PMID- 20679533
OWN - NLM
STAT- MEDLINE
DCOM- 20101026
LR  - 20211020
IS  - 1550-6606 (Electronic)
IS  - 0022-1767 (Print)
IS  - 0022-1767 (Linking)
VI  - 185
IP  - 5
DP  - 2010 Sep 1
TI  - Dendritic cell modification of neutrophil responses to infection after burn 
      injury.
PG  - 2847-53
LID - 10.4049/jimmunol.0903619 [doi]
AB  - Burn patients are highly susceptible to infections due to increased exposure 
      through wounds and impairments in a number of immune functions. Dendritic cells 
      (DCs) are important in activation of numerous immune responses that are essential 
      for the clearance of infections. We have found that prophylactic treatment of 
      burn-injured mice with the DC growth factor FLT3 ligand (FL) significantly 
      increases resistance to burn wound infections in a DC-dependent manner that is 
      correlated closely with enhanced bacterial clearance. However, as DCs are not 
      typically microbicidal, the mechanisms by which DC modulation enhances bacterial 
      clearance are not known. Due to the rapid response of neutrophils to cutaneous 
      wounds, and the reported interactions between DCs and neutrophils, we 
      investigated the role of neutrophils in FL-mediated resistance to burn wound 
      infection. This was examined both in vivo and in vitro through neutrophil 
      depletion, supplementation of neutrophils, and assessment of neutrophil 
      chemotaxis following FL treatment. To test the involvement of DCs, 
      CD11c-diphtheria toxin receptor transgenic mice were used to deplete DCs during 
      FL treatment. Studies revealed that neutrophils do play a critical role in 
      FL-mediated resistance to a burn wound infection. Additionally, treatment with FL 
      after a burn injury enhances neutrophil-mediated control of bacterial spread, 
      neutrophil migratory capacity, and myeloperoxidase production in a DC-dependent 
      manner. The results of this study provide new insight into immunological 
      mechanisms that can offer protection against infection after burn injury.
FAU - Bohannon, Julia
AU  - Bohannon J
AD  - Department of Microbiology and Immunology, University of Texas Medical Branch, 
      Galveston, TX 77555-0591, USA. jkbohann@utmb.edu
FAU - Cui, Weihua
AU  - Cui W
FAU - Sherwood, Edward
AU  - Sherwood E
FAU - Toliver-Kinsky, Tracy
AU  - Toliver-Kinsky T
LA  - eng
GR  - R01 GM072810/GM/NIGMS NIH HHS/United States
GR  - R01 GM072810-04/GM/NIGMS NIH HHS/United States
GR  - T32-07254/PHS HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20100802
PL  - United States
TA  - J Immunol
JT  - Journal of immunology (Baltimore, Md. : 1950)
JID - 2985117R
RN  - 0 (Adjuvants, Immunologic)
RN  - 0 (Membrane Proteins)
RN  - 0 (flt3 ligand protein)
SB  - IM
MH  - Adjuvants, Immunologic/administration & dosage/therapeutic use
MH  - Adoptive Transfer
MH  - Animals
MH  - Burns/*immunology/microbiology/*therapy
MH  - Cell Communication/immunology
MH  - Dendritic Cells/*immunology/microbiology/transplantation
MH  - Disease Models, Animal
MH  - Hot Temperature
MH  - Immunity, Innate
MH  - Male
MH  - Membrane Proteins/administration & dosage/therapeutic use
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Transgenic
MH  - Neutrophil Infiltration/immunology
MH  - Neutrophils/*immunology/microbiology/transplantation
MH  - Pseudomonas Infections/*immunology/microbiology/*therapy
MH  - Pseudomonas aeruginosa/growth & development/immunology
MH  - Wound Infection/*immunology/microbiology/*therapy
PMC - PMC3100157
MID - NIHMS290122
EDAT- 2010/08/04 06:00
MHDA- 2010/10/27 06:00
PMCR- 2011/09/01
CRDT- 2010/08/04 06:00
PHST- 2010/08/04 06:00 [entrez]
PHST- 2010/08/04 06:00 [pubmed]
PHST- 2010/10/27 06:00 [medline]
PHST- 2011/09/01 00:00 [pmc-release]
AID - jimmunol.0903619 [pii]
AID - 10.4049/jimmunol.0903619 [doi]
PST - ppublish
SO  - J Immunol. 2010 Sep 1;185(5):2847-53. doi: 10.4049/jimmunol.0903619. Epub 2010 
      Aug 2.