scholarly journals Diaphorina citri Nymphs Are Resistant to Morphological Changes Induced by “ Candidatus Liberibacter asiaticus” in Midgut Epithelial Cells

2018 ◽  
Vol 86 (4) ◽  
Author(s):  
Marina Mann ◽  
Somayeh Fattah-Hosseini ◽  
El-Desouky Ammar ◽  
Richard Stange ◽  
EricaRose Warrick ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cells ◽  
Molecular Mechanisms ◽  
Early Stage ◽  
Morphological Changes ◽  
Diaphorina Citri ◽  
Content Type ◽  
Citrus Greening Disease ◽  
Mitochondrial Superoxide ◽  
Liberibacter Asiaticus

ABSTRACT “ Candidatus Liberibacter asiaticus” is the causative bacterium associated with citrus greening disease. “ Ca . Liberibacter asiaticus” is transmitted by Diaphorina citri more efficiently when it is acquired by nymphs rather than adults. Why this occurs is not known. We compared midguts of D. citri insects reared on healthy or “ Ca . Liberibacter asiaticus”-infected citrus trees using quantitative PCR, confocal microscopy, and mitochondrial superoxide staining for evidence of oxidative stress. Consistent with its classification as propagative, “ Ca . Liberibacter asiaticus” titers were higher in adults than in nymphs. Our previous work showed that adult D. citri insects have basal levels of karyorrhexis (fragmentation of the nucleus) in midgut epithelial cells, which is increased in severity and frequency in response to “ Ca . Liberibacter asiaticus.” Here, we show that nymphs exhibit lower levels of early-stage karyorrhexis than adults and are refractory to the induction of advanced karyorrhexis by “ Ca . Liberibacter asiaticus” in the midgut epithelium. MitoSox Red staining showed that guts of infected adults, particularly males, experienced oxidative stress in response to “ Ca . Liberibacter asiaticus.” A positive correlation between the titers of “ Ca . Liberibacter asiaticus” and the Wolbachia endosymbiont was observed in adult and nymph midguts, suggesting an interplay between these bacteria during development. We hypothesize that the resistance of the nymph midgut to late-stage karyorrhexis through as yet unknown molecular mechanisms benefits “ Ca . Liberibacter asiaticus” for efficient invasion of midgut epithelial cells, which may be a factor explaining the developmental dependency of “ Ca . Liberibacter asiaticus” acquisition by the vector.

Intracellular life cycle of Candidatus Liberibacter asisticus inside psyllid gut cells

2021 ◽  
Author(s):  
Lin Chun-Yi ◽  
Diann Achor ◽  
Amit Levy
Keyword(s):  
Molecular Mechanisms ◽  
Management Strategies ◽  
Bacterial Invasion ◽  
Diaphorina Citri ◽  
Current Management ◽  
Insect Midgut ◽  
Rapid Spread ◽  
Candidatus Liberibacter ◽  
Infected Insect ◽  
Liberibacter Asiaticus

Candidatus Liberibacter asiaticus (CLas), the devastating pathogen related to Huanglongbing (HLB), is a phloem-limited, fastidious, insect-borne bacterium. Rapid spread of HLB disease relies on CLas propagates efficiently in its vector, the Asian citrus psyllid, Diaphorina citri, in a circulative manner. Understanding the intracellular lifecycle of CLas in psyllid midgut is fundamental to improve current management strategies. Using a microscopic approach within CLas-infected insect midgut, we observed the entry of CLas into gut cells inside vesicles by endocytosis, termed Liberibacter containing vacuoles (LCVs). Endocytosis is followed by the formation of endoplasmic reticulum-related and replication permissive vacuoles (rLCVs). rLCVs then further develop into bigger double membrane autophagosome-like structure, termed autophagy-related vacuole (aLCV). Vesicles, containing CLas egress from aLCV and fuse with the cell membrane. Immunolocalization studies showed that CLas employs endo/exocytosis-like mechanisms that mediates bacterial invasion and egress. Upregulation of autophagy-related genes indicated subversion of host autophagy by CLas in psyllid vector to promote infection. These results indicate that CLas interacts with host cellular machineries to undergo a multistage intracellular cycle through endocytic, secretory, autophagic and exocytic pathways via complex machineries. Potential tactics for HLB controlling can be made depending on further investigations on the knowledge of the molecular mechanisms of CLas intracellular cycle.

