The Granulocyte Colony-Stimulating Factor... : Journal of Infectious Diseases (original) (raw)

The Granulocyte Colony-Stimulating Factor Response after Intrapulmonary and Systemic Bacterial Challenges

Lee J. Quinton
Steve Nelson
Darren M. Boé
Ping Zhang
Qiu Zhong
Jay K. Kolls
Gregory J. Bagby

Journal of Infectious Diseases

185

(

)

1476

1482

May 15, 2002

| DOI: 10.1086/340504

In contrast to many cytokines such as tumor necrosis factor (TNF)-α, we hypothesized that, after an intrapulmonary bacterial challenge, lung-derived granulocyte colony-stimulating factor (G-CSF) would subsequently enter the systemic circulation. BALB/cmice 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-α, 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.