[Effects of nitric oxide on the airway inflammation and lymphocyte proliferation in sensitized rats].
OBJECTIVE
To investigate the relations between intrinsic nitric oxide (NO) and airway inflammation and lymphocyte proliferation in bronchial asthma.


METHODS
The rat model of asthmatic airway inflammation was established by first sensitizing and then challenging the animals with ovalbumin. NO synthase (NOS) inhibitor and NO precursor were then applied and their influences on the airway inflammatory cell numbers and on the numbers of mIL-2R positive lymphocytes were observed.


RESULTS
In vivo experiments showed that normal control rats (n = 6) did not have eosinophils in their submucosal of airways while in the sensitized animals (n = 6) eosinophils [23 +/- 5 (average cell counts per microscopic visual field, the same below) as well as lymphocytes (34 +/- 5) and mIL-2R positive cells (12 +/- 3) were found in significantly increased numbers in the airways. The application of NOS inhibitor significantly reduced eosinophils (13 + 3, P < 0.05) and mIL-2R positive cells (4.3 +/- 1.6, P < 0.05) in the sensitized animals and the number of lymphocytes was also decreased (28 +/- 4) although it did not reach the significant level. At the same time the spleen cell proliferation was inhibited (P < 0.05) and the mIL-2R positive spleen cell numbers were reduced (P < 0.05). On the contrary, the application of NO precursor resulted in the further increase of the numbers of eosinophils, lymphocytes and mIL-2R positive cells although the differences were not statistically significant. In vitro experiments showed that NOS inhibitor inhibited the proliferation of cultured spleen lymphocytes as well as their mIL-2R expression (P < 0.05). NO precursor, when used in low dose, could promote the proliferation and mIL-2R expression of spleen cells (P < 0.05); but high dose of it showed inhibiting effect on the spleen cells (P < 0.05).


CONCLUSIONS
Intrinsic NO at a suitable level is important in the regulation of the proliferation and activation of lymphocytes in the airways with allergic inflammation in the sensitized rats. This research is conducive to the understanding of the pathogenesis of the asthmatic airway inflammation and to investigating of new therapeutic approaches.
Xue
J
J
Department of Respiratory Disease, Tongji Hospital, Tongji Medical University, Wuhan 430030.
Xu
Y
Y
Zhang
Z
Z
D000818:Animals; D001120:Arginine / Q000494:pharmacology; D001249:Asthma / Q000139:chemically induced / Q000473:pathology*; D001991:Bronchitis / Q000139:chemically induced / Q000473:pathology*; D002478:Cells, Cultured; D004804:Eosinophils / Q000473:pathology; D008214:Lymphocytes / Q000473:pathology*; D008297:Male; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000378:metabolism*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors*; D010047:Ovalbumin; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D015375:Receptors, Interleukin-2 / Q000378:metabolism
D015375:Receptors, Interleukin-2; D009569:Nitric Oxide; D010047:Ovalbumin; D001120:Arginine; D019001:Nitric Oxide Synthase; D019331:NG-Nitroarginine Methyl Ester