scholarly journals Exaptation of an ancient Alu short interspersed element provides a highly conserved vitamin D-mediated innate immune response in humans and primates

BMC Genomics ◽  
2009 ◽  
Vol 10 (1) ◽  
pp. 321 ◽  
Author(s):  
Adrian F Gombart ◽  
Tsuyako Saito ◽  
H Phillip Koeffler
2015 ◽  
Vol 21 (5) ◽  
pp. 482.e1-482.e7 ◽  
Author(s):  
N.L. Ramos ◽  
M. Sekikubo ◽  
F. Kironde ◽  
F. Mirembe ◽  
M. Sääf ◽  
...  

2020 ◽  
Vol 20 (3) ◽  
Author(s):  
Yunita Arliny ◽  
Maryatun Hasan

Abstrak. Tuberkulosis (TB) merupakan salah satu penyakit infeksi yang menjadi masalah di dunia. Risiko untuk mendapatkan infeksi TB dipengaruhi oleh imunitas alamiah melawan mikobakteria. Peptida antimikroba merupakan salah satu barrier pertahanan alamiah. Cathelicidin adalah suatu peptida anti mikroba yang berperan pada proses imunitas terhadap TB. Cathelicidin Leusin Leusin-37 (LL-37) merupakan satu-satunya cathelicidin yang ada pada manusia dan dapat diekspresikan dari beberapa sel temasuk sel imun. Inducer Cathelicidin yang paling poten adalah 1,25-dihydroxyvitamin D3 yang merupakan bentuk aktif vitamin D 25(OH)D3. Tinjauan pustaka ini membahas tentang cathelicidin, vitamin D3 dam peranannya pada imunitas terhadap TB.Kata kunci: Cathelicidin, 1,25-dihydroxyvitamin D3, vitamin D 25(OH)2D3, imunitas, TuberkulosisAbstract. Tuberculosis is one of the most important infectious diseases worldwide. The susceptibility to this disease depends to great extent on the innate immune response against mycobacteria. Antimicrobial peptides are one of the natural defense barriers. Cathelicidin Leucine Leucine-37 (LL-37) is the only cathelicidin present in humans and synthesized by several cells including immune cells. The most effective inducer of Cathelicidin is 1,25-dihydroxyvitamin D3 (1,25(OH)2 D3), which is an active form of vitamin D 25(OH)D3. This review discusses cathelicidin, vitamin D3 and its role in immunity against TBKeywords: Cathelicidin, 1,25-dihydroxyvitamin D3, vitamin D 25(OH)D3, immunity, Tuberkulosis


2011 ◽  
Vol 79 (6) ◽  
pp. 2250-2256 ◽  
Author(s):  
Laura McMahon ◽  
Kyell Schwartz ◽  
Ozlem Yilmaz ◽  
Eleith Brown ◽  
Lisa K. Ryan ◽  
...  

ABSTRACTHuman gingival epithelial cells (GEC) produce peptides, such as β-defensins and the cathelicidin LL-37, that are both antimicrobial and that modulate the innate immune response. In myeloid and airway epithelial cells, the active form of vitamin D3[1,25(OH)2D3] increases the expression and antibacterial activity of LL-37. To examine the activity of vitamin D on the innate immune defense of the gingival epithelium, cultured epithelial cells were treated with either 10−8M 1,25(OH)2D3or ethanol for up to 24 h. A time-dependent induction of LL-37 mRNA up to 13-fold at 24 h in both standard monolayer and three-dimensional cultures was observed. Induction of the vitamin D receptor and the 1-α-hydroxylase genes was also observed. The hydroxylase was functional, as LL-37 induction was observed in response to stimulation by 25(OH)D3. Through microarray analysis of other innate immune genes, CD14 expression increased 4-fold, and triggering receptor expressed on myeloid cells-1 (TREM-1) was upregulated 16-fold after 24 h of treatment with 1,25(OH)2D3. TREM-1 is a pivotal amplifier of the innate immune response in macrophages, leading to increased production by inflammatory response genes. Activation of TREM-1 on the GEC led to an increase in interleukin-8 (IL-8) mRNA levels. Incubation of three-dimensional cultures with 1,25(OH)2D3led to an increase in antibacterial activity against the periodontal pathogenAggregatibacter actinomycetemcomitanswhen the bacteria were added to the apical surface. This study is the first to demonstrate the effect of vitamin D on antibacterial defense of oral epithelial cells, suggesting that vitamin D3could be utilized to enhance the innate immune defense in the oral cavity.


Critical Care ◽  
2011 ◽  
Vol 15 (S1) ◽  
Author(s):  
MJ Van den Berg ◽  
M Kox ◽  
AJ Van der Ven ◽  
JP Wielders ◽  
P Pickkers

Bone ◽  
2011 ◽  
Vol 48 ◽  
pp. S146-S147 ◽  
Author(s):  
J. Vargas-Vasserot ◽  
J.M. Mata-Granados ◽  
M. Luque de Castro ◽  
R. Guerrero Pavón ◽  
J. Quesada Gomez

2015 ◽  
Vol 29 (3) ◽  
pp. 119-129 ◽  
Author(s):  
Richard J. Stevenson ◽  
Deborah Hodgson ◽  
Megan J. Oaten ◽  
Luba Sominsky ◽  
Mehmet Mahmut ◽  
...  

Abstract. Both disgust and disease-related images appear able to induce an innate immune response but it is unclear whether these effects are independent or rely upon a common shared factor (e.g., disgust or disease-related cognitions). In this study we directly compared these two inductions using specifically generated sets of images. One set was disease-related but evoked little disgust, while the other set was disgust evoking but with less disease-relatedness. These two image sets were then compared to a third set, a negative control condition. Using a wholly within-subject design, participants viewed one image set per week, and provided saliva samples, before and after each viewing occasion, which were later analyzed for innate immune markers. We found that both the disease related and disgust images, relative to the negative control images, were not able to generate an innate immune response. However, secondary analyses revealed innate immune responses in participants with greater propensity to feel disgust following exposure to disease-related and disgusting images. These findings suggest that disgust images relatively free of disease-related themes, and disease-related images relatively free of disgust may be suboptimal cues for generating an innate immune response. Not only may this explain why disgust propensity mediates these effects, it may also imply a common pathway.


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