The granulocyte colony-stimulating factor response after intrapulmonary and systemic bacterial challenges.

In contrast to many cytokines such as tumor necrosis factor (TNF)-alpha, we hypothesized that, after an intrapulmonary bacterial challenge, lung-derived granulocyte colony-stimulating factor (G-CSF) would subsequently enter the systemic circulation. BALB/c mice were given Escherichia coli or saline, either intratracheally or intravenously. Four hours after intratracheal E. coli administration, bronchoalveolar lavage fluid (BALF) and plasma G-CSF concentrations increased, compared with concentrations in phosphate-buffered saline-treated controls. Lung G-CSF messenger RNA (mRNA) increased to 586+/-229 copies G-CSF mRNA/ng ribosomal RNA (rRNA) from the values in control animals (<0.5 copies/ng rRNA). In contrast, G-CSF mRNA was not increased in the extrapulmonary tissues examined (liver, spleen, and kidney) in mice challenged with intratracheal E. coli (<1 copy/ng rRNA). Intravenous E. coli increased plasma G-CSF and TNF-alpha, but neither cytokine was detected in BALF. These data show that, after an intrapulmonary infection, both lung and circulating G-CSF increase and that the lung is the likely source.