Year: 2006
Type: article
Abstract: Infections in Stem Ce [[ Transp[ant Recipients $25 Methods: Recipient C57Bt/6 mice received 13Gy of totat body irradiation and were rescued with BM obtained from femurs of donor C57Bt/6 mice.Resident AMs and recruited tung PMNs were harvested 3 to 5 weeks post-BMT and their eicosanoid profite were examined.We measured the Fc and non-Fc mediated phagocytosis and kitting of AMs and PMNs post-BMT.Indomethacin, a PG inhibitor, was used to brock PGE2 production in vitro and in vivo.Results: BMT AMs produce 125-times more PGE2 than controt AMs and BMT PMNs produce 27-ford more PGE2 than controt PMNs.We have shown that the increased susceptibitity of BMT mice corretates with defective AM phagocytosis and kitting of Gramnegative bacteria.Interestingty, PMNs from BMT mice do not disptay defective phagocytosis, but do show a defect in their abitity to kitt ingested Gram-negative bacteria.The pharmacotogic btockade of prostagtandin production by indomethacin in vitro restores AM phagocytosis and kitting and PMN kitting.In addition, treatment with indomethacin restores host defense to P. aeruginosa in vivo. Conclusions:We show that eicosanoid dysreguration post-BMT inhibits the effectiveness of the innate immune response.Inhibiting PGs in vitro and in vivo restores impaired putmonary host defense post-BMT.
Authors: T.R. McMillan, M.N. Ballinger, B.B. Moore
Language: English
Subfield: Oncology
Field: Medicine
Domain: Health Sciences
Open Access status: gold
Estimated APC paid: $2,900
OpenAlex ID: W2017504518