Introduction: Numerous studies have found that burn injury alters immune function, predisposing
the subject to infectious complications. We developed a mouse model of burn injury
complicated by either gram-positive or gram-negative infection and hypothesized that
post-burn infection would exacerbate the myocardial cytokine responses and contractile dysfunction
characteristic of either sepsis alone or burn alone.
Methods: Adult C57 BL6 mice were given burn injury over 40% of the total body surface
area and conventional fluid resuscitation (lactated Ringer's solution, 4 mL/kg/% burn) followed
on day 7 by intratracheal administration of 1 × 105 cfu of either Streptococcus pneumoniae
or Klebsiella pneumoniae or saline. Mice received fluid resuscitation (2 mL of lactated
Ringer's intraperitoneally) again after bacterial challenge. Cardiomyocyte cytokine secretion
and the contractile function of isolated hearts (Langendorff perfusion) were examined in vitro
24 h after bacterial challenge.
Results: Infectious challenge seven days after burn injury exaggerated the inflammatory cytokine
responses over those observed with either burn alone or gram-positive or gram-negative
infection alone (tumor necrosis factor-α: sham, 72 ± 9 pg/mL; burn alone, 176 ± 6 pg/mL,
Klebsiella pneumoniae alone, 337 ± 8 pg/mL; Streptococcus pneumoniae alone, 184 ± 2 pg/mL;
burn + Klebsiella, 476 ± 14 pg/mL; burn + Streptococcus, 351 ± 6 pg/mL). Myocardial contractile
depression was evident in the burn alone, infection alone, and burn plus infection
groups, regardless of the organism selected to produce pneumonia-related sepsis.
Conclusions: Gram-negative or gram-positive infection exacerbated the myocardial inflammation
seen with burn alone or infection alone. The availability of a mouse model of burn injury
complicated by pneumonia-related sepsis will allow use of genetically engineered mice
to examine further the mechanisms by which burn injury increases susceptibility to infection.
