Viral respiratory infection increases alveolar macrophage cytoplasmic motility in rats: Role of NO

T. Fukushima, K. Sekizawa, M. Yamaya, S. Okinaga, M. Satoh, H. Sasaki

研究成果: Article査読

14 被引用数 (Scopus)


Ingested ferrimagnetic (Fe3O4) particles were used to estimate noninvasively the motion of organelles in alveolar macrophages (AM) in intact rats during vital respiratory infection by parainfluenza type 1 (Sendai) virus. Four days after instillation of Fe3O4 particles (3 mg/kg) into the lung, remnant field strength (RFS) was measured at the body surface immediately after magnetization of Fe3O4 particles by an externally applied magnetic held. RFS decreases with time, due to particle rotation (relaxation) which is related to cytoplasmic motility of AM. Vital infection increased the relaxation rate (λ(o) per min), and increases in λ(o) reached a maximum 3 days after nasal inoculation (day 3). Viral infection (day 3)-induced increases in λ(o) were dose dependently inhibited by either the L-arginine analogue N-nitro-L-arginine or by methylene blue, an inhibitor of guanylate cyclase activity. Bronchoalveolar lavage fluid obtained from infected rats contained significantly higher levels of nitrite than that from control rats (P < 0.01). In in vitro experiments, AM from infected rats showed significantly higher λ(o), nitrite production, and intracellular guanosine 3',5'-cyclic monophosphate levels than those from control rats (P < 0.01). Sodium nitroprusside, known to release nitric oxide concentration dependently, increased λ(o) of AM from noninfected rats in vitro. These results suggest that nitric oxide plays an important role in AM cytoplasmic motility during viral respiratory infection.

ジャーナルAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
3 12-3
出版ステータスPublished - 1995

ASJC Scopus subject areas

  • Physiology
  • Pulmonary and Respiratory Medicine
  • Physiology (medical)
  • Cell Biology

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