scholarly journals Sulodexide Protects Renal Tubular Epithelial Cells from Oxidative Stress-Induced Injury via Upregulating Klotho Expression at an Early Stage of Diabetic Kidney Disease

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Yu Ning Liu ◽  
Jingwei Zhou ◽  
Tingting Li ◽  
Jing Wu ◽  
Shu Hua Xie ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Kidney Disease ◽  
Epithelial Cells ◽  
Diabetic Kidney Disease ◽  
Early Stage ◽  
Collaborative Study ◽  
Oxidative Activity ◽  
Dependent Manner ◽  
Diabetic Kidney ◽  
Collaborative Study Group

The hypoalbuminuric effect of sulodexide (SDX) on diabetic kidney disease (DKD) was suggested by some clinical trials but was denied by the Collaborative Study Group. In this study, the diabetic rats were treated with SDX either from week 0 to 24 or from week 13 to 24. We found that 24-week treatment significantly decreased the urinary protein and HAVCR1 excretion, inhibited the interstitial expansion, and downregulated the renal cell apoptosis and interstitial fibrosis. Renoprotection was also associated with a reduction in renocortical/urinary oxidative activity and the normalization of renal klotho expression. However, all of these actions were not observed when SDX was administered only at the late stage of diabetic nephropathy (from week 13 to 24). In vitro, advanced glycation end products (AGEs) dose-dependently enhanced the oxidative activity but lowered the klotho expression in cultured proximal tubule epithelial cells (PTECs). Also, H2O2 could downregulate the expression of klotho in a dose-dependent manner. However, overexpression of klotho reduced the HAVCR1 production and the cellular apoptosis level induced by AGEs or H2O2. Our study suggests that SDX may prevent the progression of DKD at the early stage by upregulating renal klotho expression, which inhibits the tubulointerstitial injury induced by oxidative stress.

Mitochondrial superoxide production during oxalate-mediated oxidative stress in renal epithelial cells

2002 ◽  
Vol 32 (12) ◽  
pp. 1339-1350 ◽  
Author(s):  
F.D. Khand ◽  
M.P. Gordge ◽  
W.G. Robertson ◽  
A.A. Noronha-Dutra ◽  
J.S. Hothersall
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cells ◽  
Superoxide Production ◽  
Renal Epithelial Cells ◽  
Mitochondrial Superoxide

scholarly journals Let-7c-3p Regulates Autophagy under Oxidative Stress by Targeting ATG3 in Lens Epithelial Cells

2020 ◽  
Vol 2020 ◽  
pp. 1-9 ◽  
Author(s):  
Ting Li ◽  
Yanhong Huang ◽  
Wenkai Zhou ◽  
Qichang Yan
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cells ◽  
Western Blot ◽  
Molecular Mechanisms ◽  
Luciferase Reporter ◽  
Human Lens ◽  
Lens Epithelial Cells ◽  
Age Related ◽  
Spot Number ◽  
Gene Assay

Background. Oxidative stress is an important factor during age-related cataract formation. Apoptosis and autophagy induced by oxidative stress have been reported as key factors in age-related cataract. In our research, we investigated the role of let-7c-3p in the regulation of autophagy and apoptosis during the formation of age-related cataract. Material and Methods. Real-time PCR and western blot were employed to detect the expression of let-7c-3p in the tissues of age-related cataract. Human lens epithelial cells (LECs) were treated with H2O2 as an age-related cataract model. The extent of apoptosis was measured by flow cytometry and western blot. To detect autophagy, immunofluorescence was used to analyze the spot number of LC3, and western blot was used to detect the expression of LC3-II/I and ATG3. The molecular mechanisms of let-7c-3p regulating autophagy via ATG3 under oxidative stress were performed by a luciferase report gene assay and rescue experiment. Results. Downregulation of let-7c-3p was found in the age-related cataract group aged >65 years relative to the age-related cataract group aged ≤65 years. Consistently, the expression of let-7c-3p was also lower under oxidative stress. The activities of LEC apoptosis and autophagy induced by oxidative stress were inhibited by let-7c-3p. By the bioinformatics database and the luciferase reporter assay, ATG3 was found to be a direct target of let-7c-3p. Let-7c-3p reduced the ATG3-mediated autophagy level, which was induced by oxidative stress in LECs. Conclusion. Let-7c-3p inhibits autophagy by targeting ATG3 in LECs in age-related cataract.

scholarly journals Asian citrus psyllid adults inoculate huanglongbing bacterium more efficiently than nymphs when this bacterium is acquired by early instar nymphs

