The role of clathrin-dependent endocytosis in bacterial internalization

Veiga, Esteban; Cossart, Pascale

doi:10.1016/j.tcb.2006.08.005

Cited by 107 publications

(107 citation statements)

References 74 publications

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“…40,41 The entry of AIEC LF82 bacteria involves lipid rafts as we observed that CTX B subunit, a drug that binds the GM1 gangliosides known to be clustered in lipid rafts, was recruited and accumulated around AIEC LF82 entering bacteria (Figure 3a). This was confirmed by treatment of macrophages with MbCD, a cholesterol-depleting molecule that induced a 1.9-fold decrease in the number of LF82 bacteria internalized in macrophages (Figure 3b).…”

Section: Inhibition Of Aiec Lf82 Endocytosis Decreased the Numbers Ofmentioning

confidence: 90%

Replication of Crohn's disease-associated AIEC within macrophages is dependent on TNF-α secretion

Bringer

Billard

Glasser

et al. 2012

Laboratory Investigation

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Adherent and invasive Escherichia coli (AIEC) associated with Crohn's disease are able to survive and to replicate extensively in active phagolysosomes within macrophages. AIEC-infected macrophages release large amounts of tumour necrosis factor-alpha (TNF-a) and do not undergo cell death. The aim of the present study was to determine what benefit AIEC bacteria could gain from inducing the release of large amounts of TNF-a by infected macrophages and to what extent the neutralization of TNF-a could affect AIEC intramacrophagic replication. Our results showed that the amount of TNF-a released by infected macrophages is correlated with the load of intramacrophagic AIEC bacteria and their intracellular replication. TNF-a secretion was not related to the number of bacteria entering host cells because when the number of bacteria internalized in macrophage was decreased by blocking lipid raft-dependent and clathrin-coated pits-dependent endocytosis, the amount of TNF-a secreted by infected macrophages was not modified. Interestingly, dose-dependent increases in the number of intracellular AIEC LF82 bacteria were observed when infected macrophages were stimulated with exogenous TNF-a, and neutralization of TNF-a secreted by AIEC-infected macrophages using anti-TNF-a antibodies induced a significant decrease in the number of intramacrophagic bacteria. These results indicate that AIEC bacteria use TNF-a as a Trojan horse to ensure their intracellular replication because replication of AIEC bacteria within macrophages induces the release of TNF-a, which in turn increases the intramacrophagic replication of AIEC. Neutralizing TNF-a secreted by infected macrophages may represent an effective strategy to control AIEC intracellular replication.

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Section: Inhibition Of Aiec Lf82 Endocytosis Decreased the Numbers Ofmentioning

confidence: 90%

Replication of Crohn's disease-associated AIEC within macrophages is dependent on TNF-α secretion

Bringer

Billard

Glasser

et al. 2012

Laboratory Investigation

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“…3A and B). Clathrin is the major protein component of a major class of coated vesicles and plays an important role in endocytosis (24)(25)(26), a pathway known to be involved in pathogen internalization (27,28). We therefore speculated that COP35 is internalized via a clathrin-dependent endocytic pathway by direct or indirect interaction with CHC in living cells.…”

Section: Discussionmentioning

confidence: 99%

COP35, a Cholangiocarcinoma-Binding Oligopeptide, Interacts with the Clathrin Heavy Chain Accompanied by GRP78

Kitahara

Masumoto

Parker

et al. 2011

Molecular Cancer Research

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Cholangiocarcinoma (CCA) is a common carcinoma of the liver, and the majority of patients with CCA have a poor prognosis due to the lack of effective nonsurgical therapies in addition to its rapid progression and inoperability at the time of diagnosis. The development of novel nonsurgical therapeutics that efficiently target CCA could significantly improve the prognosis for patients presenting with CCA. Here, we describe the iterative production and characterization of a novel peptide, designated COP35 (CCA-binding oligopeptide 35), which binds selectively to human CCA, identified by bacteriophage biopanning using the intrahepatic CCA cell line RBE and the normal cholangiocyte cell line MMNK-1. COP35 was found to augment the growth inhibitory effects of 5-fluorouracil (5-FU) against RBE cells. Utilizing pull-down assay and liquid chromatography, we identify the clathrin heavy chain accompanied by GRP78/BiP as a COP35-binding partner. In summary, we identify COP35 as a possible candidate for peptide-targeted therapies for CCA. Mol Cancer Res; 9(6); 688-701. Ó2011 AACR.

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“…Membrane dynamics regulates the internalization of different types of cargos, from small molecules, such as ligand-bound receptors, to large cargoes such as bacteria (Veiga and Cossart, 2006;Zwang and Yarden, 2009). This process is dependent on re-organization of the actin cytoskeleton, which underlies membrane remodelling and assists receptor clustering and signalling (reviewed in Smythe and Ayscough, 2006;McClatchey and Fehon, 2009;Treanor et al, 2009).…”

Section: Discussionmentioning

confidence: 99%

“…To test this possibility we turned to a different bacterium, S. enterica serovar Typhimurium, whose entry does not involve a specific receptor, but is dependent on extensive remodelling to the actin cytoskeleton (Veiga and Cossart, 2006). We ) for the indicated periods of time.…”

Section: Uch-l1 Promotes Invasion Of Epithelial Cells By S Enterica mentioning

confidence: 99%

The ubiquitin C-terminal hydrolase UCH-L1 promotes bacterial invasion by altering the dynamics of the actin cytoskeleton

Bassères

Coppotelli

Pfirrmann

et al. 2010

Cellular Microbiology

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SummaryInvasion of eukaryotic target cells by pathogenic bacteria requires extensive remodelling of the membrane and actin cytoskeleton. Here we show that the remodelling process is regulated by the ubiquitin C-terminal hydrolase UCH-L1 that promotes the invasion of epithelial cells by Listeria monocytogenes and Salmonella enterica. Knockdown of UCH-L1 reduced the uptake of both bacteria, while expression of the catalytically active enzyme promoted efficient internalization in the UCH-L1-negative HeLa cell line. The entry of L. monocytogenes involves binding to the receptor tyrosine kinase Met, which leads to receptor phosphorylation and ubiquitination. UCH-L1 controls the early membrane-associated events of this triggering cascade since knockdown was associated with altered phosphorylation of the c-cbl docking site on Tyr1003, reduced ubiquitination of the receptor and altered activation of downstream ERK1/2-and AKT-dependent signalling in response to the natural ligand Hepatocyte Growth Factor (HGF). The regulation of cytoskeleton dynamics was further confirmed by the induction of actin stress fibres in HeLa expressing the active enzyme but not the catalytic mutant UCH-L1 C90S. These findings highlight a previously unrecognized involvement of the ubiquitin cycle in bacterial entry. UCH-L1 is highly expressed in malignant cells that may therefore be particularly susceptible to invasion by bacteria-based drug delivery systems.

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The role of clathrin-dependent endocytosis in bacterial internalization

Cited by 107 publications

References 74 publications

Replication of Crohn's disease-associated AIEC within macrophages is dependent on TNF-α secretion

Replication of Crohn's disease-associated AIEC within macrophages is dependent on TNF-α secretion

COP35, a Cholangiocarcinoma-Binding Oligopeptide, Interacts with the Clathrin Heavy Chain Accompanied by GRP78

The ubiquitin C-terminal hydrolase UCH-L1 promotes bacterial invasion by altering the dynamics of the actin cytoskeleton

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