LOGIN TO YOUR ACCOUNT

Username
Password
Remember Me
Or use your Academic/Social account:

CREATE AN ACCOUNT

Or use your Academic/Social account:

Congratulations!

You have just completed your registration at OpenAire.

Before you can login to the site, you will need to activate your account. An e-mail will be sent to you with the proper instructions.

Important!

Please note that this site is currently undergoing Beta testing.
Any new content you create is not guaranteed to be present to the final version of the site upon release.

Thank you for your patience,
OpenAire Dev Team.

Close This Message

CREATE AN ACCOUNT

Name:
Username:
Password:
Verify Password:
E-mail:
Verify E-mail:
*All Fields Are Required.
Please Verify You Are Human:
fbtwitterlinkedinvimeoflicker grey 14rssslideshare1
Cruz, Laura N.; Wu, Yang; Ulrich, Henning; Craig, Alister G.; Garcia, C?lia R.S. (2016)
Publisher: Elsevier Pub. Co
Journal: Biochimica et Biophysica Acta
Languages: English
Types: Article
Subjects: wc_750, qx_135, Tumor necrosis factor, qu_55, qw_630, Plasmodium falciparum, Calcium signaling, Proliferating cell nuclear antigen-1, Cytoadhesion, Malaria, Article
Background: \ud Plasmodium has a complex biology including the ability to interact with host signals modulating their function through cellular machinery. Tumor necrosis factor (TNF) elicits diverse cellular responses including effects in malarial pathology and increased infected erythrocyte cytoadherence. As TNF levels are raised during P. falciparum infection we have investigated whether it has an effect on the parasite asexual stage.\ud \ud Methods:\ud Flow cytometry, spectrofluorimetric determinations, confocal microscopy and PCR real time quantifications were employed for characterizing TNF induced effects and membrane integrity verified by wheat germ agglutinin staining.\ud \ud Results: \ud TNF is able to decrease intracellular parasitemia, involving calcium as a second messenger of the pathway. Parasites incubated for 48h with TNF showed reduced erythrocyte invasion. Thus, TNF induced rises in intracellular calcium concentration, which were blocked by prior addition of the purinergic receptor agonists KN62 and A438079, or interfering with intra- or extracellular calcium release by thapsigargin or EGTA (ethylene glycol tetraacetic acid). Importantly, expression of PfPCNA1 which encodes the Plasmodium falciparum Proliferating-Cell Nuclear Antigen 1, decreased after P. falciparum treatment of TNF (tumor necrosis factor) or 6-Bnz cAMP (N6-Benzoyladenosine-3′,5′-cyclic monophosphate sodium salt).\ud \ud Conclusions: \ud This is potentially interesting data showing the relevance of calcium in down regulating a gene involved in cellular proliferation, triggered by TNF.\ud \ud General significance: \ud The data show that Plasmodium may subvert the immunological system and use TNF for the control of its proliferation within the vertebrate host.

Share - Bookmark

Cite this article