Um a colher de terra e um mousse de mitocondrias, por favor!

Microbial Influences
Kristen L. Mueller

Our guts are colonized by trillions of commensal microbiota, whose influence on our immune systems is just beginning to be appreciated. Altered colonization has been associated with diseases such as allergy and inflammatory bowel disease, suggesting that commensals may play an important role in regulating immune system responses; to what extent, however, is not yet understood.
Gaboriau-Routhiau et al. have addressed this issue by comparing germ-free and normally colonized mice. They found that commensal microbiota were critical for maintaining T cell homeostasis in the gut. Germ-free mice exhibited altered gene expression profiles of cytokines and transcription factors that were associated with T helper cell–mediated immune responses. Recolonization with microbiota derived from mouse fecal matter restored normal expression patterns. Surprisingly, this effect was largely restricted to one strain of bacteria: the segmented filamentous bacteria (SFB). Similar findings were obtained by Ivanov et al., who demonstrated the effects of SFB on interleukin 17–producing T helper cell responses. Thus, these results indicate that T cell immunity is regulated by both host- and microbiota-derived factors and that microbes may actively shape T cell populations in the gut.
Immunity 31, 677 (2009); Cell 139, 485 (2009).

How Antioxidants Might Help
Paula A. Kiberstis

Most studies of mammalian aging eventually lead to the mitochondrion, the energy-producing organelle. A prevailing hypothesis has been that damaging byproducts of mitochondrial respiration, called reactive oxygen species (ROS), accumulate as we age and cause mitochondrial dysfunction, which manifests at the organismal level as age-related disorders. Yet this hypothesis is at odds with growing evidence that an increase in the biogenesis of mitochondria can have beneficial anti-aging effects. Illustrating this dilemma are two studies of mice in which genetic manipulations altered mitochondrial function. For mice deficient in the proapoptotic protein Bak, Someya et al. found that mitochondria actively contribute to age-related hearing loss by mediating the death of cochlear cells in the ear. The death of these cells was triggered by oxidative stress and could be suppressed by antioxidants. Independently, Wenz et al. found that increased muscle expression of peroxisome proliferator–activated receptor- coactivator (PGC-1), a protein that up-regulates mitochondrial biogenesis, not only prevented age-associated loss of muscle mass, but also had beneficial effects on whole-body metabolism. Why the salutary effects of increased mitochondrial biogenesis are not counteracted by a parallel increase in damaging ROS remains unclear, but could involve increased turnover of the "older" ROS-damaged organelles.
Proc. Natl. Acad. Sci. U.S.A. 106, 19432; 10.1073/pnas.0911570106 (2009).