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Active leukocyte detachment and apoptosis/necrosis on PEG hydrogels and the implication in the host inflammatory response.

Abstract：

:Monocytes/Macrophages have long been recognized as key players in inflammation and wound healing and are often employed in vitro to gain an understanding of the inflammatory response to biomaterials. Previous work has demonstrated a drastic decrease in primary monocyte adherent density on biomaterial surfaces coupled with a change in monocyte behavior over time. However, the mechanism responsible for this decrease remains unclear. In this study, we explored active detachment and cellular death as possible regulating factors. Specifically, extracellular TNF-α and ROS production were analyzed as potential endogenous stimulators of cell death. MMPs, but not calpains, were found to play a key role in active monocyte detachment. Monocyte death was found to peak at 24 h and occur by both apoptosis and necrosis as opposed to polymorphonuclear leukocyte death which mainly occurred through apoptosis. Finally, TNF-α and ROS production were not found to have a causal relationship with monocyte death on TCPS or PEG surfaces. The occurrence of primary monocyte apoptosis/necrosis as well as active detachment from a material surface has implications not only in in vitro study, but also in the translation of the in vitro inflammatory response of these cells to in vivo applications.

journal_name

Biomaterials

journal_title

Biomaterials

authors

Waldeck H,Wang X,Joyce E,Kao WJ

doi

10.1016/j.biomaterials.2011.09.044

subject

Has Abstract

pub_date

2012-01-01 00:00:00

pages

29-37

issue

1

eissn

0142-9612

issn

1878-5905

pii

S0142-9612(11)01120-3

journal_volume

33

pub_type

杂志文章

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