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The granulocyte colony-stimulating factor response after intrapulmonary and systemic bacterial challenges
Lee J Quinton1, Steve Nelson, Darren M Boé
1Department of Physiology, Section of Pulmonary Critical Care Medicine, Louisiana State University Health Sciences Center, New Orleans, LA 70112, USA.
The Journal of Infectious Diseases
|May 7, 2002
Summary
Following lung infection, lung granulocyte colony-stimulating factor (G-CSF) increases in both the lungs and blood. This study suggests the lung is the primary source of this crucial immune factor.
Area of Science:
- Immunology
- Pulmonary Medicine
- Microbiology
Background:
- Cytokine responses to bacterial infections vary, with some entering systemic circulation and others remaining localized.
- Granulocyte colony-stimulating factor (G-CSF) is a key cytokine in immune response, but its pulmonary-specific response dynamics are not fully understood.
Purpose of the Study:
- To investigate the hypothesis that lung-derived granulocyte colony-stimulating factor (G-CSF) enters systemic circulation after an intrapulmonary bacterial challenge.
- To determine the lung as the primary source of G-CSF during pulmonary infection.
Main Methods:
- BALB/c mice were challenged with intratracheal or intravenous Escherichia coli (E. coli) or saline.
- Bronchoalveolar lavage fluid (BALF) and plasma G-CSF concentrations were measured.
- Lung and extrapulmonary tissue G-CSF messenger RNA (mRNA) levels were quantified.
Main Results:
- Intratracheal E. coli administration significantly increased G-CSF concentrations in both BALF and plasma compared to controls.
- Lung G-CSF mRNA levels markedly increased post-intratracheal E. coli challenge, while extrapulmonary tissues showed no significant increase.
- Intravenous E. coli increased plasma G-CSF and TNF-alpha, but these cytokines were undetectable in BALF.
Conclusions:
- Following an intrapulmonary bacterial infection, both lung and circulating G-CSF levels increase.
- The lung is identified as the likely source of increased G-CSF during pulmonary infections.
- This localized pulmonary cytokine response differs from systemic responses observed with intravenous bacterial challenge.