Splenocyte apoptosis in Plasmodium berghei ANKA infection: possible role of TNF‐α and TGF‐β. (9th January 2013)

• Record Type: Journal Article
• Authors: Keswani, T.; Bhattacharyya, A.
• Is Part Of: Parasite immunology. Volume 35:Number 2(2013:Feb.)
• Page Start: 73
• Page End: 90
• Publication Date: 2013-01-09
• Subjects: Veterinary parasitology -- Immunological aspects -- Periodicals; Host-parasite relationships -- Immunological aspects -- Periodicals; 571.96
• DOI: 10.1111/pim.12005
• Languages: English
• ISSNs: 0141-9838

Abstract

<abstract abstract-type="main" xml:lang="en" id="pim12005-abs-0001"> <title>Summary</title> <p>Cerebral malaria is associated with the circulating levels of tumour necrosis factor alpha (TNF‐α) and transforming growth factor β (TGF‐β), but association between these two cytokines and implications in splenocyte apoptosis remain largely obscured. We have evaluated the outcome of TGF‐β and TNF‐α production in the context of splenocyte apoptosis during <italic>Plasmodium berghei ANKA (PbA)</italic> infection. Blood‐stage <italic>PbA</italic> infection confirmed blood–brain barrier disruption, disarray of white pulp, increase in percentage of sub‐G0/G1 and splenocyte apoptosis. Flow cytometric analysis reveals up‐regulation of Fas‐L followed by caspase‐8 and caspase‐3 activation and signifies possible involvement of Fas‐L‐mediated splenocyte apoptosis. We have observed down‐regulation of TGF‐β and up‐regulation of TNF‐α in tissue and serum level, respectively, during <italic>PbA</italic> infection. Association between the production of TGF‐β and the severity of malaria infection in splenocytes was verified with TGF‐β inhibitor that exacerbated the apoptotic process. In contrary, TNF‐α inhibitor causes significant delay in apoptotic process, but could not alter the lethality of parasite. Thus, results from this study suggest that the critical balance between TGF‐β and TNF‐α might have a key role on Fas‐L‐mediated splenocyte apoptosis during experimental cerebral malaria.</p> </abstract>