Research

14 pages, 6241 KiB

Open AccessArticle

Lipid Droplet Motility Increases Following Viral Immune Stimulation

by Ebony A. Monson, Donna R. Whelan and Karla J. Helbig

Int. J. Mol. Sci. 2021, 22(9), 4418; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22094418 - 23 Apr 2021

Cited by 11 | Viewed by 3617

Lipid droplets (LDs) have traditionally been thought of as solely lipid storage compartments for cells; however, in the last decade, they have emerged as critical organelles in health and disease. LDs are highly dynamic within cells, and their movement is critical in organelle–organelle [...] Read more.

Lipid droplets (LDs) have traditionally been thought of as solely lipid storage compartments for cells; however, in the last decade, they have emerged as critical organelles in health and disease. LDs are highly dynamic within cells, and their movement is critical in organelle–organelle interactions. Their dynamics are known to change during cellular stress or nutrient deprivation; however, their movement during pathogen infections, especially at very early timepoints, is under-researched. This study aimed to track LD dynamics in vitro, in an astrocytic model of infection. Cells were either stimulated with a dsRNA viral mimic, poly I:C, or infected with the RNA virus, Zika virus. Individual LDs within infected cells were analysed to determine displacement and speed, and average LD characteristics for multiple individual cells calculated. Both LD displacement and mean speed were significantly enhanced in stimulated cells over a time course of infection with an increase seen as early as 2 h post-infection. With the emerging role for LDs during innate host responses, understanding their dynamics is critical to elucidate how these organelles influence the outcome of viral infection. Full article

(This article belongs to the Special Issue Intracellular Organelle Rearrangement Induced by Pathogenic Infections)

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16 pages, 2939 KiB

Open AccessArticle

Chlamydia psittaci PmpD-N Modulated Chicken Macrophage Function by Triggering Th2 Polarization and the TLR2/MyD88/NF-κB Signaling Pathway

by Jun Chu, Xiaohui Li, Guanggang Qu, Yihui Wang, Qiang Li, Yongxia Guo, Lei Hou, Jue Liu, Francis O. Eko and Cheng He

Int. J. Mol. Sci. 2020, 21(6), 2003; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21062003 - 15 Mar 2020

Cited by 14 | Viewed by 3032 | Correction

Abstract

The polymorphic membrane protein D (PmpD) is a highly conserved outer membrane protein which plays an important role in pathogenesis during Chlamydia psittaci infection. In this study, we evaluated the ability of the N-terminus of PmpD (PmpD-N) to modulate the functions of chicken [...] Read more.

The polymorphic membrane protein D (PmpD) is a highly conserved outer membrane protein which plays an important role in pathogenesis during Chlamydia psittaci infection. In this study, we evaluated the ability of the N-terminus of PmpD (PmpD-N) to modulate the functions of chicken macrophages and the signaling pathway(s) involved in PmpD-N-induced Toll-like receptors (TLRs), as well as interleukin (IL)-6 and IL-10 cytokine secretions. Thus, HD11 macrophages were treated with exogenous and intracellular PmpD-N of C. psittaci. The chlamydial growth was evaluated by enumeration of chlamydial loads in the infected macrophages. The phagocytic function of macrophages following PmpD-N treatment was detected by fluorescein-labeled Escherichia coli (E. coli). The concentration of nitric oxide (NO) secreted by HD11 macrophages was measured by the amount of NO₂^- in the culture supernatant using the Griess method. The cytokine secretions were assessed using multiplex cytokine ELISA kits. Expression levels of TLRs, myeloid differentiation factor 88 (MyD88), and nuclear factor kappa B (NF-κB) were analyzed by a Western blotting assay, as well as a luciferase assay, while NF-κB p65 nuclear translocation was assessed by confocal microscopy. The nuclear translocation of the transcription factor NF-κB was confirmed by evaluating its ability to combine with the corresponding promoter using the electrophoretic mobility shift assay (EMSA). After treatment with exogenous or endogenous PmpD-N, chlamydial loads and phagocytic functions were reduced significantly compared with those of the plasmid vector group, while NO secretions were reduced significantly compared with those of the lipopolysaccharide (LPS) treatment. Stimulation of HD11 cells with PmpD-N provoked the secretion of the Th2 cytokines, IL-6, and IL-10 and upregulated the expression of TLR2, TLR4, MyD88, and NF-κB. Furthermore, inhibition of TLR2, MyD88, and NF-κB in HD11 cells significantly decreased IL-6 and IL-10 cytokine levels, while NO production and phagocytosis increased significantly, strongly suggesting their involvement in PmpD-N-induced Th2 cytokine secretion and macrophage dysfunction. Our data indicate that C. psittaci PmpD-N inhibited macrophage functions by activating the Th2 immune response and the TLR2/MyD88/NF-κB signaling pathway. Full article

(This article belongs to the Special Issue Intracellular Organelle Rearrangement Induced by Pathogenic Infections)

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Review

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23 pages, 2644 KiB

Open AccessReview

Manipulation of Host Cell Organelles by Intracellular Pathogens

by Malte Kellermann, Felix Scharte and Michael Hensel

Int. J. Mol. Sci. 2021, 22(12), 6484; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22126484 - 17 Jun 2021

Cited by 23 | Viewed by 7752

Abstract

Pathogenic intracellular bacteria, parasites and viruses have evolved sophisticated mechanisms to manipulate mammalian host cells to serve as niches for persistence and proliferation. The intracellular lifestyles of pathogens involve the manipulation of membrane-bound organellar compartments of host cells. In this review, we described [...] Read more.

