PMID- 15616027
OWN - NLM
STAT- MEDLINE
DCOM- 20050414
LR  - 20190516
IS  - 0012-1797 (Print)
IS  - 0012-1797 (Linking)
VI  - 54
IP  - 1
DP  - 2005 Jan
TI  - Impairment of host resistance to Listeria monocytogenes infection in liver of 
      db/db and ob/ob mice.
PG  - 182-9
AB  - Leptin is an adipocyte-derived hormone that regulates a number of physiological 
      functions, including energy homeostasis and immune function. In immune responses, 
      leptin plays a role in the induction of inflammation. We investigated a role of 
      leptin in Listeria monocytogenes infection using leptin receptor-deficient db/db 
      mice and leptin-deficient ob/ob mice. These mutant mice were highly susceptible 
      to L. monocytogenes, and the elimination of bacteria from the liver was 
      inhibited. After infection, the induction of monocyte chemoattractant protein-1 
      (MCP-1) and KC mRNA in the liver of db/db mice and the MCP-1 mRNA expression in 
      the liver of ob/ob mice was decreased compared with their heterozygote 
      littermates. Leptin replacement in ob/ob mice resulted in improvement of 
      anti-listerial resistance and the MCP-1 mRNA expression. The elimination of L. 
      monocytogenes was significantly enhanced, and the expression of MCP-1 and KC mRNA 
      was completely reversed in db/db mice by insulin treatment. These results suggest 
      that leptin is required for host resistance to L. monocytogenes infection and 
      that hyperglycemia caused by leptin deficiency is involved in the inefficient 
      elimination of bacteria from the liver. Moreover, defect of MCP-1 expression in 
      the liver may be involved in the attenuated host resistance in these mutant mice.
FAU - Ikejima, Shin
AU  - Ikejima S
AD  - Department of Bacteriology, Hirosaki University School of Medicine, Zaifu-cho 5, 
      Hirosaki, Aomori 036-8562, Japan.
FAU - Sasaki, Sanae
AU  - Sasaki S
FAU - Sashinami, Hiroshi
AU  - Sashinami H
FAU - Mori, Fumiaki
AU  - Mori F
FAU - Ogawa, Yoshiji
AU  - Ogawa Y
FAU - Nakamura, Teruo
AU  - Nakamura T
FAU - Abe, Yoshinao
AU  - Abe Y
FAU - Wakabayashi, Koichi
AU  - Wakabayashi K
FAU - Suda, Toshihiro
AU  - Suda T
FAU - Nakane, Akio
AU  - Nakane A
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Diabetes
JT  - Diabetes
JID - 0372763
RN  - 0 (Ccl2 protein, mouse)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Cytokines)
RN  - 0 (DNA Primers)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Cell Surface)
RN  - 0 (Receptors, Leptin)
SB  - IM
MH  - Animals
MH  - Chemokine CCL2/genetics
MH  - Colony-Forming Units Assay
MH  - Cytokines/genetics
MH  - DNA Primers
MH  - Disease Susceptibility
MH  - Immunity, Innate
MH  - Inflammation
MH  - Listeria monocytogenes
MH  - Listeriosis/*genetics
MH  - Liver/physiopathology
MH  - Mice
MH  - Mice, Knockout
MH  - Mice, Obese
MH  - RNA, Messenger/genetics
MH  - Receptors, Cell Surface/*deficiency/genetics
MH  - Receptors, Leptin
MH  - Reverse Transcriptase Polymerase Chain Reaction
EDAT- 2004/12/24 09:00
MHDA- 2005/04/15 09:00
CRDT- 2004/12/24 09:00
PHST- 2004/12/24 09:00 [pubmed]
PHST- 2005/04/15 09:00 [medline]
PHST- 2004/12/24 09:00 [entrez]
AID - 54/1/182 [pii]
AID - 10.2337/diabetes.54.1.182 [doi]
PST - ppublish
SO  - Diabetes. 2005 Jan;54(1):182-9. doi: 10.2337/diabetes.54.1.182.