PMID- 11564157
OWN - NLM
STAT- MEDLINE
DCOM- 20020122
LR  - 20180822
IS  - 0818-9641 (Print)
IS  - 0818-9641 (Linking)
VI  - 79
IP  - 5
DP  - 2001 Oct
TI  - Induction of multiple chemokine and colony-stimulating factor genes in 
      experimental Burkholderia pseudomallei infection.
PG  - 490-501
AB  - Melioidosis is a disease of the tropics caused by the facultative intracellular 
      bacterium Burkholderia pseudomallei. In human infection, increased levels of 
      IFN-gamma in addition to the chemokines interferon-gamma-inducible protein 10 
      (IP-10) and monocyte interferon-gamma-inducible protein (Mig) have been 
      demonstrated. However, the role of these and other chemokines in the pathogenesis 
      of melioidosis remains unknown. Using BALB/c and C57BL/6 mice as models of the 
      acute and chronic forms of human melioidosis, the induction of mRNA was assessed 
      for various chemokines and CSF (G-CSF, M-CSF, GM-CSF, IP-10, Mig, RANTES, MCP-1, 
      KC and MIP-2) in spleen and liver following B. pseudomallei infection. Patterns 
      of chemokine and CSF induction were similar in liver and spleen; however, 
      responses were typically greater in spleen, which reflected higher tissue 
      bacterial loads. In BALB/c mice, high-level expression of mRNA for all chemokines 
      and CSF investigated was demonstrated at day 3 postinfection, correlating with 
      peak bacterial load and extensive infiltration of leucocytes. In contrast, 
      increased mRNA expression and bacterial numbers in C57BL/6 mice were greatest 
      between 4 and 14 days following infection. This paralleled increases in the size 
      and number of abscesses in liver and spleen of C57BL/6 mice at days 3 and 14 
      postinfection. Earlier induction of cytokine-induced neutrophil chemoattractant 
      (KC), macrophage inflammatory protein-2 (MIP-2), monocyte chemoattractant 
      protein-1 (MCP-1), granulocyte-macrophage CSF (GM-CSF) and macrophage CSF (M-CSF) 
      mRNA was demonstrated in spleen, while MIP-2, MCP-1, IP-10 and Mig were 
      demonstrated in liver of BALB/c mice when compared to spleen and liver of 
      C57BL/6. The magnitude of cellular responses observed in the tissue correlated 
      with increased levels of the chemokines and CSF investigated, as well as 
      bacterial load. Compared with C57BL/6 mice, greater infiltration of neutrophils 
      was observed in liver and spleen of BALB/c mice at day 3. In contrast, early 
      lesions in C57BL/6 mice predominantly comprised macrophages. These results 
      suggest that the inability of BALB/c mice to contain the infection at sites of 
      inflammation may underlie the susceptible phenotype of this mouse strain towards 
      B. pseudomallei infection.
FAU - Barnes, J L
AU  - Barnes JL
AD  - School of Biomedical Science, James Cook University, Townsville, Queensland, 
      Australia. jodie.barnes@jcu.edu.au
FAU - Ulett, G C
AU  - Ulett GC
FAU - Ketheesan, N
AU  - Ketheesan N
FAU - Clair, T
AU  - Clair T
FAU - Summers, P M
AU  - Summers PM
FAU - Hirst, R G
AU  - Hirst RG
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Immunol Cell Biol
JT  - Immunology and cell biology
JID - 8706300
RN  - 0 (Chemokines)
RN  - 0 (Colony-Stimulating Factors)
RN  - 0 (RNA, Messenger)
SB  - IM
MH  - Animals
MH  - Burkholderia pseudomallei/growth & development/*immunology/physiology
MH  - Chemokines/*genetics/metabolism
MH  - Colony-Stimulating Factors/*genetics/metabolism
MH  - Disease Models, Animal
MH  - *Gene Expression Regulation
MH  - Humans
MH  - Liver/immunology/microbiology
MH  - Melioidosis/genetics/*immunology/microbiology
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Inbred C57BL
MH  - RNA, Messenger/genetics/metabolism
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Spleen/immunology/microbiology
EDAT- 2001/09/21 10:00
MHDA- 2002/01/23 10:01
CRDT- 2001/09/21 10:00
PHST- 2001/09/21 10:00 [pubmed]
PHST- 2002/01/23 10:01 [medline]
PHST- 2001/09/21 10:00 [entrez]
AID - icb1038 [pii]
AID - 10.1046/j.1440-1711.2001.01038.x [doi]
PST - ppublish
SO  - Immunol Cell Biol. 2001 Oct;79(5):490-501. doi: 10.1046/j.1440-1711.2001.01038.x.