ABSTRACT
Pebrine disease, caused by Nosema bombycis (Nb) infection in silkworms, is a severe and long-standing disease that threatens sericulture. As parasitic pathogens, a complex relationship exists between microsporidia and their hosts at the mitochondrial level. Previous studies have found that the translocator protein (TSPO) is involved in various biological functions, such as membrane potential regulation, mitochondrial autophagy, immune responses, calcium ion channel regulation, and cell apoptosis. In the present study, we found that TSPO expression in silkworms (BmTSPO) was upregulated following Nb infection, leading to an increase in cytoplasmic calcium, adenosine triphosphate, and reactive oxygen species levels. Knockdown and overexpression of BmTSPO resulted in the promotion and inhibition of Nb proliferation, respectively. We also demonstrated that the overexpression of BmTSPO promotes host cell apoptosis and significantly increases the expression of genes involved in the immune deficiency and Janus kinase-signal transducer and the activator of the transcription pathways. These findings suggest that BmTSPO activates the innate immune signalling pathway in silkworms to regulate Nb proliferation. Targeting TSPO represents a promising approach for the development of new treatments for microsporidian infections.
Subject(s)
Bombyx , Insect Proteins , Nosema , Nosema/physiology , Animals , Bombyx/microbiology , Bombyx/metabolism , Bombyx/genetics , Insect Proteins/metabolism , Insect Proteins/genetics , Receptors, GABA/metabolism , Receptors, GABA/genetics , Apoptosis , Larva/metabolism , Larva/microbiology , Larva/growth & developmentABSTRACT
Image intensifiers are used internationally as advanced military night-vision devices. They have better imaging performance in low-light-level conditions than CMOS/CCD. The intensified CMOS (ICMOS) was developed to satisfy the digital demand of image intensifiers. In order to make the ICMOS capable of color imaging in low-light-level conditions, a liquid-crystal tunable filter based color imaging ICMOS was developed. Due to the time-division color imaging scheme, motion artifacts may be introduced when a moving target is in the scene. To solve this problem, a deformable kernel prediction neural network (DKPNN) is proposed for joint denoising and motion artifact removal, and a data generation method which generates images with color-channel motion artifacts is also proposed to train the DKPNN. The results show that, compared with other denoising methods, the proposed DKPNN performed better both on generated noisy data and on real noisy data. Therefore, the proposed DKPNN is more suitable for color ICMOS denoising and motion artifact removal. A new exploration was made for low-light-level color imaging schemes.
Subject(s)
Artifacts , Neural Networks, Computer , MotionABSTRACT
We introduce and verify a single-channel time-division filtering low-light-level (LLL) color night vision system (3LCNV). The imaging scheme, comprising a tunable liquid crystal filter, three-generation GaAsP image intensifier, and CMOS camera, achieves LLL color imaging and ensures sensitivity. The image enhancement and color reconstruction algorithm flow suitable for LLL night vision combines overexposure-against white balance, color correction matrix (CCM) color correction, and color image denoising to improve color visibility and reduce color difference and image noise. The proposed night vision system extends the minimum working illuminance to 10-4 lx and achieves natural and clear color LLL imaging, improving night-time observations.
ABSTRACT
Lipid droplets (LDs) are dynamic organelles that participate in the regulation of lipid metabolism and cellular homeostasis inside of cells. LD-associated proteins, also known as perilipins (PLINs), are a family of proteins found on the surface of LDs that regulate lipid metabolism, immunity, and other functions. In silkworms, pébrine disease caused by infection by the microsporidian Nosema bombycis (Nb) is a severe threat to the sericultural industry. Although we found that Nb relies on lipids from silkworms to facilitate its proliferation, the relationship between PLINs and Nb proliferation remains unknown. Here, we found Nb infection caused the accumulation of LDs in the fat bodies of silkworm larvae. The characterized perilipin1 gene (plin1) promotes the accumulation of intracellular LDs and is involved in Nb proliferation. plin1 is similar to perilipin1 in humans and is conserved in all insects. The expression of plin1 was mostly enriched in the fat body rather than in other tissues. Knockdown of plin1 enhanced Nb proliferation, whereas overexpression of plin1 inhibited its proliferation. Furthermore, we confirmed that plin1 increased the expression of the Domeless and Hop in the JAK-STAT immune pathway and inhibited Nb proliferation. Taken together, our current findings demonstrate that plin1 inhibits Nb proliferation by promoting the JAK-STAT pathway through increased expression of Domeless and Hop. This study provides new insights into the complicated connections among microsporidia pathogens, LD surface proteins, and insect immunity.IMPORTANCELipid droplets (LDs) are lipid storage sites in cells and are present in almost all animals. Many studies have found that LDs may play a role in host resistance to pathogens and are closely related to innate immunity. The present study found that a surface protein of insect lipid droplets could not only regulate the morphological changes of lipid droplets but also inhibit the proliferation of a microsporidian pathogen Nosema bombycis (Nb) by activating the JAK-STAT signaling pathway. This is the first discovery of the relationship between microsporidian pathogen and insect lipid surface protein perilipin and insect immunity.
Subject(s)
Bombyx , Insect Proteins , Janus Kinases , Lipid Droplets , Nosema , Perilipin-1 , Signal Transduction , Bombyx/microbiology , Bombyx/metabolism , Bombyx/genetics , Animals , Nosema/metabolism , Nosema/genetics , Insect Proteins/metabolism , Insect Proteins/genetics , Lipid Droplets/metabolism , Janus Kinases/metabolism , Janus Kinases/genetics , Perilipin-1/metabolism , Perilipin-1/genetics , STAT Transcription Factors/metabolism , STAT Transcription Factors/genetics , Fat Body/metabolism , Larva/microbiology , Larva/metabolism , Lipid MetabolismABSTRACT
The silkworm (Bombyx mori) is a model species of lepidopteran insect. Microsporidium spp. are obligate intracellular eukaryotic parasites. Infection by the microsporidian Nosema bombycis (Nb) results in an outbreak of Pébrine disease in silkworms and causes substantial losses to the sericulture industry. It has been suggested that Nb depends on nutrients from host cells for spore growth. However, little is known about changes in lipid levels after Nb infection. In this study, ultra-high performance liquid chromatography-tandem mass spectrometry (UHPLC-MS/MS) was performed to analyze the effect of Nb infection on lipid metabolism in the midgut of silkworms. A total of 1601 individual lipid molecules were detected in the midgut of silkworms, of which 15 were significantly decreased after Nb challenge. Classification, chain length, and chain saturation analysis revealed that these 15 differential lipids can be classified into different lipid subclasses, of which 13 belong to glycerol phospholipid lipids and two belong to glyceride esters. The results indicated that Nb uses the host lipids to complete its own replication, and the acquisition of host lipid subclasses is selective; not all lipid subclasses are required for microsporidium growth or proliferation. Based on lipid metabolism data, phosphatidylcholine (PC) was found to be an important nutrient for Nb replication. Diet supplementation with lecithin substantially promoted the replication of Nb. Knockdown and overexpression of the key enzyme phosphatidate phosphatase (PAP) and phosphatidylcholine (Bbc) for PC synthesis also confirmed that PC is necessary for Nb replication. Our results showed that most lipids in the host midgut decreased when silkworms were infected with Nb. Reduction of or supplementation with PC may be a strategy to suppress or promote microsporidial replication.