Pathogenic intracellular bacteria, parasites and viruses have evolved sophisticated mechanisms to manipulate mammalian host cells to serve as niches for persistence and proliferation. The intracellular lifestyles of pathogens involve the manipulation of membrane-bound organellar compartments of host cells. In this review, we described how normal structural organization and cellular functions of endosomes, endoplasmic reticulum, Golgi apparatus, mitochondria, or lipid droplets are targeted by microbial virulence mechanisms. We focus on the specific interactions of Salmonella, Legionella pneumophila, Rickettsia rickettsii, Chlamydia spp. and Mycobacterium tuberculosis representing intracellular bacterial pathogens, and of Plasmodium spp. and Toxoplasma gondii representing intracellular parasites. The replication strategies of various viruses, i.e., Influenza A virus, Poliovirus, Brome mosaic virus, Epstein-Barr Virus, Hepatitis C virus, severe acute respiratory syndrome virus (SARS), Dengue virus, Zika virus, and others are presented with focus on the specific manipulation of the organelle compartments. We compare the specific features of intracellular lifestyle and replication cycles, and highlight the communalities in mechanisms of manipulation deployed. Full article

(This article belongs to the Special Issue Intracellular Organelle Rearrangement Induced by Pathogenic Infections)

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26 pages, 1393 KiB

Open AccessReview

Viral Interactions with Adaptor-Protein Complexes: A Ubiquitous Trait among Viral Species

by Ivana Strazic Geljic, Paola Kucan Brlic, Lucija Musak, Dubravka Karner, Andreja Ambriović-Ristov, Stipan Jonjic, Peter Schu and Tihana Lenac Rovis

Int. J. Mol. Sci. 2021, 22(10), 5274; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22105274 - 17 May 2021

Cited by 5 | Viewed by 3750

Abstract

Numerous viruses hijack cellular protein trafficking pathways to mediate cell entry or to rearrange membrane structures thereby promoting viral replication and antagonizing the immune response. Adaptor protein complexes (AP), which mediate protein sorting in endocytic and secretory transport pathways, are one of the [...] Read more.

Numerous viruses hijack cellular protein trafficking pathways to mediate cell entry or to rearrange membrane structures thereby promoting viral replication and antagonizing the immune response. Adaptor protein complexes (AP), which mediate protein sorting in endocytic and secretory transport pathways, are one of the conserved viral targets with many viruses possessing AP-interacting motifs. We present here different mechanisms of viral interference with AP complexes and the functional consequences that allow for efficient viral propagation and evasion of host immune defense. The ubiquity of this phenomenon is evidenced by the fact that there are representatives for AP interference in all major viral families, covered in this review. The best described examples are interactions of human immunodeficiency virus and human herpesviruses with AP complexes. Several other viruses, like Ebola, Nipah, and SARS-CoV-2, are pointed out as high priority disease-causative agents supporting the need for deeper understanding of virus-AP interplay which can be exploited in the design of novel antiviral therapies. Full article

(This article belongs to the Special Issue Intracellular Organelle Rearrangement Induced by Pathogenic Infections)

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14 pages, 1991 KiB

Open AccessReview

SEIPIN: A Key Factor for Nuclear Lipid Droplet Generation and Lipid Homeostasis

by Yi Jin, Yanjie Tan, Pengxiang Zhao and Zhuqing Ren

Int. J. Mol. Sci. 2020, 21(21), 8208; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21218208 - 02 Nov 2020

Cited by 17 | Viewed by 3925

Abstract

Lipid homeostasis is essential for normal cell physiology. Generally, lipids are stored in a lipid droplet (LD), a ubiquitous organelle consisting of a neutral lipid core and a single layer of phospholipid membrane. It is thought that LDs are generated from the endoplasmic [...] Read more.

