Immunohistochemical Quantification of the Tumor Necrosis Factor (TNF) Receptor II Expression in the Hepatic Tissue after Systemic Administration of the DNA-SWCNT
Abstract
The Tumor Necrosis Factor is a key mediator in hepatic inflammatory response during acute exposure to xenobiotics. The cellular effects of TNF are mediated via two cell surface receptors, TNF receptor 1 and TNF receptor 2. The purpose of this study was to examine the expression and to identify the cellular localization of TNFR2 in hepatic tissue by immunohistochemistry after systemic administration of the SWCNT. In the same time the cellular infiltration and the weight of the liver was correlated with the TNF alpha receptor 2 expression. Mice were exposed intraperitoneally (ip) to either vehicle, phosphate-buffered saline (PBS), or SWCNT-DNA (1.5ml, 2.925 mg/kg) for 48 h. The hepatic response associated with SWCNT systemic administration was characterized by increased expression of the TNF receptor II especially in the hepatocytes from the centrilobular and midzonal areas of hepatic lobule. This induced elevation of the TNF receptor II is not followed by hepatic necrosis, inflammatory infiltration or significant changes in liver weight.
a) Authors retain copyright and grant the journal right of first publication with the work simultaneously licensed under a Creative Commons Attribution License that allows others to share the work with an acknowledgement of the work's authorship and initial publication in this journal.
b) Authors are able to enter into separate, additional contractual arrangements for the non-exclusive distribution of the journal's published version of the work (e.g., post it to an institutional repository or publish it in a book), with an acknowledgement of its initial publication in this journal.
c) Authors are permitted and encouraged to post their work online (e.g., in institutional repositories or on their website) prior to and during the submission process, as it can lead to productive exchanges, as well as earlier and greater citation of published work (See The Effect of Open Access).