PMID- 10948149
OWN - NLM
STAT- MEDLINE
DCOM- 20000908
LR  - 20210526
IS  - 0019-9567 (Print)
IS  - 1098-5522 (Electronic)
IS  - 0019-9567 (Linking)
VI  - 68
IP  - 9
DP  - 2000 Sep
TI  - Induction of interleukin-4 (IL-4) by legionella pneumophila infection in BALB/c 
      mice and regulation of tumor necrosis factor alpha, IL-6, and IL-1beta.
PG  - 5234-40
AB  - Infection of BALB/c mice with a sublethal concentration of Legionella pneumophila 
      causes an acute disease that is resolved by innate immune responses. The 
      infection also initiates the development of adaptive Th1 responses that protect 
      the mice from challenge infections. To study the early responses, cytokines 
      induced during the first 24 h after infection were examined. In the serum, 
      interleukin-12 (IL-12) was detectable by 3 h and peaked at 10 h, while gamma 
      interferon was discernible by 5 h and peaked at 8 h. Similar patterns were 
      observed in ex vivo cultures of splenocytes. A transient IL-4 response was also 
      detected by 3 h postinfection in ex vivo cultures. BALB/c IL-4-deficient mice 
      were more susceptible to L. pneumophila infection than were wild-type mice. The 
      infection induced higher serum levels of acute-phase cytokines (tumor necrosis 
      factor alpha [TNF-alpha], IL-1beta, and IL-6), and reducing TNF-alpha levels with 
      antibodies protected the mice from death. Moreover, the addition of IL-4 to L. 
      pneumophila-infected macrophage cultures suppressed the production of these 
      cytokines. Thus, the lack of IL-4 in the deficient mice resulted in unchecked 
      TNF-alpha production, which appeared to cause the mortality. Monocyte 
      chemoattractant protein-1 (MCP-1), a chemokine that is induced by IL-4 during 
      Listeria monocytogenes infection, was detected at between 2 and 30 h after 
      infection. However, MCP-1 did not appear to be induced by IL-4 or to be required 
      for the TNF-alpha regulation by IL-4. The data suggest that the early increase in 
      IL-4 serves to regulate the mobilization of acute phase cytokines and thus 
      controls the potential harmful effects of these cytokines.
FAU - Newton, C
AU  - Newton C
AD  - Department of Medical Microbiology and Immunology, University of South Florida 
      College of Medicine, Tampa, Florida 33612, USA. cnewton@hsc.usf.edu
FAU - McHugh, S
AU  - McHugh S
FAU - Widen, R
AU  - Widen R
FAU - Nakachi, N
AU  - Nakachi N
FAU - Klein, T
AU  - Klein T
FAU - Friedman, H
AU  - Friedman H
LA  - eng
GR  - R01 AI045169/AI/NIAID NIH HHS/United States
GR  - AI45169-01/AI/NIAID 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 (Interleukin-1)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 187348-17-0 (Interleukin-12)
RN  - 207137-56-2 (Interleukin-4)
RN  - 82115-62-6 (Interferon-gamma)
SB  - IM
MH  - Animals
MH  - Cells, Cultured
MH  - Chemokine CCL2/biosynthesis
MH  - Female
MH  - Interferon-gamma/biosynthesis
MH  - Interleukin-1/*biosynthesis
MH  - Interleukin-12/biosynthesis
MH  - Interleukin-4/*physiology
MH  - Legionnaires' Disease/*immunology
MH  - Macrophages/metabolism
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Tumor Necrosis Factor-alpha/*biosynthesis
PMC - PMC101783
EDAT- 2000/08/19 11:00
MHDA- 2000/09/19 11:01
PMCR- 2000/09/01
CRDT- 2000/08/19 11:00
PHST- 2000/08/19 11:00 [pubmed]
PHST- 2000/09/19 11:01 [medline]
PHST- 2000/08/19 11:00 [entrez]
PHST- 2000/09/01 00:00 [pmc-release]
AID - 1935 [pii]
AID - 10.1128/IAI.68.9.5234-5240.2000 [doi]
PST - ppublish
SO  - Infect Immun. 2000 Sep;68(9):5234-40. doi: 10.1128/IAI.68.9.5234-5240.2000.