immunobiology
JT  - Immunobiology
JID - 8002742
RN  - 0 (Chemokines)
SB  - IM
MH  - Animals
MH  - Chemokines/*immunology
MH  - Humans
MH  - Influenza A virus/*immunology
MH  - Influenza, Human/*immunology
MH  - Monocytes/immunology
RF  - 31
EDAT- 2002/02/16 10:00
MHDA- 2002/07/27 10:01
CRDT- 2002/02/16 10:00
PHST- 2002/02/16 10:00 [pubmed]
PHST- 2002/07/27 10:01 [medline]
PHST- 2002/02/16 10:00 [entrez]
AID - S0171-2985(04)70048-0 [pii]
AID - 10.1078/0171-2985-00099 [doi]
PST - ppublish
SO  - Immunobiology. 2001 Dec;204(5):603-13. doi: 10.1078/0171-2985-00099.