Lipid homeostasis is essential for normal cell physiology. Generally, lipids are stored in a lipid droplet (LD), a ubiquitous organelle consisting of a neutral lipid core and a single layer of phospholipid membrane. It is thought that LDs are generated from the endoplasmic reticulum and then released into the cytosol. Recent studies indicate that LDs can exist in the nucleus, where they play an important role in the maintenance of cell phospholipid homeostasis. However, the details of nuclear lipid droplet (nLD) generation have not yet been clearly characterized. SEIPIN is a nonenzymatic protein encoded by the Berardinelli-Seip congenital lipodystrophy type 2 (BSCL2) gene. It is associated with lipodystrophy diseases. Many recent studies have indicated that SEIPIN is essential for LDs generation. Here, we review much of this research in an attempt to explain the role of SEIPIN in nLD generation. From an integrative perspective, we conclude by proposing a theoretical model to explain how SEIPIN might participate in maintaining homeostasis of lipid metabolism. Full article

(This article belongs to the Special Issue Intracellular Organelle Rearrangement Induced by Pathogenic Infections)

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18 pages, 2188 KiB

Open AccessReview

Hijacking of Lipid Droplets by Hepatitis C, Dengue and Zika Viruses—From Viral Protein Moonlighting to Extracellular Release

by Alexandra P.M. Cloherty, Andrea D. Olmstead, Carla M.S. Ribeiro and François Jean

Int. J. Mol. Sci. 2020, 21(21), 7901; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21217901 - 24 Oct 2020

Cited by 44 | Viewed by 5379

Abstract

Hijacking and manipulation of host cell biosynthetic pathways by human enveloped viruses are essential for the viral lifecycle. Flaviviridae members, including hepatitis C, dengue and Zika viruses, extensively manipulate host lipid metabolism, underlining the importance of lipid droplets (LDs) in viral infection. LDs [...] Read more.

Hijacking and manipulation of host cell biosynthetic pathways by human enveloped viruses are essential for the viral lifecycle. Flaviviridae members, including hepatitis C, dengue and Zika viruses, extensively manipulate host lipid metabolism, underlining the importance of lipid droplets (LDs) in viral infection. LDs are dynamic cytoplasmic organelles that can act as sequestration platforms for a unique subset of host and viral proteins. Transient recruitment and mobilization of proteins to LDs during viral infection impacts host-cell biological properties, LD functionality and canonical protein functions. Notably, recent studies identified LDs in the nucleus and also identified that LDs are transported extracellularly via an autophagy-mediated mechanism, indicating a novel role for autophagy in Flaviviridae infections. These developments underline an unsuspected diversity and localization of LDs and potential moonlighting functions of LD-associated proteins during infection. This review summarizes recent breakthroughs concerning the LD hijacking activities of hepatitis C, dengue and Zika viruses and potential roles of cytoplasmic, nuclear and extracellular LD-associated viral proteins during infection. Full article

(This article belongs to the Special Issue Intracellular Organelle Rearrangement Induced by Pathogenic Infections)

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26 pages, 2254 KiB

Open AccessReview

Morphology Remodeling and Selective Autophagy of Intracellular Organelles during Viral Infections

by Shanhui Ren, Chan Ding and Yingjie Sun

Int. J. Mol. Sci. 2020, 21(10), 3689; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21103689 - 23 May 2020

Cited by 8 | Viewed by 3343

Abstract

Viruses have evolved different strategies to hijack subcellular organelles during their life cycle to produce robust infectious progeny. Successful viral reproduction requires the precise assembly of progeny virions from viral genomes, structural proteins, and membrane components. Such spatial and temporal separation of assembly [...] Read more.

Viruses have evolved different strategies to hijack subcellular organelles during their life cycle to produce robust infectious progeny. Successful viral reproduction requires the precise assembly of progeny virions from viral genomes, structural proteins, and membrane components. Such spatial and temporal separation of assembly reactions depends on accurate coordination among intracellular compartmentalization in multiple organelles. Here, we overview the rearrangement and morphology remodeling of virus-triggered intracellular organelles. Focus is given to the quality control of intracellular organelles, the hijacking of the modified organelle membranes by viruses, morphology remodeling for viral replication, and degradation of intracellular organelles by virus-triggered selective autophagy. Understanding the functional reprogram and morphological remodeling in the virus-organelle interplay can provide new insights into the development of broad-spectrum antiviral strategies. Full article

(This article belongs to the Special Issue Intracellular Organelle Rearrangement Induced by Pathogenic Infections)

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Other

Jump to: Research, Review

2 pages, 177 KiB

Open AccessCorrection

Correction:Chlamydia psittaci PmpD-N Modulated Chicken Macrophage Function by Triggering Th2 Polarization and the TLR2/MyD88/NF-κB Signaling Pathway

by Jun Chu, Xiaohui Li, Guanggang Qu, Yihui Wang, Qiang Li, Yongxia Guo, Lei Hou, Jue Liu, Francis O. Eko and Cheng He

Int. J. Mol. Sci. 2020, 21(7), 2639; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21072639 - 10 Apr 2020

Cited by 2 | Viewed by 1819

Abstract

The authors would like to make the following corrections to their paper, published in the International Journal of Molecular Sciences [...] Full article

(This article belongs to the Special Issue Intracellular Organelle Rearrangement Induced by Pathogenic Infections)

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