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
El-Desouky Ammar ◽  
Justin George ◽  
Kasie Sturgeon ◽  
Lukasz L. Stelinski ◽  
Robert G. Shatters
Keyword(s):  
Latent Period ◽  
Salivary Glands ◽  
Emerging Adults ◽  
Citrus Greening ◽  
Asian Citrus Psyllid ◽  
Diaphorina Citri ◽  
Citrus Greening Disease ◽  
Early Instar ◽  
Liberibacter Asiaticus ◽  
Greening Disease

Abstract The Asian citrus psyllid (Diaphorina citri) transmits the bacterium ‘Candidatus Liberibacter asiaticus’ (CLas), which causes huanglongbing (citrus greening) disease, in a circulative-propagative manner. We compared CLas inoculation efficiency of D. citri nymphs and adults into healthy (uninfected) citron leaves when both vector stages were reared from eggs on infected plants. The proportion of CLas-positive leaves was 2.5% for nymphs and 36.3% for adults. CLas acquisition by early instar nymphs followed by dissections of adults and 4th instar nymphs revealed that CLas bacterium had moved into the head-thorax section (containing the salivary glands) in 26.7–30.0% of nymphs and 37–45% of adults. Mean Ct values in these sections were 31.6–32.9 and 26.8–27.0 for nymphs and adults, respectively. Therefore, CLas incidence and titer were higher in the head-thorax of adults than in nymphs. Our results suggest that following acquisition of CLas by early instar D. citri nymphs, emerging adults inoculate the bacteria into citrus more efficiently than nymphs because adults are afforded a longer latent period necessary for multiplication and/or translocation of CLas into the salivary glands of the vector. We propose that CLas uses D. citri nymphs mainly for pathogen acquisition and multiplication, and their adults mainly for pathogen inoculation and spread.

scholarly journals Near-Complete Genome Sequences of a Wolbachia Strain Isolated from Diaphorina citri Kuwayama (Hemiptera: Liviidae)

2020 ◽  
Vol 9 (35) ◽  
Author(s):  
Surendra Neupane ◽  
Sylvia I. Bonilla ◽  
Andrew M. Manalo ◽  
Kirsten S. Pelz-Stelinski
Keyword(s):  
Complete Genome ◽  
Wolbachia Strain ◽  
Insect Vector ◽  
Diaphorina Citri ◽  
Genome Sequences ◽  
Content Type ◽  
Liberibacter Asiaticus

ABSTRACT Wolbachia strains are one of three endosymbionts associated with the insect vector of “Candidatus Liberibacter asiaticus,” Diaphorina citri Kuwayama (Hemiptera: Liviidae). We report three near-complete genome sequences of samples of Wolbachia from D. citri (wDi), with sizes of 1,518,595, 1,542,468, and 1,538,523 bp.

scholarly journals 2020 J. Leonard Goldner Award Winner: Inhibition of HMGB1 by Metformin Prevents Mechanical Overloading-Induced Tendinopathy

2020 ◽  
Vol 5 (4) ◽  
pp. 2473011420S0008
Author(s):  
Jianying Zhang ◽  
Feng Li ◽  
Kentaro Onishi ◽  
MaCalus V. Hogan ◽  
James HC Wang
Keyword(s):  
Molecular Mechanisms ◽  
Early Stage ◽  
Morphological Changes ◽  
High Mobility ◽  
Histochemical Staining ◽  
Normal Tendon ◽  
Chondrogenic Marker ◽  
Collagen Ii ◽  
Group 2 ◽  
The Right

