The effects of inhaled carbon monoxide on lung injury in rats caused by lipopolysaccharide

BACKGROUND: Carbon monoxide (CO) has long been considered a toxic substance. Recent studies have revealed that CO may play an important role in intercellular signaling. We hypothesized that CO modulates the inflammatory mechanisms. METHODS: SD rats (each study group consisting of 7 animals) inhaled 250 ppm of CO one hour prior to LPS challenges. These animals were incubated for a particular period of time (four different length of time; 1, 2, 4, and 8 hours). The control group (each study group consisting of 6 animals) had been left in the room air. Both groups were instilled with LPS (1 mg) into the lungs. At the end of each period, animals were exsanguinated, broncho-alveolar lavage (BAL) and blood sampling were performed, and a part of the small intestine was harvested. PMN numbers, protein, TNF, and IL-10 concentrations in BAL fluid were measured. Plasma TNF and IL-10 were also measured. The Wet/Dry ratio of a small intestine was calculated. RESULTS: In the CO-inhalation group, the anti-inflammatory cytokine IL-10 concentration in the BAL fluid was higher at 8 hours after LPS challenge than the counterpart of room air group (37.6 +/- 11.4 pg.ml-1 vs. 92.8 +/- 31.5 pg.ml-1, P < 0.05). W/D ratio decreased (3.29 +/- 0.2 vs. 2.94 +/- 0.06, P < 0.05). CONCLUSION: These findings indicated that CO inhalation might modulate the inflammatory response to LPS. Further study is needed to prove the therapeutic role of CO inhalation without serious adverse effects.