The development of pneumonia and other infections is one of the most common complications of a traumatic brain injury (TBI). Prior studies have also found that patients suffering from TBI also develop immune dysfunction consistent with an immunosuppressed state shortly after the traumatic event. Specifically, it has been shown that patients with a TBI have impaired delayed type hypersensitivity (DTH), cellular immunity and humoral immunity. The humoral arm of the immune system is particularly involved in defending the host against extracellular bacteria and is primarily composed of B-cells, immunoglobulins and complement. Surgery and trauma impair the clonal expansion of antibody producing B lymphocytes causing hypogammaglobulinemia, through a mechanism involving T lymphocytes. In addition, during the systemic inflammatory process, pro-inflammatory cytokines such as tumor necrosis factor alpha (TNF-alpha), interleukin 1 (IL-1beta) and interleukin 6 (IL-6) are released. Nuclear factor kappa beta (NF-kB) is a transcriptional regulatory protein that is involved in the expression of proinflammatory cytokines and appears to act at a critical step in the transcription of many proinflammatory genes.
The hypothesis of this study is that the hypogammaglobulinemia from the immune dysfunction and the induction of NF-kB from the inflammatory process are, in part, responsible for the development of pneumonia and other infectious complications identified after TBI. This study has two specific aims: The primary specific aim of this study is to determine the association between serum immunoglobulin or NF-kB levels and the development of pneumonia in patients suffering from traumatic brain injury (TBI). The secondary specific aim of this study is to determine the relative contribution of clinical variables such as APACHE II-III Score and Injury Severity Score as compared to immunological variables (serum immunoglobulins and NF-kB) to the development of pneumonia in patients suffering from TBI.