BACKGROUND: @entity1223 (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 @entity35 (each study group consisting of 7 animals) inhaled 250 ppm of CO one hour prior to @entity558 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 @entity558 (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, @entity1505 , and @entity13358 concentrations in BAL fluid were measured. Plasma @entity1505 and @entity13358 were also measured. The Wet/Dry ratio of a small intestine was calculated. RESULTS: In the CO-inhalation group, the anti-inflammatory cytokine @entity13358 concentration in the BAL fluid was higher at 8 hours after @entity558 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 @entity558 . Further study is needed to prove the therapeutic role of CO inhalation without serious adverse effects.

[The effects of inhaled XXXX on lung injury in @entity35 caused by lipopolysaccharide].

@entity558 :: ('MESH:C536528', 'Disease') :: ['LPS'] @entity1223 :: ('MESH:D002248', 'Chemical') :: ['Carbon monoxide'] @entity13358 :: ('25325(Tax:10116)', 'Gene') :: ['IL-10'] @entity1505 :: ('24835(Tax:10116)', 'Gene') :: ['TNF'] @entity35 :: ('10116', 'Species') :: ['rats']
@entity1223 :: (MESH:D002248,Chemical) :: ['carbon monoxide']
