scholarly journals The Role of Autophagy in the Innate Immune Response to Fungal Keratitis Caused by Aspergillus fumigatus Infection

2020 ◽  
Vol 61 (2) ◽  
pp. 25 ◽  
Author(s):  
Chenyu Li ◽  
Cui Li ◽  
Jing Lin ◽  
Guiqiu Zhao ◽  
Qiang Xu ◽  
...  
2017 ◽  
Vol 11 (01) ◽  
pp. 89-97 ◽  
Author(s):  
Guiqiu Zhao ◽  
Qiang Xu ◽  
Jing Lin ◽  
Wenjun Chen ◽  
Tingting Cui ◽  
...  

Introduction: This study aimed to detect the early expression of macrophage-inducible C-type lectin (Mincle) and investigate its role in the innate immune response of fungal keratitis (FK). Methodology: Wistar rats were used to make fungal keratitis models. The inflammatory responses and corneal lesions were observed by slit-lamp microscope.RT-PCR, immunohistochemistry, and immunofluorescence were used to detect the expression of Mincle in the rat corneal epithelium. The expression of eight cytokines (CXCL1, CXCL2, IL-1β, IL-6, IL-10, TNF-α, CCL2, CCL3) were detected by real-time RT-PCR and immunohistochemistry. Lastly, corneal epithelium of 54 patients with Aspergillus fumigatus keratitis and 13 ocular trauma patients were collected to detect expression of Mincle by real-time RT-PCR, and 12 FK and 10 ocular trauma paraffin samples were collected to confirm expression of Mincle by immunohistochemistry. Results: The expression of Mincle was significantly upregulated at 4, 8, 16, and 24 hours after fungal infection. There were significant differences in the expression of the eight inflammatory cytokines between the blank control group and the fungus-infected group. Mincle expression was correlated with the expression of TNF-a, IL-1β, IL-10, and CCL3 in the cornea. The mRNA expressions of Mincle in the corneas of both normal and FK patients were significantly different. Conclusions: The expression of Mincle increases significantly during the early period of Aspergillus fumigatus infection, while expression of eight corresponding cytokines changes. Mincle, as a pattern recognition receptor, may play a role in the early innate immune response of the corneal resistance against fungus.


2015 ◽  
Vol 6 (1) ◽  
Author(s):  
Viktoria V. Мokrozub ◽  
Liudmyla M. Lazarenko ◽  
Liubov M. Sichel ◽  
Lidia P. Babenko ◽  
Petro M. Lytvyn ◽  
...  

2017 ◽  
Vol 10 (2) ◽  
pp. 85-93 ◽  
Author(s):  
Keaton M. Crosse ◽  
Ebony A. Monson ◽  
Michael R. Beard ◽  
Karla J. Helbig

The ability of a host to curb a viral infection is heavily reliant on the effectiveness of an initial antiviral innate immune response, resulting in the upregulation of interferon (IFN) and, subsequently, IFN-stimulated genes (ISGs). ISGs serve to mount an antiviral state within a host cell, and although the specific antiviral function of a number of ISGs has been characterized, the function of many of these ISGs remains to be determined. Recent research has uncovered a novel role for a handful of ISGs, some of them directly induced by IFN regulatory factor 3 in the absence of IFN itself. These ISGs, most with potent antiviral activity, are also able to augment varying arms of the innate immune response to viral infection, thereby strengthening this response. This new understanding of the role of ISGs may, in turn, help the recent advancement of novel therapeutics aiming to augment innate signaling pathways in an attempt to control viral infection and pathogenesis.


2008 ◽  
Vol 36 (6) ◽  
pp. 1211-1215 ◽  
Author(s):  
Andrew E. Williams ◽  
Mark M. Perry ◽  
Sterghios A. Moschos ◽  
Hanna M. Larner-Svensson ◽  
Mark A. Lindsay

In mammalian cells, miRNAs (microRNAs) are the most abundant family of small non-coding RNAs that regulate mRNA translation through the RNA interference pathway. In general, it appears that the major function of miRNAs is in development, differentiation and homoeostasis, which is indicated by studies showing aberrant miRNA expression during the development of cancer. Interestingly, changes in the expression of miR-146a have been implicated in both the development of multiple cancers and in the negative regulation of inflammation induced via the innate immune response. Furthermore, miR-146a expression is driven by the transcription factor NF-κB (nuclear factor κB), which has been implicated as an important causal link between inflammation and carcinogenesis. In the present article, we review the evidence for a role of miR-146a in innate immunity and cancer and assess whether changes in miR-146a might link these two biological responses.


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