Thermal injury is known to be a potent modulator of many host immune function. Exposure of experimental animals to thermal injury induces a reduction in their ability to initate and effectuate various types of cellular immune responses. In this
study,
the effects of artificial thermal injury on resistance to Listeria monocytogenes(LM) or Pseudomonas aeruginosa(Ps) were examined at the cellular level.
The number of cultivable LM recovered from the spleens of burnt mice were decreased at 2 and 3 days postinfection compared with those of the untreated control mice. However, the acquired immunity, which developed in either burnt, LPS or IL-1
pretreated
mice 7 days after immunization with streptomycin(SM) sensitive LM, was weaker than that developed in the untreated, control mice.
To elucidate the possible mechanisms underlying the observation that thermal injury did increases innate immunity but decresaed acquired immunity of mice to infection with LM, we assessed the effects of thermal injury of mice on the production of
IL-2
and IFN-γ by activated splenocytes and TNF-α by peritoneal macrophages. Activated splenocytes from burnt mice exhibited a reduced capacity to produce IFN-γ and IL-2. However, the peritoneal macrophasges from burnt mice produced more TNF-α in
the
presence of LPS.
Pretreatment of mice with LPS or IL-1β showed similar results to burnt mice in the production of II 2 or IFN-γ by activated splenecytes and resistance te LM. When burnt mice were treated with dehydroepiandrosterone (DHEA), a native adrenal
steroid
hormone, the acquired immunity to LM as restored with increased production of IL-2 and IFN-γ by activated splenocytes.
These findings suggest that the dual effects of thermal injury on the innate and acquired immunity of mice to the LM infection may be associated with altered capacities of splenocytes and peritoneal macrophages of the mice to produce cytokines
including
IL-1 and DHEA seemed to restore the acquired immunity to LM. DHEA deserves intensive study for used in the therapeutic modulation of infection caused by immunodeficiencies.
|