Objective.
Trauma patients (TP) frequently develop an imbalanced immune response that often causes infectious postinjury complications. Monocytes show a diminished capability of both producing proinflammatory
cytokines and antigen presentation after
trauma. TLR2, TLR4, and TLR9 recognize pathogens and subsequently activate monocytes. While there are conflictive data about TLR2 and TLR4 expression after
trauma, no studies about the expression of TLR2, TLR4, TLR9, and
HLA-DR on monocytes from TP after their secondary ex vivo-in vitro "hit" have been reported. Methods/Results. Ex vivo-in vitro
lipopolysaccharide- (LPS-) stimulated blood from TP showed diminished
interleukin- (IL-) 1β-release in TP for five postinjury days compared to healthy volunteers (HV). The recovery was observed at day 5. In parallel, monocytes from TP showed an impaired capability of TLR2, TLR4, and TLR9 expression after secondary stimulation compared to HV, while the measurement of unstimulated samples showed significant reduction of TLR4 and TLR9 at ED. Furthermore,
HLA-DR decreased after
trauma and was even more profound by stimulation of monocytes. Ratio of monocytes to leukocytes was significantly increased at days 6 and 7 after
trauma compared to HV. Conclusion. Impaired expression of TLRs and
HLA-DR in acute inflammatory conditions may be responsible for the well-described monocyte
paralysis after severe
trauma.