Dominance of T-Helper 2–Type Cytokines After Severe Injury

Mack, Vivian; McCarter, Martin D.; Naama, Hassan A.; Calvano, Steve E.; Daly, J.M.

doi:10.1001/archsurg.1996.01430240057007

Cited by 111 publications

(73 citation statements)

References 32 publications

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“…On admission the mean age of the trauma patients ( n = 31) was 32·8 (range, 18-59), the mean ISS was 32·0 (17-59), APACHE II score of 13·5 (4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22) and mean GCS of 8·7 (3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15). There were 25 men and six women.…”

Section: Resultsmentioning

confidence: 99%

Primary immune response to keyhole limpet haemocyanin following trauma in relation to low plasma glutamine

Boelens¹,

Fonk

Houdijk³

et al. 2004

Clinical and Experimental Immunology

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SUMMARYSevere trauma can lead to a compromised immune response, thereby increasing susceptibility to infections. Here we will study to what extent these early changes in the immune status upon trauma affect a primary immune response to keyhole limpet haemocyanin (KLH). Because glutamine is the preferred respiratory substrate for immune competent cells and known to be depleted after trauma, we studied the immune status and the primary sensitization in relation to the glutamine plasma concentration in a group of severe trauma patients [injury severity score (ISS) > 17]. Trauma patients ( n = 31) were sensitized with KLH within 12 h after trauma; plasma glutamine concentrations and immune parameters were determined, after which KLH-specific immune responsiveness was evaluated on days 9 and 14. Low plasma glutamine concentrations were found after trauma. Significantly elevated numbers of granulocytes and CD14-positive leucocytes were found, whereas the HLA-DR expression on CD14-positive cells was significantly lower in trauma patients than in healthy controls. Trauma did not change the in vitro proliferative capacity of lymphocytes when cultured with glutamine; however, when lymphocytes were cultured without glutamine, trauma resulted in lower proliferation than healthy controls. Phytohaemagglutinin-(PHA)-induced interferon (IFN)-g and interleukin (IL)-10 production was significantly lower after trauma, whereas IL-4 production was not affected. KLH sensitization following trauma resulted in poor skin test reactivity and low in vitro KLH-induced lymphocyte proliferation compared to controls. In contrast, the development of anti-KLH IgM, IgG, IgA, IgG1, IgG2, IgG3 and IgG4 production on days 9 and 14 following trauma was not different from that in healthy controls. Major trauma was associated with a reduced cell-mediated immune response, correlating with low plasma glutamine concentrations, while no effects of trauma were found on the development of a primary humoral immune response.

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Section: Resultsmentioning

confidence: 99%

Primary immune response to keyhole limpet haemocyanin following trauma in relation to low plasma glutamine

Boelens¹,

Fonk

Houdijk³

et al. 2004

Clinical and Experimental Immunology

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“…Next, we wanted to determine whether burn-injured mice exhibit a similar difference in mortality if challenged with the same doses of these SAg at 7 days after injury, a time point when injured mice are know to express a Th2 phenotype (8,10,25). We found that burn-injured mice did not die when given either SEA or SEB at 7 days after burn injury at doses that were fatal at 1 day after injury.…”

Section: Discussionmentioning

confidence: 99%

Burn Injury Initiates a Shift in Superantigen-Induced T Cell Responses and Host Survival

Zang

Dolan

Choileain

et al. 2004

The Journal of Immunology

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Severe injury induces a temporal shift in immune reactivity that can cause serious complications or even death. We previously reported that mice exposed to bacterial superantigen (SAg) early after injury undergo a strong SAg response with lethal consequences. This study compares the early and late effects of burn injury on SAg reactivity in vivo to establish how injury influences adaptive immune responses. We found that mice challenged with ordinarily sublethal doses of staphylococcal enterotoxin A or staphylococcal enterotoxin B at 1 day after burn injury exhibited high mortality, whereas no mortality occurred at 7 days after injury. This shift in mortality correlated with higher Th2-type cytokines (IL-4 and IL-10) being expressed by CD4+ and CD8+ T cells from burn as opposed to sham mice at 7 days after injury. Lymph node cells from burn-injured mice also produced higher levels of Th2-type cytokines at 7 days after injury. The results of cell-mixing studies using CD4+ and CD8+ T cells mixed with APCs from sham or burn mice suggested that changes in both T cells and APCs are involved in the altered SAg response. Finally, the biological significance of altered SAg reactivity following injury was shown by demonstrating that blocking IL-10 activity in vivo caused higher SAg-induced mortality at 7 days after injury. These findings support the idea that injury promotes a Th2-type shift in adaptive immune reactivity. Although prior studies link this counterinflammatory-type response to lowered resistance to infection, the present results suggest it may sometimes benefit the injured host.

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“…eosinophils vs. neutrophils) Summaries of the T-helper cytokine response and its role in inflammation are available in the literature (Cameron et al, 2001;DiPiro, 1997;Miller et al, 2007). As a third cytokine-dependent mechanism, the cytokine milleu of CARS is also characterized by an upregulation of T H 2 cytokine responses (Mack et al, 1996). This upregulation of T H 2 cytokines serves to blunt the T H 1-dominant SIRS response through the modulation of leukocyte gene expression.…”

Section: Early Phase Cars: Suppressor Cells and Immunosuppressive Cytmentioning

confidence: 99%

Immune Cell Dysfunction as a Consequence of Severe Sepsis

Carson¹,

Kunkel²

2012

Severe Sepsis and Septic Shock - Understanding a Serious Killer

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Dominance of T-Helper 2–Type Cytokines After Severe Injury

Cited by 111 publications

References 32 publications

Primary immune response to keyhole limpet haemocyanin following trauma in relation to low plasma glutamine

Primary immune response to keyhole limpet haemocyanin following trauma in relation to low plasma glutamine

Burn Injury Initiates a Shift in Superantigen-Induced T Cell Responses and Host Survival

Immune Cell Dysfunction as a Consequence of Severe Sepsis

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