title: Increased levels of serum sulfite in patients with acute pneumonia.
abstract: Sulfite, a common air pollutant, is toxic for humans, causing hypersensitivity or chronic airway diseases. We previously reported that sulfite is actively produced from neutrophils by stimulation with bacterial endotoxin, lipopolysaccharide (LPS). We also found that the serum sulfite concentration is increased in a rat model of sepsis induced by systemic injection of LPS. However, information on sulfite metabolism in human inflammatory conditions is limited. In the current study, the serum concentration of sulfite was determined in 25 patients with acute pneumonia. Serum sulfite concentration in pneumonia patients was significantly higher than that in control subjects (3.75 +/- 0.88 vs. 1.23 +/- 0.48 microM, respectively, P < 0.05). Among 20 patients, serum sulfite was serially determined before and after antibiotic therapy. The levels of serum sulfite were significantly reduced during the recovery phase compared with those during the acute phase (1.34 +/- 0.56 vs. 3.65 +/- 0.92 microM, respectively, P < 0.05). Moreover, neutrophils obtained from three patients during the acute phase of pneumonia spontaneously produced higher amounts of sulfite in vitro than those obtained after recovery. There was a close positive correlation (r = 0.71, P < 0.05) between serum sulfite and C-reactive protein (CRP) in patients with pneumonia. Taken together, the current findings suggest that serum sulfite increases during systemic inflammation in humans. Activated neutrophils might be responsible, at least in part, for the up-regulation of sulfite. Given various biological effects reported previously, sulfite may act as a mediator in inflammation.
authors.affiliation: Department of Medicine and Clinical Science, Gunma Graduate School of Medicine, Maebashi, Japan.
authors.forename: Hideki
authors.initials: H
authors.lastname: Mitsuhashi
authors.forename: Hidekazu
authors.initials: H
authors.lastname: Ikeuchi
authors.forename: Shin
authors.initials: S
authors.lastname: Yamashita
authors.forename: Takashi
authors.initials: T
authors.lastname: Kuroiwa
authors.forename: Yoriaki
authors.initials: Y
authors.lastname: Kaneko
authors.forename: Keijyu
authors.initials: K
authors.lastname: Hiromura
authors.forename: Kazue
authors.initials: K
authors.lastname: Ueki
authors.forename: Yoshihisa
authors.initials: Y
authors.lastname: Nojima
mesh_terms: D000208:Acute Disease; D000210:Acute-Phase Reaction; D000368:Aged; D000890:Anti-Infective Agents / Q000627:therapeutic use; D002097:C-Reactive Protein / Q000096:biosynthesis; D016022:Case-Control Studies; D005260:Female; D006801:Humans; D007249:Inflammation; D007962:Leukocytes / Q000378:metabolism; D008070:Lipopolysaccharides; D008297:Male; D018375:Neutrophil Activation; D009504:Neutrophils / Q000378:metabolism; D011014:Pneumonia / Q000097:blood* / Q000188:drug therapy; D013447:Sulfites / Q000097:blood*; D013997:Time Factors; D015854:Up-Regulation
chemical_list: D000890:Anti-Infective Agents; D008070:Lipopolysaccharides; D013447:Sulfites; D002097:C-Reactive Protein