CD64 and CD16 were differentially modulated by sepsis. CD64, CD64/CD16 and PCT may be biomarkers of sepsis. CD64 was better than PCT for identifying patients who required treatment with antibiotics.

Neutrophils appeared to play an important role in ALI. Time-dependent treatment with IL-10 after intra-tracheal instillation of LPS was effective in protecting rats from ALI, probably by suppressing pulmonary infiltration with activated neutrophils.

Soluble and surface TREM-1 are valuable markers in establishing the aetiology of pleural effusions.

The pathophysiological role of soluble immune complexes (SICXs) and its relationship with neutrophils were investigated in LPS-induced acute lung injury (ALI) animal model (Sprague-Dawley rat) and through the in vitro studies. Results showed that LPS-induced SICX was timely related to changes of tumor necrosis factor alpha and macrophage inflammatory protein 2 (inflammatory cytokines) in bronchoalveolar lavage fluid. In vitro study showed that SICX can bind to Fc gammaR (CD64 and CD32 or CD16) to prevent the apoptosis of neutrophils. The SICX-mediated apoptosis inhibition was extracellular signal-regulated kinase (ERK) or phosphoinositide 3 kinase dependent and was interrupted by PD98059 and LY294002. In vivo, additional amount of SICX exacerbated the lung injury caused by LPS. LPS-induced lung injury and macrophage inflammatory protein 2 release, however, were prevented by CD64 and CD32 blockers (decoy antibodies). In conclusion, excessive amount of SICX in lung can act through Fc gammaRs to protect bronchoalveolar lavage fluid neutrophils from apoptosis that eventually lead to delayed resolution of ALI caused by LPS. Blockade of SICX engagement of CD32 and CD64 (with decoy antibodies) could interrupt SICX-mediated protection of neutrophils and protect lung from LPS-induced injury. The decoy antibodies may therefore have therapeutic utility in ALI.