当前位置： SCI文献检索 > INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES期刊下所有文献 > Aspergillus niger lectin elicits MyD88 dependent proliferation and apoptosis at lower and higher doses in immortalized human corneal epithelial cells leading to pathogenesis.

Aspergillus niger lectin elicits MyD88 dependent proliferation and apoptosis at lower and higher doses in immortalized human corneal epithelial cells leading to pathogenesis.

Abstract：

:An L-fucose lectin, ANL from the corneal smears of a mycotic keratitis patient was reported earlier. Interaction of ANL with immortalized Human Corneal Epithelial Cells (HCECs) was studied in order to assign the role of ANL in pathogenesis. ANL showed strong binding to HCECs which could be blocked by L-fucose and mucin. At concentrations below 0.6 μg/mL ANL showed proliferative effect and highest at 0.07 μg/mL leading to expression of proinflammatory cytokines IL-6 and IL-8. ANL induced proinflammatory response is mediated by TLR-2,-4, MyD88, NFkB and C-Jun dependent signaling. In contrast, ANL at concentrations above 0.6 μg/mL showed growth inhibitory effect at 48 h with an IC50 of 2.75 μg/mL. Western blot analysis revealed that HCECs treated with ANL at lower concentration induced the expression of proinflammatory signaling proteins TLR-2, 4, MyD88, NFkB and C-Jun which maintain high cell proliferating state. At higher concentration ANL induced apoptotic effect in HCECs with an increase in early apoptotic population as demonstrated by Annexin V-PI assay. ANL induced the expression of apoptotic proteins FADD, Caspase 8 and -3 mediated by MyD88. These findings demonstrate implication of ANL in pathogenesis and the findings are of clinical significance in developing strategy for controlling the infection leading to mycotic keratitis.

journal_name

Int J Biol Macromol

journal_title

International journal of biological macromolecules

authors

Jagadeesh N,Belur S,Chachadi VB,Roy S,Inamdar SR

doi

10.1016/j.ijbiomac.2020.10.020

subject

Has Abstract

pub_date

2020-12-15 00:00:00

pages

2089-2095

issue

Pt B

eissn

0141-8130

issn

1879-0003

pii

S0141-8130(20)34642-0

journal_volume

165

pub_type

杂志文章

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