PMID- 25609031
OWN - NLM
STAT- MEDLINE
DCOM- 20150616
LR  - 20181113
IS  - 1470-8736 (Electronic)
IS  - 0143-5221 (Print)
IS  - 0143-5221 (Linking)
VI  - 128
IP  - 11
DP  - 2015 Jun
TI  - Breaking the co-operation between bystander T-cells and natural killer cells 
      prevents the development of immunosuppression after traumatic skeletal muscle 
      injury in mice.
PG  - 825-38
LID - 10.1042/CS20140835 [doi]
AB  - Nosocomial infections represent serious complications after traumatic or surgical 
      injuries in intensive care units. The pathogenesis of the underlying 
      immunosuppression is only incompletely understood. In the present study, we 
      investigated whether injury interferes with the function of the adaptive immune 
      system in particular with the differentiation of antigen-specific T helper 
      (Th)-cell responses in vivo. We used a mouse model for traumatic gastrocnemius 
      muscle injury. Ovalbumin (OVA), which served as a foreign model antigen, was 
      injected into the hind footpads for determination of the differentiation of 
      OVA-specific Th-cells in the draining popliteal lymph node (pLN). The release of 
      interferon (IFN)-gamma from OVA-specific Th-cells was impaired within 24 h after 
      injury and this impairment persisted for at least 7 days. In contrast, the 
      proliferation of OVA-specific Th-cells remained unaffected. Injury did not 
      modulate the function of antigen-presenting cells (APCs) in the pLN. Adoptive 
      transfer of total T-cells from pLNs of injured mice inhibited IFN-gamma production by 
      OVA-specific Th-cells in naive mice. Suppressed Th1 priming did not occur in 
      lymphocyte-deficient mice after injury but was restored by administration of 
      T-cells before injury. Moreover, the suppression of Th1 differentiation required 
      the presence of natural killer (NK) cells that were recruited to the pLN after 
      injury; this recruitment was dependent on lymphocytes, toll-like receptor 4 
      (TLR4) and myeloid differentiation factor 88 (MyD88). In summary, upon traumatic 
      skeletal muscle injury T-cells and NK cells together prevent the development of 
      protective Th1 immunity. Breaking this co-operation might be a novel approach to 
      reduce the risk of infectious complications after injury.
FAU - Wirsdorfer, Florian
AU  - Wirsdorfer F
AD  - *Surgical Research, Department of Trauma Surgery, University Hospital Essen, 
      University Duisburg-Essen, 45147 Essen, Germany.
FAU - Bangen, Jorg M
AU  - Bangen JM
AD  - *Surgical Research, Department of Trauma Surgery, University Hospital Essen, 
      University Duisburg-Essen, 45147 Essen, Germany.
FAU - Pastille, Eva
AU  - Pastille E
AD  - *Surgical Research, Department of Trauma Surgery, University Hospital Essen, 
      University Duisburg-Essen, 45147 Essen, Germany.
FAU - Hansen, Wiebke
AU  - Hansen W
AD  - double daggerInstitute of Medical Microbiology, University Hospital Essen, University 
      Duisburg-Essen, 45147 Essen, Germany.
FAU - Flohe, Stefanie B
AU  - Flohe SB
AD  - *Surgical Research, Department of Trauma Surgery, University Hospital Essen, 
      University Duisburg-Essen, 45147 Essen, Germany.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Clin Sci (Lond)
JT  - Clinical science (London, England : 1979)
JID - 7905731
RN  - 0 (Myd88 protein, mouse)
RN  - 0 (Myeloid Differentiation Factor 88)
RN  - 0 (Toll-Like Receptor 4)
RN  - 82115-62-6 (Interferon-gamma)
RN  - 9006-59-1 (Ovalbumin)
SB  - IM
MH  - Animals
MH  - Antigen-Presenting Cells/immunology
MH  - Bystander Effect/immunology
MH  - Cell Differentiation/immunology
MH  - Cells, Cultured
MH  - Flow Cytometry
MH  - Immune Tolerance/*immunology
MH  - Interferon-gamma/immunology/metabolism
MH  - Killer Cells, Natural/*immunology
MH  - Lymph Nodes/cytology/immunology
MH  - Male
MH  - Mice, Inbred BALB C
MH  - Mice, Knockout
MH  - Muscle, Skeletal/*immunology/injuries
MH  - Myeloid Differentiation Factor 88/genetics/immunology/metabolism
MH  - Ovalbumin/immunology
MH  - Th1 Cells/immunology/metabolism
MH  - Toll-Like Receptor 4/genetics/immunology/metabolism
PMC - PMC4557401
EDAT- 2015/01/23 06:00
MHDA- 2015/06/17 06:00
PMCR- 2015/03/19
CRDT- 2015/01/23 06:00
PHST- 2015/01/23 06:00 [entrez]
PHST- 2015/01/23 06:00 [pubmed]
PHST- 2015/06/17 06:00 [medline]
PHST- 2015/03/19 00:00 [pmc-release]
AID - CS20140835 [pii]
AID - 10.1042/CS20140835 [doi]
PST - ppublish
SO  - Clin Sci (Lond). 2015 Jun;128(11):825-38. doi: 10.1042/CS20140835.