Thus, further investigations will be necessary to conclude that neutrophils play an important role in the host defense to S. pneumoniae infection via secreting TNF-α as well as killing this bacterium. Furthermore, we JQ1 cell line demonstrated the production of TNF-α by additional cells expressing a lower level of Gr-1 that were not neutrophils, but rather macrophage-like cells. Because Gr-1 is well known as a cell surface marker of neutrophils, the current observation may suggest the possible contribution of a population found in the macrophage lesion to the host defense to pneumococcal infection.

In an earlier study by Mordue & Sibley (2003), a population of unusual macrophages expressing Gr-1 was reported to accumulate in the peritoneal cavity during infection selleck kinase inhibitor with T. gondii. These cells contribute to the host defense to this parasite by producing IL-12p40 and generating a reactive nitrogen intermediate. Interestingly, they express F4/80, CD11b and CD68, another macrophage marker, but do not express CD11c, a dendritic cell marker. These cells are likely to also exist in the peritoneal cavity of uninfected mice, and their expression of F4/80 and CD11b is reduced after infection. By contrast, the Gr-1dull+ cells described in the current study are not

detected in BALF before infection, although the pleural cavity and extra-airway spaces in lungs have not been addressed for

their existence. In addition, the Gr-1dull+ cells express CD11c, suggesting that they may be dendritic cells. However, these cells are Celastrol not likely in this case, as shown by the macrophage-like morphology and the marginal expression of CD80. Thus, Gr-1+ macrophages and Gr-1dull+ cells described in the two independent studies may not necessarily be identical, although it is not known whether they are in the distinct lineage or whether some of them contain overlapped lineages. A recent study by Kirby et al. (2006) has found that alveolar macrophages, originally CD11cbright+ MHC class IIdull+ CD11b−, increase after intranasal pneumococcal infection, which is associated with elevated expression of CD11b. Interestingly, these cells are negative for Gr-1 expression. They suggest that these cells may be derived from blood monocytes, in which the expression of CD11c and Gr-1 is upregulated and downregulated, respectively, during transit from the circulation into the infected lung tissues. On the other hand, Gonzalez-Juarrero et al. (2003) described the dynamics of macrophage cell populations during murine pulmonary tuberculosis and speculated the differentiation of macrophages entering the lungs in response to the infection, which is defined as the changes in their surface expression of CD11b and CD11c.