| Apoptosis of infected host macrophages by
Leishmania spp. is mainly addressed as one of the survival
mechanisms of the parasite. However, there is no eligible
data about whether tumor suppressor p53 could induce the
apoptosis of host lymphocytes-treated Leishmania major
via the mitochondrial intrinsic pathway. In this study, the
amastigotes of L. major obtained from ten cutaneous leishmaniases (CL) patients were separately isolated and cultured in N.N.N and RPMI 1640 media. L. major was definitely confirmed by targeting Cyt b gene following sequencing. Subsequently, 2–3 × 106 lymphocytes obtained
from ten healthy individuals were isolated and co-cultured
with 1–2 × 106 L. major promastigotes. Following 6 h of
exposure time, the enzymatic activity of caspase-3 was
determined by fluorometric assay in each L. major-treated
lymphocytes and cell control (only lymphocyte). The
mRNA expressions of Bax, Bcl-2, p53, and caspase-3
genes were assessed by quantitative real-time-PCR analysis following 6 to 9 h of exposure times. The Bcl-2 mRNA
expression in L. major-treated lymphocytes was 100-fold
down-regulated relative to cell control. The mRNA expressions of p53 and caspase-3 were over-expressed 1.8- and
3.2-fold up-regulated relative to control lymphocytes, respectively. The Bax/Bcl-2 ratio and caspase-3 activity were
higher than the control group (Pv <0.05). The current new
findings indicate that the apoptotic effects of L. majortreated host lymphocytes dependent on p53 tumor suppressor via mitochondrial pathway may probably address as an
auxiliary survival mechanism of L. major in CL patients.
However, here is much work ahead to figure out the multiple functions played by apoptosis in the evasion of
L. major. |