Anergy, Immunosuppressive Serum, and Impaired Lymphocyte Blastogenesis in Burn Patients

Wolfe, John H.; Wu, Amy D.; O’Connor, Nick; Saporoschetz, Inna B.; Mannick, John A.

doi:10.1001/archsurg.1982.01380340002002

Cited by 97 publications

(30 citation statements)

References 20 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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“…Early observations of the immunodeficiency that follows thermal injury were linked to works on "burn toxins" published by Wertheim, Avdakoff, and Sevitt (17,384,455). More recently, these observations have been supported by the findings of prolonged allograft survival, anergy, and increased susceptibility to infection in burn patients (75,227,324,402,405,462). Despite improvements in the early care of burn patients, systemic inflammatory response syndrome, severe sepsis, and multiple-organ dysfunction syndrome remain major causes of morbidity and mortality (47,194,382).…”

Section: Immunological Response To Burn Injurymentioning

confidence: 93%

Burn Wound Infections

Church

Elsayed

Reid³

et al. 2006

Clin Microbiol Rev

1,595

1,345

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SUMMARYBurns are one of the most common and devastating forms of trauma. Patients with serious thermal injury require immediate specialized care in order to minimize morbidity and mortality. Significant thermal injuries induce a state of immunosuppression that predisposes burn patients to infectious complications. A current summary of the classifications of burn wound infections, including their diagnosis, treatment, and prevention, is given. Early excision of the eschar has substantially decreased the incidence of invasive burn wound infection and secondary sepsis, but most deaths in severely burn-injured patients are still due to burn wound sepsis or complications due to inhalation injury. Burn patients are also at risk for developing sepsis secondary to pneumonia, catheter-related infections, and suppurative thrombophlebitis. The introduction of silver-impregnated devices (e.g., central lines and Foley urinary catheters) may reduce the incidence of nosocomial infections due to prolonged placement of these devices. Improved outcomes for severely burned patients have been attributed to medical advances in fluid resuscitation, nutritional support, pulmonary and burn wound care, and infection control practices.

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“…The susceptibility to infection, and resultant mortality, is greatly increased after burn, as a result of suppression of cell-mediated immunity (Moss et al 1988, Dinkel & Lebok 1994. The immune defects observed after burn include anergy to delayed type hypersensitivity (DTH) antigens (Tchervenkov et al 1988), decreased activation and proliferation of lymphocytes in response to mitogenic (concanavalin A (Con A)) or antigenic stimulation and decreased cytokine secretion (Wolfe et al 1982, Teodorczyk-Injeyan et al 1986, Moss et al 1988). …”

Section: Introductionmentioning

confidence: 99%

“…It has been well established that one of the main factors contributing to decreased T lymphocyte function, and thus cellular immunity, after burn injury is a dramatic decline in IL-2 production (Wolfe et al 1982, Wood et al 1984, Horgan et al 1994a, b, O'Riordain et al 1995. Clinically, the ability of peripheral blood mononuclear cells to produce IL-2 in vitro is positively correlated with survival after burn injury (Teodorczyk-Injeyan et al 1986, Sparkes 1993.…”

Section: Introductionmentioning

confidence: 99%

Testosterone receptor blockade restores cellular immunity in male mice after burn injury

Messingham¹,

Shirazi²,

Duffner³

et al. 2001

Journal of Endocrinology

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Males are known to have increased risk for septic complications after traumatic injury, which appears to be mediated by the inhibitory effects of testosterone on immune function. The role of testosterone in immunity after burn injury, however, remains unclear. Herein, we examined the effects of a testosterone receptor antagonist, flutamide, on delayed type hypersensitivity response (DTH), splenocyte proliferation, interleukin (IL)-2 secretion, and IL-2 receptor (IL-2R) expression in male BALB/c mice subjected to a 15% total body surface area burn or sham injury. Burn-or sham-injured mice were given flutamide s.c. at 30 min and 24 h after injury. At 48 h, burn injury caused a 48% (P<0·001) decrease in DTH response; however, mice that received flutamide treatment did not demonstrate significant suppression of DTH. Likewise, splenocyte proliferation and IL-2 production were depressed in burned animals in comparison with sham-injured controls, and flutamide treatment resulted in a partial restoration of these responses. In vitro studies indicated that splenocytes from sham-and burninjured mice were equally sensitive to the suppressive effects of 5 -dihydrotestosterone in regard to proliferation and IL-2 production. Further evaluation revealed a decrease in IL-2R expression on splenocytes from burned mice and a partial restoration of this expression with flutamide treatment. Thus blocking testosterone receptor activation improves the cellular immunity in thermally injured mice, possibly through restoration of IL-2 production and IL-2R expression. It remains to be determined whether the effects of testosterone in this injury model are direct or indirect.

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Anergy, Immunosuppressive Serum, and Impaired Lymphocyte Blastogenesis in Burn Patients

Cited by 97 publications

References 20 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 Wound Infections

Testosterone receptor blockade restores cellular immunity in male mice after burn injury

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