Enhancement of stress resistances and downregulation of Imd pathway by lower developmental temperature in Drosophila melanogaster

2010 ◽  
Vol 45 (12) ◽  
pp. 984-987 ◽  
Author(s):  
Keetae Kim ◽  
Yuh-Ru Lin ◽  
Yongkyu Park
2021 ◽  
Vol 12 ◽  
Author(s):  
Joelle R. Madi ◽  
Amani Al Outa ◽  
Mirna Ghannam ◽  
Hadi M. Hussein ◽  
Marwa Shehab ◽  
...  

The Epstein-Barr virus (EBV) commonly infects humans and is highly associated with different types of cancers and autoimmune diseases. EBV has also been detected in inflamed gastrointestinal mucosa of patients suffering from prolonged inflammation of the digestive tract such as inflammatory bowel disease (IBD) with no clear role identified yet for EBV in the pathology of such diseases. Since we have previously reported immune-stimulating capabilities of EBV DNA in various models, in this study we investigated whether EBV DNA may play a role in exacerbating intestinal inflammation through innate immune and regeneration responses using the Drosophila melanogaster model. We have generated inflamed gastrointestinal tracts in adult fruit flies through the administration of dextran sodium sulfate (DSS), a sulfated polysaccharide that causes human ulcerative colitis- like pathologies due to its toxicity to intestinal cells. Intestinal damage induced by inflammation recruited plasmatocytes to the ileum in fly hindguts. EBV DNA aggravated inflammation by enhancing the immune deficiency (IMD) pathway as well as further increasing the cellular inflammatory responses manifested upon the administration of DSS. The study at hand proposes a possible immunostimulatory role of the viral DNA exerted specifically in the fly hindgut hence further developing our understanding of immune responses mounted against EBV DNA in the latter intestinal segment of the D. melanogaster gut. These findings suggest that EBV DNA may perpetuate proinflammatory processes initiated in an inflamed digestive system. Our findings indicate that D. melanogaster can serve as a model to further understand EBV-associated gastroinflammatory pathologies. Further studies employing mammalian models may validate the immunogenicity of EBV DNA in an IBD context and its role in exacerbating the disease through inflammatory mediators.


Fly ◽  
2017 ◽  
Vol 12 (1) ◽  
pp. 1-12 ◽  
Author(s):  
Neda N. Moghadam ◽  
Pia Mai Thorshauge ◽  
Torsten N. Kristensen ◽  
Nadieh de Jonge ◽  
Simon Bahrndorff ◽  
...  

Gerontology ◽  
1986 ◽  
Vol 32 (1) ◽  
pp. 28-36 ◽  
Author(s):  
A.C. Economos ◽  
F.A. Lints

Evolution ◽  
1995 ◽  
Vol 49 (4) ◽  
pp. 670 ◽  
Author(s):  
Jean-Marie Delpuech ◽  
Brigitte Moreteau ◽  
Joelle Chiche ◽  
Eliane Pla ◽  
Joseph Vouidibio ◽  
...  

2020 ◽  
Author(s):  
Crystal M. Vincent ◽  
Marc S. Dionne

AbstractMale and female animals exhibit differences in infection outcomes. One possible source of sexually dimorphic immunity is sex-specific costs of immune activity or pathology, but little is known about the independent effects of immune-induced versus microbe-induced pathology, and whether these may differ for the sexes. Here, through measuring metabolic and physiological outputs in wild-type and immune-compromised Drosophila melanogaster, we test whether the sexes are differentially impacted by these various sources of pathology and identify a critical regulator of this difference. We find that the sexes exhibit differential immune activity but similar bacteria-derived metabolic pathology. We show that female-specific immune-inducible expression of PGRP-LB, a negative regulator of the Imd pathway, enables females to reduce immune activity in response to reductions in bacterial numbers. In the absence of PGRP-LB, females are more resistant of infection, confirming the functional importance of this regulation and suggesting that female-biased immune restriction comes at a cost.


Author(s):  
Ewa Chrostek ◽  
Nelson Martins ◽  
Marta S Marialva ◽  
Luis Teixeira

AbstractWolbachia is a maternally transmitted bacterium widespread in arthropods and filarial nematodes, and confers strong antiviral protection in Drosophila melanogaster and other insects. Wolbachia-transinfected Aedes aegypti are currently being deployed to fight transmission of dengue and Zika viruses. However, the mechanism of antiviral protection and factors influencing it are still not fully understood. Here we show that temperature modulates Wolbachia-conferred protection in Drosophila melanogaster. Temperature after infection directly impacts Drosophila C virus replication and modulates Wolbachia protection. At higher temperatures virus proliferates more and is more lethal, while Wolbachia confers lower protection. Strikingly, host developmental temperature is a determinant of Wolbachia-conferred antiviral protection. While there is a strong protection when flies are raised from egg to adult at 25°C, the protection is highly reduced or completely abolished when flies develop at 18°C. However, Wolbachia-induced changes during development are not sufficient to limit virus-induced mortality, as Wolbachia is still required to be present in adults at the time of infection. This developmental effect is general, since it was present in different host genotypes, Wolbachia variants and upon infection with different viruses. Overall, we show that Wolbachia-conferred antiviral protection is temperature dependent, being present or absent depending on the environmental conditions. This interaction likely impacts Wolbachia-host interactions in nature and, as a result, frequencies of host and symbionts in different climates. Dependence of Wolbachia-mediated pathogen blocking on developmental temperature could be used to dissect the mechanistic bases of protection and should be considered by programmes deploying Wolbachia as an antiviral agent in the field.Significance StatementInsects are often infected with beneficial intracellular bacteria. The bacterium Wolbachia can protect insects from pathogenic viruses. This effect can be used to prevent transmission of dengue and Zika viruses by Wolbachia-infected mosquitoes. To deploy Wolbachia in the field successfully and understand the biology of insects in the wild we need to discover which factors affect Wolbachia-conferred antiviral protection. Here we show that the temperature in which insects develop from eggs to adults can determine presence or absence of antiviral protection. The environment, therefore, influences this insect-bacterium interaction. Our work may help to provide insights into the mechanism of viral blocking by Wolbachia and inform programs using Wolbachia in mosquito-borne disease control.


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