Category: Basic Sciences/Biologics; Sports Introduction/Purpose: Tendinopathy is a debilitating tendon disorder that affects millions of Americans and costs billions of healthcare dollars every year. Mechanical overloading is considered to cause the development of tendinopathy, but the underlying molecular mechanisms of tendinopathy remain unclear. High mobility group box-1 (HMGB1), an upstream potent inflammatory mediator, has been identified in high levels in early stage tendinopathy patients [1]. However, whether HMGB1 mediates tendinopathy development due to mechanical overloading is completely unknown. Metformin (Met), a hypoglycemic drug commonly used for the treatment of type II diabetes, has shown to inhibit the activity of HMGB1 via binding the acidic tail of HMGB1 [2]. In this study, we tested the hypothesis that Met prevents mechanical overloading-induced tendinopathy by inhibiting HMGB1. Methods: A total of 24 mice were divided into 4 groups and treated for 24 weeks as follows: Group 1 (Cage) with cage activities; Group 2 (Met) received daily IP injection of metformin (50 mg/kg body weight); Group 3 (ITR) ran on treadmill at 15 meters/min for 3 h/ day, 5 days a week; Group 4 (ITR+Met) ran the same protocol as that of ITR group but with daily IP injection of metformin. Six mice/group were sacrificed at 24 weeks and the Achilles and patellar tendon tissues were harvested. The tendons from the left legs were used for histochemical staining and the right for immunostaining. Results: We found that mechanical overloading induced HMGB1 release into tendon matrix (Fig. 1G, K, O). Metformin inhibited HMGB1 release (Fig. 1H, L, P). ITR induced degenerative tendinopathy as evidenced by the cell morphological changes from elongated shape in normal tendon (Fig. 2A, E, I, M) to round shape (Fig. 2C, G, K, O) and the accumulation of proteoglycans (Fig. 2K, O) in ITR tendon. Metformin injection inhibited ITR effect, which is shown by less round shaped cells and low proteoglycan levels found in metformin injected ITR tendons (Fig. 2D, H, L, P). ITR promoted the expression of chondrogenic markers (collagen II and SOX-9) in tendon (Fig. 3C, G, K, O), and metformin inhibited the expression of chondrogenic makers (Fig. 3D, H, L, P). Conclusion: Our study demonstrated that mechanical overloading induced degenerative changes in mouse tendons characterized by the presence of chondrocyte-like cells, accumulation of proteoglycans, high levels of chondrogenic marker SOX-9 and Collagen II expression. Administration of metformint reduced the degenerative responses in overloaded tendon and blocked the development of tendinopathy. These findings support the notion that mechanical overloading induces tendinopathy development by initiation of tendon inflammation via HMGB1, which leads to eventual tendon degeneration. Thus, metformin, a commonly prescribed and FDA approved drug that specifically inhibits HMGB1, can be used to prevent tendinopathy development due to mechanical overloading placed on the tendon.

scholarly journals The Helicobacter pylori CZB Cytoplasmic Chemoreceptor TlpD Forms an Autonomous Polar Chemotaxis Signaling Complex That Mediates a Tactic Response to Oxidative Stress

2016 ◽  
Vol 198 (11) ◽  
pp. 1563-1575 ◽  
Author(s):  
Kieran D. Collins ◽  
Tessa M. Andermann ◽  
Jenny Draper ◽  
Lisa Sanders ◽  
Susan M. Williams ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Helicobacter Pylori ◽  
Molecular Mechanisms ◽  
Reactive Oxygen ◽  
Host Cells ◽  
Oxygen Species ◽  
Content Type ◽  
Signaling Complex ◽  
H Pylori

ABSTRACTCytoplasmic chemoreceptors are widespread among prokaryotes but are far less understood than transmembrane chemoreceptors, despite being implicated in many processes. One such cytoplasmic chemoreceptor isHelicobacter pyloriTlpD, which is required for stomach colonization and drives a chemotaxis response to cellular energy levels. Neither the signals sensed by TlpD nor its molecular mechanisms of action are known. We report here that TlpD functions independently of the other chemoreceptors. When TlpD is the sole chemoreceptor, it is able to localize to the pole and recruits CheW, CheA, and at least two CheV proteins to this location. It loses the normal membrane association that appears to be driven by interactions with other chemoreceptors and with CheW, CheV1, and CheA. These results suggest that TlpD can form an autonomous signaling unit. We further determined that TlpD mediates a repellent chemotaxis response to conditions that promote oxidative stress, including being in the presence of iron, hydrogen peroxide, paraquat, and metronidazole. Last, we found that all testedH. pyloristrains express TlpD, whereas other chemoreceptors were present to various degrees. Our data suggest a model in which TlpD coordinates a signaling complex that responds to oxidative stress and may allowH. pylorito avoid areas of the stomach with high concentrations of reactive oxygen species.IMPORTANCEHelicobacter pylorisenses its environment with proteins called chemoreceptors. Chemoreceptors integrate this sensory information to affect flagellum-based motility in a process called chemotaxis. Chemotaxis is employed during infection and presumably aidsH. pyloriin encountering and colonizing preferred niches. A cytoplasmic chemoreceptor named TlpD is particularly important in this process, and we report here that this chemoreceptor is able to operate independently of other chemoreceptors to organize a chemotaxis signaling complex and mediate a repellent response to oxidative stress conditions.H. pyloriencounters and must cope with oxidative stress during infection due to oxygen and reactive oxygen species produced by host cells. TlpD's repellent response may allow the bacteria to escape niches experiencing inflammation and elevated reactive oxygen species (ROS) production.

