Host cell egress of <i>Brucella abortus</i> requires <scp>BNIP3L</scp>‐mediated mitophagy

Verbeke, Jérémy; Fayt, Youri; Martin, Lisa J.; Yilmaz, Oya; Sędzicki, Jarosław; Reboul, Ariel; Jadot, Michel; Renard, Patricia; Dehio, Christoph; Renard, Henri-François; Letesson, Jean‐Jacques; Bolle, Xavier De; Arnould, Thierry

doi:10.15252/embj.2022112817

Cited by 13 publications

(10 citation statements)

References 97 publications

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“…To determine the role of host ferroptosis in Brucella egress, a 24-period bacterial egress quantification procedure was conducted as reported previously [11,47,48]. RAW264.7 macrophages were seeded into 24-well plates and infected with Brucella M5 at a MOI of 100.…”

Section: Bacterial Egress Assaymentioning

confidence: 99%

Brucella Manipulates Host Cell Ferroptosis to Facilitate Its Intracellular Replication and Egress in RAW264.7 Macrophages

Zhang,

Hu,

Yin

et al. 2024

Antioxidants

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Brucella virulence relies on its successful intracellular life cycle. Modulating host cell death is a strategy for Brucella to survive and replicate intracellularly. Ferroptosis is a novel regulated cell death characterized by iron-triggered excessive lipid peroxidation, which has been proven to be associated with pathogenic bacteria infection. Thus, we attempted to explore if smooth-type Brucella infection triggers host cell ferroptosis and what role it plays in Brucella infection. We assessed the effects of Brucella infection on the lactate dehydrogenase release and lipid peroxidation levels of RAW264.7 macrophages; subsequently, we determined the effect of Brucella infection on the expressions of ferroptosis defense pathways. Furthermore, we determined the role of host cell ferroptosis in the intracellular replication and egress of Brucella. The results demonstrated that Brucella M5 could induce ferroptosis of macrophages by inhibiting the GPX4-GSH axis at the late stage of infection but mitigated ferroptosis by up-regulating the GCH1-BH4 axis at the early infection stage. Moreover, elevating host cell ferroptosis decreased Brucella intracellular survival and suppressing host cell ferroptosis increased Brucella intracellular replication and egress. Collectively, Brucella may manipulate host cell ferroptosis to facilitate its intracellular replication and egress, extending our knowledge about the underlying mechanism of how Brucella completes its intracellular life cycle.

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Section: Bacterial Egress Assaymentioning

confidence: 99%

Brucella Manipulates Host Cell Ferroptosis to Facilitate Its Intracellular Replication and Egress in RAW264.7 Macrophages

Zhang,

Hu,

Yin

et al. 2024

Antioxidants

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“…The intracellular pathogens L. monocytogenes , B. abortus , and Mycobacterium bovis induce mitophagy through varied mechanisms [ 92 , 93 , 94 ]. P. aeruginosa also induces mitophagy through the action of clustered regularly interspaced short palindromic repeats (CRISPR)-associated systems (CRISPR-Cas) [ 95 ].…”

Section: How Bacteria Cause Mitochondrial Dysfunctionmentioning

confidence: 99%

“…Therefore, it is not surprising that some pathogens such as M. bovis promote mitophagy to competitively suppress host xenophagy and increase intracellular survival [ 92 ]. Finally, B. abortus -mediated mitophagy plays an important role in the propagation of infection to neighboring cells through the regulation of the packaging and egress of bacteria-containing vacuoles [ 94 ].…”

Section: How Bacteria Cause Mitochondrial Dysfunctionmentioning

confidence: 99%

Mitochondrial Dysfunction in Bacterial Infections

Maurice

Sadikot

2023

Pathogens

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Mitochondria are critical in numerous cellular processes, including energy generation. Bacterial pathogens target host cell mitochondria through various mechanisms to disturb the host response and improve bacterial survival. We review recent advances in the understanding of how bacteria cause mitochondrial dysfunction through perturbations in mitochondrial cell-death pathways, energy production, mitochondrial dynamics, mitochondrial quality control, DNA repair, and the mitochondrial unfolded protein response. We also briefly highlight possible therapeutic approaches aimed at restoring the host mitochondrial function as a novel strategy to enhance the host response to bacterial infection.

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“…In addition, B . abortus simultaneously triggers mitophagy in an iron-HIF-1α-BNIP3L-dependent manner [ 90 ]. As for the actors of autophagy initiation, this mitophagy response also plays a role in B .…”

Section: The Battle Between Bacterial Pathogens and Host Mitophagy: R...mentioning

confidence: 99%

“…As for the actors of autophagy initiation, this mitophagy response also plays a role in B . abortus exit of host cells through an alteration of aBCVs formation [ 90 ]. This could mean that B .…”

Section: The Battle Between Bacterial Pathogens and Host Mitophagy: R...mentioning

confidence: 99%

To eat or not to eat mitochondria? How do host cells cope with mitophagy upon bacterial infection?

2023

Self Cite

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Mitochondria fulfil a plethora of cellular functions ranging from energy production to regulation of inflammation and cell death control. The fundamental role of mitochondria makes them a target of choice for invading pathogens, with either an intracellular or extracellular lifestyle. Indeed, the modulation of mitochondrial functions by several bacterial pathogens has been shown to be beneficial for bacterial survival inside their host. However, so far, relatively little is known about the importance of mitochondrial recycling and degradation pathways through mitophagy in the outcome (success or failure) of bacterial infection. On the one hand, mitophagy could be considered as a defensive response triggered by the host upon infection to maintain mitochondrial homeostasis. However, on the other hand, the pathogen itself may initiate the host mitophagy to escape from mitochondrial-mediated inflammation or antibacterial oxidative stress. In this review, we will discuss the diversity of various mechanisms of mitophagy in a general context, as well as what is currently known about the different bacterial pathogens that have developed strategies to manipulate the host mitophagy.

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Host cell egress of Brucella abortus requires BNIP3L‐mediated mitophagy

Cited by 13 publications

References 97 publications

Brucella Manipulates Host Cell Ferroptosis to Facilitate Its Intracellular Replication and Egress in RAW264.7 Macrophages

Brucella Manipulates Host Cell Ferroptosis to Facilitate Its Intracellular Replication and Egress in RAW264.7 Macrophages

Mitochondrial Dysfunction in Bacterial Infections

To eat or not to eat mitochondria? How do host cells cope with mitophagy upon bacterial infection?

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