Alterations in lung prostaglandin synthesis and release in murine respiratory mycoplasmosis.
Pathogenetic mechanisms in murine respiratory mycoplasmosis are poorly understood; however, non-specific immune responses appear to be important in controlling the growth of Mycoplasma pulmonis in vitro. To date, no study has examined the role of pulmonary prostaglandin production during the development of M. pulmonis infection. The present study was designed to determine if alterations in pulmonary prostaglandin synthesis and release occur in M. pulmonis infection and the possible role for prostaglandins in the modulation/pathogenesis of murine respiratory mycoplasmosis. Ten to 20 days after intranasal inoculation of pathogen-fee F344 rats with M. pulmonis, lung lavage concentrations of prostaglandin E (PGE) and thromboxane A2 (TxA2) were significantly elevated. To confirm a role for prostaglandins in the pathogenesis of murine mycoplasmosis we blocked the cyclo-oxygenase pathway with indomethacin. Indomethacin-treated rats had significantly lower lavage levels of PGE and TxA2 and significantly increased numbers of M. pulmonis in the lung. These data indicate that prostaglandins may be involved in the pathogenesis of murine respiratory mycoplasmosis, possibly through alteration of mycoplasmacidal and/or mycoplasmastatic mechanisms.
Reinhard
M K
MK
Department of Medicine, University of Alabama, Birmingham.
Chandler
D B
DB
D000818:Animals; D007213:Indomethacin / Q000494:pharmacology; D008168:Lung / Q000378:metabolism*; D008297:Male; D009175:Mycoplasma Infections / Q000378:metabolism*; D011458:Prostaglandins E / Q000096:biosynthesis*; D051381:Rats; D011916:Rats, Inbred F344; D013047:Specific Pathogen-Free Organisms; D013928:Thromboxane A2 / Q000096:biosynthesis*
D011458:Prostaglandins E; D013928:Thromboxane A2; D007213:Indomethacin