scholarly journals The role of Mincle in innate immune to fungal keratitis

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.

2014 ◽  
Vol 128 ◽  
pp. 117-128 ◽  
Author(s):  
Ayilam Ramachandran Rajalakshmy ◽  
Jambulingam Malathi ◽  
Hajib Naraharirao Madhavan

2019 ◽  
Author(s):  
Grace E. Weber ◽  
Katherine Koenig ◽  
Maria Khrestian ◽  
Yvonne Shao ◽  
Elizabeth D. Tuason ◽  
...  

AbstractIndividuals with Down syndrome (DS) develop Alzheimer’s disease (AD) - related neuropathology, characterized by amyloid plaques with amyloid β (Aβ) and neurofibrillary tangles with tau accumulation more frequently and at an earlier age than their neurotypical counterparts. Peripheral inflammation and the innate immune response are elevated in DS. Triggering receptor expressed in myeloid cells 2 (TREM2) genetic variants are risk factors for AD and other neurodegenerative diseases. A soluble cleavage product of TREM2 (sTREM2) has been described as elevated in AD cerebrospinal fluid and positively correlates with Aβ and cognitive decline. There is relatively little information about TREM2 in DS. The objective of this study was to examine the relationship between sTREM2 and inflammatory markers in DS, prior to the development of dementia symptoms. Since TREM2 plays a role in the innate immune response and has been associated with dementia, the hypothesis of this exploratory study was that young adults with DS pre-dementia (n=15, mean age 29.5 years) would exhibit a different relationship between sTREM2 and inflammatory markers in plasma, compared to neurotypical, age-matched controls (n=16, mean age 29.6 years). Indeed, young adults with DS had significantly elevated plasma sTREM2 and inflammatory markers. In addition, in young adults with DS, sTREM2 correlated positively with 24 of the measured cytokines, while there were no significant correlations in the control group. Hierarchical clustering of sTREM2 and cytokine concentrations also differed between the group with DS and controls, supporting the hypothesis that its function is altered in people with DS pre-dementia. This exploratory study provides a basis for future studies investigating the relationship between TREM2 and the broader immune response pre-dementia.


2020 ◽  
Author(s):  
Di Yang ◽  
Lin Shen ◽  
Ri Chen ◽  
Yu Fu ◽  
Li Zhang ◽  
...  

Abstract Background: Talaromyces Marneffei (T.marneffei) is an destructive opportunistic dimorphic fungal which can cause lethiferous Talaromycosis, but the clearance of T.marneffei mainly depends on the innate immune response. Objectives: To investigate the effect of T.marneffei on CD86 expression in THP-1 cells after infection and discuss the potential mechanisms. Methods: Western blot and immunoelectron microscopy were used to detect the CD86 expression on T.marneffei cultured on BHI medium at 37℃. Western blot、enzyme-linked immunoassay and immunofluorescence were used to detect the change of CD86 expression on macrophages incubating with T.marneffei. Enzyme-linked immunoassay was used to detect the content of CD86 in supernatant in the co-culture system. Immunohistochemistry and immunoelectron microscopy were used to detect the expression of CD86 on T.marneffei incubating with macrophages. Results: T.marneffei didn’t express CD86 when cultured separately at 37℃ detected by western blot and immunoelectron microscopy, but it did express CD86 when incubated with macrophages detected by immunohistochemistry and immunoelectron microscopy. The CD86 expression of macrophages significantly decreased at 72 hours when infected with T.marneffei while the content of CD86 in supernatant significantly increased at 72 hours compared with the control group which were detected by western blot, enzyme-linked immunoassay and immunofluorescence. Conclusion: 1.After T.marneffei infection,CD86 expression on THP-1 decreased,and with the progression of infection, insufficient polarization of M1 macrophages gradually appeared;2.T.marneffei may adsorb or uptake CD86 in supernatant produced by macrophages during the contact with THP-1 cells, thus leading to the consumption of CD86 in macrophages.


Author(s):  
А.В. Цепокина ◽  
М.Ю. Синицкий ◽  
М.А. Асанов ◽  
Я.В. Казачек ◽  
А.В. Евтушенко ◽  
...  

Изучены образцы створок клапанов сердца, полученные в ходе кардиохирургического вмешательства от 26 пациентов с установленным диагнозом «инфекционный эндокардит» (ИЭ), и от 12 пациентов без данной патологии (контрольная группа). Оценка уровня экспрессии генов врожденного иммунного ответа TLR1, TLR2, TLR4 и TLR6 проводилась методом количественной полимеразной цепной реакции. Установлено, что экспрессия гена TLR2 у пациентов с ИЭ практически не отличалась от контрольной группы, в то время как уровень мРНК генов TLR1, TLR4 и TLR6 в группе пациентов был значительно ниже, чем в контроле. We studied samples of heart valves obtained during cardiac surgery from 26 patients with infective endocarditis (IE) and 12 patients without this pathology (control group). The expression of innate immune response genes (TLR1, TLR2, TLR4 and TLR6) was evaluated by quantitative polymerase chain reaction. It was found that the TLR2 expression in patients with IE was similar to the control group, while the mRNA level of the TLR1, TLR4 and TLR6 genes in the patients was significantly lower compared to the control.


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