Suppression of Cellular Immune Activity Following Severe Head Injury

Abstract

Infection is a major cause of morbidity following multiple traumatic and head injury. Although immunosuppression has been demonstrated after multiple traumatic injury, the effects of head injury on immune function have not been thoroughly investigated. In a prospective study of 10 severely head-injured patients, in vitro and in vivo parameters of cellular immune activity were assessed. In vitro measurements of lymphocyte surface antigen expression following mitogen stimulation were made serially over a 3-week period in 10 patients with severe head injury. The control group consisted of 20 healthy subjects. Phenotyping of peripheral blood lymphocytes (PBLs) was performed following incubation with and without mitogens. Phenotypes were determined by flow cytometry using monoclonal antibodies (MABs) to T lymphocyte subsets and the alpha subunit of interleukin 2 (IL-2) receptors. In vivo cellular immune function was determined by measuring patient responses to delayed-type hypersensitivity (DTH) skin testing within 24 h of injury. When head-injured patients were compared to controls, PBLs incubated in the presence of phytohemagglutinin (PHA) demonstrated a decrease in cells marking as T cells (p = 0.005), helper-inducer T cells (p = 0.001), and in the number of IL-2 receptor-bearing cells (p = 0.001). The functional ability of these lymphocyte subpopulations to proliferate in the presence of PHA was significantly suppressed within 24 h of injury and normalized within 3 weeks of injury. DTH skin testing to Candida, mumps, trichophyton, and PPD antigens was performed within 24 h of injury and resulted in anergic responses in all 10 patients when measured at 24, 48, and 72 h following administration. The overall infection rate was 60%, with the majority of infections occurring within the first 4 days following injury. The results of this study indicate that severe head injury results in suppression of cellular immune function with a corresponding high rate of infection. The possible significance of the decrease in the percentage of helper-inducer T cells and in the number of cells bearing IL-2 receptors following mitogen stimulation is discussed.

Concept of autoimmunity following spinal cord injury: Possible roles for T lymphocytes in the traumatized central nervous system

“…However, these data are difficult to interpret as some patients received steroid injections immediately after injury and criteria used for their entry into the study were not defined. Similar findings have been reported in head injury patients (Quattrocchi et al, 1990(Quattrocchi et al, , 1992a.…”

Mortality following Traumatic Brain Injury among Individuals Unable to Follow Commands at the Time of Rehabilitation Admission: A National Institute on Disability and Rehabilitation Research Traumatic Brain Injury Model Systems Study

“…This may be related to trauma induced glucocorticoid secretion and poorly understood neuroinflammation. [27][28][29] Individuals who remain physically dependent may be more likely to be at higher risk of community acquired and nosocomial infections. They also may acquire from prolonged hospitalizations, and are at higher risk of pressure sores, aspiration pneumonia, and require indwelling urinary catheters.…”

Safety and Tolerability of Cyclosporin A in Severe Traumatic Brain Injury Patients: Results from a Prospective Randomized Trial

“…It is also well-known that immunological function may be impaired in the early phase after TBI, as well in as trauma in general, due to a complex multifactorial effect of suppression of T-cell mediated immune function, and changes in soluble mediators, such as an increase in PGE 2 biosynthesis, and reductions in the levels of the key immunoregulatory cytokines IL-2 and IFN-g (Boddie et al, 2003;Quattrocchi et al, 1990Quattrocchi et al, , 1991aQuattrocchi et al, ,b, 1992. The administration of any medication that might induce further immunological suppression should therefore be undertaken with caution, in order to avoid any additional or synergistic suppression of immune function after severe TBI.…”