PMID- 12785005
OWN - NLM
STAT- MEDLINE
DCOM- 20040224
LR  - 20190916
IS  - 1073-2322 (Print)
IS  - 1073-2322 (Linking)
VI  - 19
IP  - 6
DP  - 2003 Jun
TI  - Mast cells and resistance to peritoneal sepsis after burn injury.
PG  - 513-8
AB  - A mouse model of burn injury demonstrates increasing mortality to an infectious 
      challenge in the form of cecal ligation and puncture (CLP) reaching a peak at 10 
      days after injury. Because it is widely believed that peritoneal mast cells play 
      an important role in the defense against peritoneal sepsis, we wished to explore 
      the possibility that peritoneal mast cell dysfunction contributed to increased 
      CLP mortality after burn injury. Kit(W-v) C57BL/6 mice, which were shown to lack 
      peritoneal mast cells by cytospin and flow cytometry, and normal littermate 
      control animals were subjected to 25% burn or sham burn injury and 10 days later 
      underwent CLP. Burn injured Kit(W-v) and normal littermates had a high CLP 
      mortality when compared with sham-injured Kit(W-v) and normal littermates (P < 
      0.003), but the sham- and burn-injured Kit(W-v) and normal littermate animals did 
      not differ from one another with respect to CLP mortality. This result prompted a 
      comparison of CLP mortality in untreated WBB6F1 Kit(W/W-v) mice, known to be mast 
      cell deficient, and normal littermate controls, as well as untreated C57BL/6 
      Kit(W-v) and normal littermates. The WBB6F1 Kit(W/W-v) mice showed significantly 
      increased mortality after CLP as compared with the littermate controls (P = 
      0.03), whereas both C57BL/6 Kit(W-v) and littermate controls had very low 
      mortality after CLP. A study of peritoneal cell populations 24 h after CLP failed 
      to reveal an obvious cause for the difference in CLP survival between the two 
      mast cell-deficient strains. Tumor necrosis factor-alpha (TNF-alpha) measurements 
      in peritoneal fluid showed appreciable amounts of TNF-alpha in the littermate 
      controls of both strains and little in the fluid obtained from the mast 
      cell-deficient animals of both strains. We conclude that peritoneal mast cell 
      dysfunction is unlikely to be a major cause of decreased resistance to peritoneal 
      sepsis in burn-injured animals and that the importance of peritoneal mast cells 
      in combating peritoneal sepsis in the mouse appears to be strain dependent.
FAU - Shelley, Odhran
AU  - Shelley O
AD  - Department of Surgery, Julian and Eunice Cohen Laboratory, Harvard Medical 
      School, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA.
FAU - Murphy, Thomas
AU  - Murphy T
FAU - Lederer, James A
AU  - Lederer JA
FAU - Mannick, John A
AU  - Mannick JA
FAU - Rodrick, Mary L
AU  - Rodrick ML
LA  - eng
GR  - GM3563317/GM/NIGMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Shock
JT  - Shock (Augusta, Ga.)
JID - 9421564
SB  - IM
MH  - Animals
MH  - Burns/*complications
MH  - Cecum/surgery
MH  - Disease Models, Animal
MH  - Immunity, Innate
MH  - Male
MH  - Mast Cells/*physiology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Inbred Strains
MH  - Peritoneal Diseases/etiology/prevention & control
MH  - Sepsis/etiology/*prevention & control
MH  - Spleen/physiology/physiopathology
MH  - Survival Analysis
MH  - Time Factors
EDAT- 2003/06/06 05:00
MHDA- 2003/12/03 05:00
CRDT- 2003/06/06 05:00
PHST- 2003/06/06 05:00 [pubmed]
PHST- 2003/12/03 05:00 [medline]
PHST- 2003/06/06 05:00 [entrez]
AID - 10.1097/.01.shk0000055239.25446.2d [doi]
PST - ppublish
SO  - Shock. 2003 Jun;19(6):513-8. doi: 10.1097/.01.shk0000055239.25446.2d.