Cytosolic lipid inclusions formed during infection by viral and bacterial pathogens

Stehr, Matthias; Elamin, Ayssar A.; Singh, Mahavir

doi:10.1016/j.micinf.2012.08.001

Cited by 28 publications

(22 citation statements)

References 97 publications

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“…Obesity is a particularly serious health concern because of its prevalence, and its predisposition to serious illnesses such as diabetes, fatty liver disease, heart disease and cancer (Bozza and Viola, 2010;Cohen et al, 2011;Greenberg et al, 2011). LDs are also required for the infectious cycle of pathogens such as hepatitis C virus, Dengue virus and Chlamydia, which target fat metabolic cells and/or lipid metabolic pathways for their propagation (Saka and Valdivia, 2012;Stehr et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

Targeting of the Arf-GEF GBF1 to lipid droplets and Golgi membranes

Bouvet

Golinelli-Cohen

Contremoulins

et al. 2013

Journal of Cell Science

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SummaryLipid droplet metabolism and secretory pathway trafficking both require activation of the Arf1 small G protein. The spatiotemporal regulation of Arf1 activation is mediated by guanine nucleotide exchange factors (GEFs) of the GBF and BIG families, but the mechanisms of their localization to multiple sites within cells are poorly understood. Here we show that GBF1 has a lipid-binding domain (HDS1) immediately downstream of the catalytic Sec7 domain, which mediates association with both lipid droplets and Golgi membranes in cells, and with bilayer liposomes and artificial droplets in vitro. An amphipathic helix within HDS1 is necessary and sufficient for lipid binding, both in vitro and in cells. The HDS1 domain of GBF1 is stably associated with lipid droplets in cells, and the catalytic Sec7 domain inhibits this potent lipid-droplet-binding capacity. Additional sequences upstream of the Sec7 domain-HDS1 tandem are required for localization to Golgi membranes. This mechanism provides insight into crosstalk between lipid droplet function and secretory trafficking.

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Section: Introductionmentioning

confidence: 99%

Targeting of the Arf-GEF GBF1 to lipid droplets and Golgi membranes

Bouvet

Golinelli-Cohen

Contremoulins

et al. 2013

Journal of Cell Science

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“…Distinct from some bacteria and parasites that usurp lipid droplets [14,18], it is unlikely that P. gingivalis uses lipid droplets as a nutrient source or as assembly platforms during their infection. This notion is based on the findings that P. gingivalis was not localized in the lipid droplets and that prolonged persistence of the bacteria was not observed in hepatic steatosis-induced HepG2 cells.…”

Section: Discussionmentioning

confidence: 99%

“…Some intracellular pathogens use lipid droplets either for nutritional purposes or as part of an anti-immunity strategy [14]. For example, Mycobacterium and Chlamydia species are parasitic on lipid droplets in macrophages, which they use as a nutrient source and to build up their own lipid inclusions [18]. However, the interaction between lipid droplets and P. gingivalis in hepatocytes remains unknown.…”

Section: Introductionmentioning

confidence: 99%

Lipid droplets affect elimination of Porphyromonas gingivalis in HepG2 cells by altering the autophagy-lysosome system

Zaitsu

Iwatake

Satô

et al. 2016

Microbes and Infection

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“…Successful pathogens subvert host defense mechanisms that normally control infection. Thus, the ability of Mycobacterium tuberculosis, M. leprae and other intracellular pathogens to import lipids from the cholesteryl ester-rich lipid droplets that they induce in their host cell [91,92] may be an example for subversion of antimicrobial cholesteryl ester accumulation as part of the innate defense.…”

Section: Bacterial Mechanisms That Manipulate Host-derived Lipidsmentioning

confidence: 99%

Antimicrobial lipids: Emerging effector molecules of innate host defense

Porter

Daniel²,

Alvarez³

et al. 2015

WJI

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The antimicrobial properties of host-derived derived lipids have become increasingly recognized and evidence is mounting that antimicrobial lipids (AMLs), like antimicrobial peptides, are effector molecules of the innate immune system and are regulated by its conserved pathways. This review, with primary focus on the human body, provides some background on the biochemistry of lipids, summarizes their biological functions, expands on their antimicrobial properties and site-specific composition, presents modes of synergism with antimicrobial peptides, and highlights the more recent reports on the regulation of AML production as well as bacterial resistance mechanisms. Based on extant data a concept of innate epithelial defense is proposed where epithelial cells, in response to microbial products and proinflammatory cytokines and through activation of conserved innate signaling pathways, increase their lipid uptake and up-regulate transcription of enzymes involved in antimicrobial lipid biosynthesis, and induce transcription of antimicrobial peptides as well as cytokines and chemokines. The subsequently secreted antimicrobial peptides and lipids then attack and eliminate the invader, assisted by or in synergism with other antimicrobial molecules delivered by other defense cells that have been recruited to the site of infection, in most of the cases. This review invites

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Cytosolic lipid inclusions formed during infection by viral and bacterial pathogens

Cited by 28 publications

References 97 publications

Targeting of the Arf-GEF GBF1 to lipid droplets and Golgi membranes

Targeting of the Arf-GEF GBF1 to lipid droplets and Golgi membranes

Lipid droplets affect elimination of Porphyromonas gingivalis in HepG2 cells by altering the autophagy-lysosome system

Antimicrobial lipids: Emerging effector molecules of innate host defense

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