Hh. Winkler et al., EFFECT OF GAMMA-INTERFERON ON PHOSPHOLIPID HYDROLYSIS AND FATTY-ACID INCORPORATION IN L929 CELLS INFECTED WITH RICKETTSIA-PROWAZEKII, Infection and immunity, 61(8), 1993, pp. 3412-3415
Treatment of Rickettsia prowazekii-infected L929 cells with gamma inte
rferon (IFN-gamma) immediately after infection altered the lipid metab
olism of the host cells as determined by measurement of phospholipid h
ydrolysis and oleic acid incorporation into phospholipids and neutral
lipids. At 48 h postinfection, there was increased phospholipid hydrol
ysis in infected cultures relative to mock-infected cultures and a fur
ther increase in radiolabeled phospholipid hydrolysis in IFN-gamma-tre
ated infected cultures. Oleic acid, the radiolabeled product of hydrol
ysis, was found in both the free fatty acid and neutral lipid fraction
s. None of the mock-infected cultures demonstrated increased hydrolysi
s of their radiolabeled phospholipids in response to treatment with IF
N-gamma. Most of the radiolabeled oleic acid incorporated into culture
s in the interval between 24 and 48 h after infection and IFN-gamma tr
eatment was present in the phospholipid fraction. However, the neutral
lipid fraction from the infected cultures that had been IFN-gamma tre
ated was labeled to a greater extent than that from the untreated cult
ures. Thin-layer chromatographic analysis of the neutral lipid fractio
ns from both the hydrolysis and incorporation experiments demonstrated
that most of the radiolabel was in triglycerides. The infected cultur
es at 30 h were intact as assessed by the exclusion of trypan blue, bu
t at 48 h postinfection in the IFN-gamma-treated infected cultures mor
e than half of the cells were unable to exclude trypan blue. In no cas
e did the mock-infected cells show substantial damage as a result of I
FN-gamma treatment.