scholarly journals Extensive Differences in Antifungal Immune Response in TwoDrosophilaSpecies Revealed by Comparative Transcriptome Analysis

2013 ◽  
Vol 2013 ◽  
pp. 1-15 ◽  
Author(s):  
Yosuke Seto ◽  
Koichiro Tamura

The innate immune system ofDrosophilais activated by ingestion of microorganisms.D. melanogasterbreeds on fruits fermented bySaccharomyces cerevisiae, whereasD. virilisbreeds on slime flux and decaying bark of tree housing a variety of bacteria, yeasts, and molds. In this study, it is shown thatD. virilishas a higher resistance to oral infection of a species of filamentous fungi belonging to the genusPenicilliumcompared toD. melanogaster. In response to the fungal infection, a transcriptome profile of immune-related genes was considerably different betweenD. melanogasterandD. virilis: the genes encoding antifungal peptides, Drosomycin and Metchnikowin, were highly expressed inD. melanogasterwhereas, the genes encoding Diptericin and Defensin were highly expressed inD. virilis. On the other hand, the immune-induced molecule (IM) genes showed contrary expression patterns between the two species: they were induced by the fungal infection inD. melanogasterbut tended to be suppressed inD. virilis. Our transcriptome analysis also showed newly predicted immune-related genes inD. virilis. These results suggest that the innate immune system has been extensively differentiated during the evolution of theseDrosophilaspecies.

2014 ◽  
Vol 307 (5) ◽  
pp. R501-R504 ◽  
Author(s):  
Madhu V. Singh ◽  
François M. Abboud

Hypertension and associated inflammatory processes that accelerate cardiovascular damage are regulated by the innate immune system. Toll-like receptors (TLR) are major components of the innate immune system that recognize endogenous damage-associated molecular patterns to activate prominent inflammatory signaling including activation of nuclear factor-κB (NF-κB). However, the role of TLR in the etiology of hypertension is not well understood. TLR signaling is dependent on adaptor proteins that, along with the TLR expression patterns, confer specificity of the inflammatory response and its pathological targets. Here we review the conceptual framework of how TLR and their adaptor proteins may differentially affect hypertension and cardiac hypertrophy by different stimuli.


2020 ◽  
Vol 177 ◽  
pp. 107481
Author(s):  
Chuanfei Yuan ◽  
Jia Wu ◽  
Yun Peng ◽  
Yufeng Li ◽  
Shu Shen ◽  
...  

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Yasuhiro Nihon-Yanagi ◽  
Megumi Wakayama ◽  
Naobumi Tochigi ◽  
Fumi Saito ◽  
Hideaki Ogata ◽  
...  

Purpose. We hypothesized that innate immune response pathways might be involved in thyroid carcinogenesis. To investigate this hypothesis, we aimed at analyzing the expression of several receptors and molecules in the innate immune system in papillary thyroid carcinoma (PTC) and anaplastic thyroid carcinoma (ATC) tissues. Methods. Of the surgically resected specimens, 11 ATC tissues, 25 PTC tissues, and 8 nodular hyperplasia (NH) tissues were selected and examined for the expression of toll-like receptor (TLR) 2, TLR3, TLR4, TLR5, TLR7, TLR9, the myeloid differentiation primary response gene 88 (MyD88), and toll-interleukin-1 receptor domain-containing adaptor inducing INF-β (TRIF) by immunohistochemistry (IHC). Results. Several TLRs were expressed in each tissue. TLR3 was strongly expressed in all tissues. In contrast, TLR4 was not detected in any tissues. While TLR5 was moderately expressed in NH but significantly reduced in PTC and ATC, TLR9 was absent in NH tissue but moderately expressed in both PTC and ATC. On MyD88 expression, no significant difference was found between PTC and ATC. TRIF was significantly upregulated in PTC and ATC compared to NH. Surprisingly, PTC and ATC tissues exhibited similar expression patterns of TLRs, MyD88, and TRIF. Conclusion. These data suggest the involvement of the innate immune system in both PTC and ATC. Specifically, TLR3-mediated TRIF activation was confirmed in PTC and ATC. This provides new insight into thyroid carcinogenesis.


2021 ◽  
Vol 12 ◽  
Author(s):  
Michelle Broekhuizen ◽  
Emilie Hitzerd ◽  
Thierry P. P. van den Bosch ◽  
Jasper Dumas ◽  
Robert M. Verdijk ◽  
...  

Preeclampsia is a severe placenta-related pregnancy disorder that is generally divided into two subtypes named early-onset preeclampsia (onset <34 weeks of gestation), and late-onset preeclampsia (onset ≥34 weeks of gestation), with distinct pathophysiological origins. Both forms of preeclampsia have been associated with maternal systemic inflammation. However, alterations in the placental immune system have been less well characterized. Here, we studied immunological alterations in early- and late-onset preeclampsia placentas using a targeted expression profile approach. RNA was extracted from snap-frozen placenta samples (healthy n=13, early-onset preeclampsia n=13, and late-onset preeclampsia n=6). The expression of 730 immune-related genes from the Pan Cancer Immune Profiling Panel was measured, and the data were analyzed in the advanced analysis module of nSolver software (NanoString Technology). The results showed that early-onset preeclampsia placentas displayed reduced expression of complement, and toll-like receptor (TLR) associated genes, specifically TLR1 and TLR4. Mast cells and M2 macrophages were also decreased in early-onset preeclampsia compared to healthy placentas. The findings were confirmed by an immunohistochemistry approach using 20 healthy, 19 early-onset preeclampsia, and 10 late-onset preeclampsia placentas. We conclude that the placental innate immune system is altered in early-onset preeclampsia compared to uncomplicated pregnancies. The absence of these alterations in late-onset preeclampsia placentas indicates dissimilar immunological profiles. The study revealed distinct pathophysiological processes in early-onset and late-onset preeclampsia placentas and imply that a tailored treatment to each subtype is desirable.


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