Role of Hypothalamic Pituitary Adrenal (HPA) Axis and Tumor Necrosis Factor (TNF) in Development of Post-Traumatic Nosocomial Pneumonia

Abstract

T. Mozes1, K. Gornicsar, A. Grosz, Ta. Mozes, Kh. Diab and E. Madarasz

Background and purpose: Infection after experimental focal ischemia may result from brain-induced immune depression. A strong cytokine mediated anti-inflammatory response was recently observed in stroke patients at higher risk of infection, although infection due to the decreased pro-inflammatory mediators can be expected as well. To investigate this question the following experiment was performed.

Methods: 105 over 60 years hip fracture patients were included in the study. Sera and lympho/monocytes were separated from blood samples taken on different days (day 1, 3, 6, 9). Isolated lympho/ monocytes were cultured for one day with or without endotoxin (LPS). TNFα levels in sera and in the culture supernatants were determined by bioassays using WEHI 164 cells. Plasma ACTH and cortisol values were measured by RIA kits.

Results: From 105 hip fracture patients 7 nosocomial pneumonia patients were found, (4 survivors and 3 nonsurvivors) furthermore 2 non-survivors with cardiovascular death without infection. On the day of trauma the level of circulating TNFα activity was extremely low in nosocomial pneumonia patients in comparison to uneventful healing patients. In pneumonia patients TNFα started to increase on day 3, increased till day 9 then reached the values of uneventful healing group. In two patients with later cardiovascular complications, extremely high TNF alpha activities were detected throughout the entire observation period. The plasma cortisol values were high in nosocomial pneumonia patients in comparison to uneventful healing persons, and decreased slightly by the 9th post-trauma day. In the two cardiovascular patients, serum cortisol was extremely low on the day of trauma and increased gradually during the investigation period. ACTH level was stable in the sera of uneventfully healing patients, while showed large individual and also time-dependent fluctuations people with post-traumatic complications.

Conclusions: An excessive decrease in pro-inflammatory response is a key facilitating factor for the development of infection.

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