Viral respiratory infection increases alveolar macrophage cytoplasmic motility in rats: role of NO
Fukushima, T.; Sekizawa, K.; Yamaya, M.; Okinaga, S.; Satoh, M.; Sasaki, H.
American Journal of Physiology 268(3 Pt 1): L399-L406
1995
ISSN/ISBN: 0002-9513 PMID: 7900821 Document Number: 451141
Ingested ferrimagnetic (Fe-3O-4) particles were used to estimate noninvasively the motion of organelles in alveolar macrophages (AM) in intact rats during viral respiratory infection by parainfluenza type 1 (Sendai) virus. Four days after instillation of Fe-3O-4 particles (3 mg/kg) into the lung, remnant field strength (RFS) was measured at the body surface immediately after magnetization of Fe-3O-4 particles by an externally applied magnetic field. RFS decreases with time, due to particle rotation (relaxation) which is related to cytoplasmic motility of AM. Viral infection increased the relaxation rate (lambda-o per min), and increases in lambda-o reached a maximum 3 days after nasal inoculation (day 3). Viral infection (day 3)-induced increases in lambda-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 lt 0.01). In in vitro experiments, AM from infected rats showed significantly higher lambda-o, nitrite production, and intracellular guanosine 3',5'-cyclic monophosphate levels than those from control rats (P lt 0.01). Sodium nitroprusside, known to release nitric oxide concentration dependently, increased lambda-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.