A recent study has shown that respiratory infections in the human lung initiated by TLR2 agonist lipoteichoic acid (LTA, a component of Gram-positive bacteria) and TLR4 agonist LPS (a component of Gram-negative bacteria) exhibit different inflammatory responses (56) . The study was performed on healthy subjects with LPS or LTA instillation into the contralateral lung. Alveolar macrophages (AMφ) isolated from bronchoalveolar lavage fluid were analyzed by multiplex ligation-dependent probe amplification. The results show that whereas both LPS and LTA elicited neutrophil recruitment, only LPS instillation was associated with activation of neutrophils (PMN) (CD11b surface expression and degranulation) and consistent rises of chemokine/cytokine levels. Moreover, LPS but not LTA activated AM, as reflected by enhanced expression of proinflammatory mediators and increased spontaneous cytokine release upon incubation ex vivo. Remarkably, only LTA induced C5a release. These data suggest that stimulation of TLR2 or TLR4 results in differential pulmonary inflammation, which may be of relevance for understanding the differences during Gram-positive and Gram-negative respiratory tract infection (56) .