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Review
. 2024 Jul 1;223(7):e202310134.
doi: 10.1083/jcb.202310134. Epub 2024 May 15.

Bacteria-organelle communication in physiology and disease

Yi-Tang Lee #  1   2   3 , Mumine Senturk #  2   4 , Youchen Guan  5   6 , Meng C Wang  4   6
Affiliations
Review

Bacteria-organelle communication in physiology and disease

Yi-Tang Lee et al. J Cell Biol. .

Abstract

Bacteria, omnipresent in our environment and coexisting within our body, exert dual beneficial and pathogenic influences. These microorganisms engage in intricate interactions with the human body, impacting both human health and disease. Simultaneously, certain organelles within our cells share an evolutionary relationship with bacteria, particularly mitochondria, best known for their energy production role and their dynamic interaction with each other and other organelles. In recent years, communication between bacteria and mitochondria has emerged as a new mechanism for regulating the host's physiology and pathology. In this review, we delve into the dynamic communications between bacteria and host mitochondria, shedding light on their collaborative regulation of host immune response, metabolism, aging, and longevity. Additionally, we discuss bacterial interactions with other organelles, including chloroplasts, lysosomes, and the endoplasmic reticulum (ER).

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Conflict of interest statement

Disclosures: The authors declare no competing interests exist.

Figures

Figure 1.
Figure 1.
Bacteria exhibit communal behavior through various communication strategies. Biofilms serve as a form of communal existence, where bacteria aggregate, forming extracellular polymeric substance (EPS) matrices that offer protection, nutrient absorption, habitat diversity, and social interactions. Bacteria can also employ quorum sensing (QS), releasing signals to coordinate gene expression based on population density. Bacterial membrane vesicles (MVs) facilitate the transfer of diverse cargos, including hydrophobic signals involved in QS.
Figure 2.
Figure 2.
Pathogens and mitochondria interact during infection. Shigella flexneri, Legionella pneumophila, and Helicobacter pylori drive mitochondrial fragmentation in a DRP1-dependent manner, while Listeria monocytogenes do so via a DRP1-independent mechanism, facilitating pathogenic infection through various pathways. Toxoplasma gondii remodels the mitochondria outer membrane into SPOT structure that contains mitochondrial fusion machinery such as MFN1/2, blocking the host metabolic defense and favoring infection. On the other hand, mitochondria serve as the host intracellular response center to defend against bacterial infection via promoting metabolic reprogramming and inducing mitoROS-mediated immune response.
Figure 3.
Figure 3.
Bacterial metabolites signal through host mitochondria to regulate somatic and reproductive aging in C. elegans. Colanic acids released from bacteria direct the intestinal mitochondrial network toward fragmentation, promoting somatic longevity in C. elegans. Bacterial vitamin B12 causes perinuclear clustering of mitochondria in the oocyte, resulting in accelerated reproductive decline in C. elegans.
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