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International audience; The study of Legionella pneumophila interactions with host mitochondria during infection has been historically limited by the techniques available to analyze and quantify mitochondrial dynamics and activity in living cells. Recently, new, powerful techniques such as high-content microscopy or mitochondrial respiration assays (Seahorse) have been developed to quantitatively analyze mitochondrial parameters. Here we present state-of-the-art methods adapted to analyze mitochondrial dynamics and activity during Legionella infection of living human primary macrophages.

Several vacuolar bacteria and parasites, such as Legionella, Chlamydia, and Toxoplasma, have been reported to grow associated with host mitochondria. The reason behind this phenomenon remains elusive. In this issue of Cell Metabolism, Pernas et al. (2018) propose that fusion of host mitochondria limits the availability of fatty acids needed for Toxoplasma gondii replication.

We present a patient with mitochondrial myopathy who developed rhabdomyolysis following treatment with clindamycin. While clindamycin is not yet linked to drug-induced rhabdomyolysis in the literature, other drugs with mechanisms of action similar to clindamycin have been shown to damage human host mitochondria. Given this, we contend that clindamycin may also be capable of causing mitochondrial injury, and that while in otherwise healthy patients it may not produce any negative clinical outcome, it can precipitate rhabdomyolysis in certain patients whose mitochondria are already vulnerable.

The microbiome has emerged as a major determinant of the functioning of host organisms, affecting both health and disease. Here, Han et al. use the workhorse of aging research, C. elegans, to identify specific mechanisms by which gut bacteria influence mitochondrial dynamics and aging, a first step toward analogous manipulations to modulate human aging.

Microbes residing in the host gut actively produce various metabolic molecules that exert crucial effects on host health. However, the exact molecular relationship between microbe-derived metabolites and host metabolism and longevity remains largely unknown. Through high-throughput genetic screens and metabolomic profiling, we have identified specific microbe-derived metabolites that specifically regulate lipid metabolism and longevity in Caenorhabditis elegans. We further delineated molecular pathways regulated by these microbial metabolites in the host, and discovered host mitochondrial dynamics as a converged cellular mechanism for these metabolic and longevity regulations. Together, our work reveals microbe-host metabolic axes that control mitochondrial dynamics with critical consequences for host metabolic health and longevity.

In Sonchus oleraceus L. (Asteraceae) infected with the beet yellow stunt virus (BYSV) the virions are found in phloem cells, including the sieve elements. In parenchymatous phloem cells, the virus is present mainly in the cytoplasm. In some parenchymatous cells, containing massive accumulations of virus, the flexuous rodlike virus particles are found partly inserted into mitochondrial cristae. The mitochondrial envelope is absent where virus is present in the cristae. A similar relation between virus and host mitochondria apparently has not been recorded for any other plant virus.