当前位置： SCI文献检索 > INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES期刊下所有文献 > Naja kaouthia venom protein, Nk-CRISP, upregulates inflammatory gene expression in human macrophages.

Naja kaouthia venom protein, Nk-CRISP, upregulates inflammatory gene expression in human macrophages.

Abstract：

:Cysteine-Rich Secretory Proteins (CRISP) are widespread in snake venoms and known to target ion channels. More recently, CRISPs have been shown to mediate inflammatory responses. Involvement of potential receptor in CRISP-induced inflammatory reactions, however, remains unknown. A CRISP protein named as Nk-CRISP, was isolated from the venom of Naja kaouthia. The molecular mass of the purified protein was found to be ~25 kDa and the primary sequence was determined by MALDI TOF-TOF. The involvement of this protein in proinflammatory effects were evaluated in THP-1 macrophage-like cells. Nk-CRISP treated cells induced up-regulation of several inflammatory marker genes in dose dependent manner. Toll like receptor 4 (TLR4)-myeloid differentiation factor 2 (MD2) complex are known to play crucial role in recognition of damage/pathogen-associated molecular patterns and activation of innate immune response. Therefore, we hypothesized that snake venom CRISP could also modulate the innate immune response via TLR4-MD2 complex. In-silico molecular docking study of cobra CRISP with TLR4-MD2 receptor complex reveals CRISP engages its cysteine-rich domain (CRD) to interact with complex. Inhibition of TLR4 signalling pathway using CLI-095 confirmed the role of TLR4 in Nk-CRISP induced inflammatory responses. Collectively, these findings imply that TLR4 initiates proinflammatory signalling following recognition of cobra CRISP and alteration of TLR4 receptor might improve or control CRISP induced inflammation.

journal_name

Int J Biol Macromol

journal_title

International journal of biological macromolecules

authors

Deka A,Sharma M,Mukhopadhyay R,Devi A,Doley R

doi

10.1016/j.ijbiomac.2020.05.169

subject

Has Abstract

pub_date

2020-10-01 00:00:00

pages

602-611

eissn

0141-8130

issn

1879-0003

pii

S0141-8130(20)33328-6

journal_volume

160

pub_type

杂志文章

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