Expression and validation of PvPGIP genes for resistance to white mold (Sclerotinia sclerotiorum) in common beans (Phaseolus vulgaris L.).

The interaction between polygalacturonase-inhibiting proteins (PGIPs), produced by plants, and endopolygalacturonases (PGs), produced by fungi, limits the destructive potential of PGs and can trigger plant defense responses. This study aimed to i) investigate variation in the expression of different common bean (Phaseolus vulgaris L.) genotypes and its relationship with resistance to white mold (Sclerotinia sclerotiorum); ii) determine the expression levels of PvPGIP genes at different time points after inoculation with white mold; and iii) investigate differences in PvPGIP gene expression between two white mold isolates with different levels of aggressiveness. Four bean lines were analyzed, including two lines from a recurrent selection for white mold (50/5 and 84/6), one resistant line that was not adapted to Brazilian conditions (Cornell 605), and one susceptible line (Corujinha). Gene expression was investigated at 0, 1, 2, 3, and 5 days after inoculation. The isolate UFLA 03 caused no significant difference in the relative expression of any gene examined, and was inefficient in discriminating among the genotypes. For the isolate UFLA 116, all of the genes were differentially expressed, as they were associated with resistance to white mold, and the expressions increased until the third day after inoculation. The 50/5 line was not significantly different from the Corujinha line for all of the genes analyzed. However, this line had a resistance level that was similar to that of Cornell 605, according to the straw test. Therefore, the incorporation of PvPGIP genes can increase the resistance of lines derived from recurrent selection.

Suppressor activity in Leishmania donovani-infected hamster serum: reversion by delipidated bovine serum albumin and role in cell cycle events.

Visceral leishmaniasis, caused by Leishmania donovani, is a chronic disease with a high mortality rate. This protozoan induces a serious dysfunction of the immune system characterized by suppression of the cellular response to parasite antigens. We provide evidence for the involvement of lipids in the immunological alterations of experimental leishmaniasis. Sera obtained from 60-day-infected hamsters present increased triglyceride levels. Inhibition of cell proliferation was observed when splenocytes from normal hamsters were stimulated with concanavalin A in the presence of 3% infected hamster serum (IHS) (Control 50 +/- 3 (x10(3)) cpm; IHS 5 +/- 1 (x10(3)) cpm). This inhibition was reversed by the addition of 5 mg/ml of delipidated bovine serum albumin (BSA) to the cultures (Control 65 +/- 1 (x10(3)) cpm; IHS 75 +/- 3 (x10(3)) cpm). The inhibitory effect of IHS was demonstrable only when added to the culture simultaneously with the mitogen. This effect was not as intense on fresh, pre-activated cells or on the CTLL-2 cells. This cell line stimulated by IL-2 in the presence of IHS is only marginally inhibited (about 20% inhibition). The suppressor effect on CTLL-2 was not reversed by the addition of increasing doses of IL-2 (up to 100 U/ml) to cultures. The inhibition of the proliferative response of the CTLL-2 cells caused by IHS was also reversed by the addition of delipidated BSA. Our data suggest a role for fatty acids in the infected hamster serum-induced suppression of normal or L. donovani-infected cell proliferation.

Suppressor activity in Leishmania donovani-infected hamster serum: reversion by delipidated bovine serum albumin and role in cell cycle events

Visceral leishmaniasis caused by Leishmania donovani, is a chroníc disease with a high mortality rate. This protozoan induces a serious dysfunction of the immune system characterized by suppression of the cellular response to parasite antigens. We provide evidence for the involvement of lipids in the immunological alterations of experimental leishmaniasis. Sera obtained from 60-day-infected hamsters present increased triglyceride levels. Inhibition of cell proliferation was observed when splenocytes from normal hamsters were stimulated with concanavalin A in the presence of 3 per cent infected hamster serum (IHS) (Control 50 + 3 (x 10(3)) Cpm; IHS 5 ñ 1 (X 10(3)) cpm). This inhibition was reversed by the addition of 5 mg/ml of delipidated bovine serum albumin (BSA) to the cultures (Control 65 ñ 1 (X 10(3)) cpm; IHS 75 ñ 3 (x 10(3)) cpm). The inhibitory effect of IHS was demonstrable only when added to the culture simultaneously with the mitogen. This effect was not as intense on fresh, pre-activated cells or on the CTLL-2 cells. This cell line stimulated by IL-2 in the presence of IHS is only marginally inhibited (about 20 per cent inhibition). The suppressor effect on CTLL-2 was not reversed by the addition of increasing doses of IL-2 (up to 100 U/ml) to cultures. The inhibition of the proliferative response of the CTLL-2 cells caused by IHS was also reversed by the addition of delipidated BSA. Our data suggest a role for fatty acids in the infected hamster serum-induced suppression of normal or L. donovani-infected cell proliferation.