5 research outputs found
Delay in maturation of the submandibular gland in Chagas disease correlates with lower DNA synthesis
Delay in maturation of the submandibular gland in Chagas disease correlates with lower DNA synthesis
It has been demonstrated that the acute phase of Trypanosoma cruzi
infection promotes several changes in the oral glands. The present
study examined whether T. cruzi modulates the expression of host cell
apoptotic or mitotic pathway genes. Rats were infected with T. cruzi
then sacrificed after 18, 32, 64 or 97 days, after which the
submandibular glands were analyzed by immunohistochemistry.
Immunohistochemical analyses using an anti-bromodeoxyuridine antibody
showed that, during acute T. cruzi infection, DNA synthesizing cells in
rat submandibular glands were lower than in non-infected animals (p
< 0.05). However, after 64 days of infection (chronic phase), the
number of immunolabeled cells are similar in both groups. However,
immunohistochemical analysis of Fas and Bcl-2 expression did not find
any difference between infected and non-infected animals in both the
acute and chronic stages. These findings suggest that the delay in
ductal maturation observed at the acute phase of Chagas disease is
correlated with lower expression of DNA synthesis genes, but not
apoptotic genes
Epidermal growth factor receptors, testosterone levels and parotid gland changes in rats infected with Trypanosoma cruzi
It has been demonstrated that parotid glands of rats infected with
Trypanosoma cruzi present severe histological alterations; changes
include reduction in density and volume of the acini and duct systems
and an increase in connective tissue. We evaluated the association
between morphological changes in parotid glands, circulating
testosterone levels and epidermal growth factor receptor (EGF-R)
expression in experimental Chagas disease in rats. Animals at 18 days
of infection (acute phase) showed a significant decrease in body
weight, serum testosterone levels and EGF-R expression in the parotid
gland compared with a control group. Since decreases in body weight
could lead to a reduction in circulating testosterone concentration, we
believe that the reduction in EGF-R expression in parotid glands of
infected rats is due to alterations in testosterone levels and atrophy
of parotid glands is caused by changes in EGF-R expression.
Additionally, at 50 days (chronic phase) of infection parotid glands
showed a normal histological aspect likely due to the normalization of
the body weight. These findings suggest that the testosterone-EGF-R
axis is involved in the histological changes