Distribution of genes for parathyroid hormone (PTH)—related peptide, Indian hedgehog, PTH receptor and patched in the process of experimental spondylosis in mice

2002 ◽  
Vol 97 (1) ◽  
pp. 82-87 ◽  
Author(s):  
Takanobu Nakase ◽  
Kenta Ariga ◽  
Wenxiang Meng ◽  
Motoki Iwasaki ◽  
Tetsuya Tomita ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Messenger Rna ◽  
Molecular Mechanisms ◽  
Early Stage ◽  
Indian Hedgehog ◽  
Molecular Signaling ◽  
Content Type ◽  
Chondrocyte Maturation ◽  
Related Peptide ◽  
Fine Print

Object. Little is known about the molecular mechanisms underlying the process of spondylosis. The authors determined the extent of genetic localization of major regulators of chondrogenesis such as Indian hedgehog (Ihh) and parathyroid hormone (PTH)—related peptide (PTHrP) and their receptors during the development of spondylosis in their previously established experimental mouse model. Methods. Experimental spondylosis was induced in 5-week-old ICR mice. The cervical spines were chronologically harvested, and histological sections were prepared. Messenger (m) RNA for PTHrP, Ihh, PTH receptor (PTHR; a receptor for PTHrP), patched (Ptc; a receptor for Ihh), bone morphogenetic protein (BMP)—6, and collagen type X (COL10; a marker for mature chondrocyte) was localized in the tissue sections by performing in situ hybridization. In the early stage, mRNA for COL10, Ihh, and BMP-6 was absent; however, mRNA for PTHrP, PTHR, and Ptc was detected in the anterior margin of the cervical discs. In the late stage, evidence of COL10 mRNA began to be detected, and transcripts for Ihh, PTHrP, and BMP-6 were localized in hypertrophic chondrocytes adjacent to the bone-forming area in osteophyte. Messenger RNA for Ptc and PTHR continued to localize at this stage. In control mice, expression of these genes was absent. Conclusions. The localization of PTHrP, Ihh, BMP-6, and the receptors PTHR and Ptc demonstrated in the present experimental model indicates the possible involvement of molecular signaling by PTHrP (through the PTHR), Ihh (through the Ptc), and BMP-6 in the regulation of chondrocyte maturation leading to endochondral ossification in spondylosis.

scholarly journals Phobalysin, a Small β-Pore-Forming Toxin of Photobacterium damselae subsp. damselae

2015 ◽  
Vol 83 (11) ◽  
pp. 4335-4348 ◽  
Author(s):  
Amable J. Rivas ◽  
Gisela von Hoven ◽  
Claudia Neukirch ◽  
Martina Meyenburg ◽  
Qianqian Qin ◽  
...  
Keyword(s):  
Lactate Dehydrogenase ◽  
Epithelial Cells ◽  
Necrotizing Fasciitis ◽  
Vibrio Cholerae ◽  
Gene Product ◽  
Morphological Changes ◽  
Marine Animals ◽  
Content Type ◽  
Membrane Pores ◽  
Photobacterium Damselae

ABSTRACTPhotobacterium damselaesubsp.damselae, an important pathogen of marine animals, may also cause septicemia or hyperaggressive necrotizing fasciitis in humans. We previously showed that hemolysin genes are critical for virulence of this organism in mice and fish. In the present study, we characterized thehlyAgene product, a putative small β-pore-forming toxin, and termed it phobalysin P (PhlyP), for “photobacterial lysin encoded on a plasmid.” PhlyP formed stable oligomers and small membrane pores, causing efflux of K+, with no significant leakage of lactate dehydrogenase but entry of vital dyes. The latter feature distinguished PhlyP from the relatedVibrio choleraecytolysin. Attack by PhlyP provoked a loss of cellular ATP, attenuated translation, and caused profound morphological changes in epithelial cells. In coculture experiments with epithelial cells,Photobacterium damselaesubsp.damselaeled to rapid hemolysin-dependent membrane permeabilization. Unexpectedly, hemolysins also promoted the association ofP. damselaesubsp.damselaewith epithelial cells. The collective observations of this study suggest that membrane-damaging toxins commonly enhance bacterial adherence.

Sign in / Sign up

Export Citation Format

Share Document