Dietary Intake Regulates the Circulating Inflammatory Monocyte Pool

Jordan, Stefan; Tung, Navpreet; Casanova-Acebes, María; Chang, Christie; Cantoni, Claudia; Zhang, Dachuan; Wirtz, Theresa H.; Naik, Shruti; Rose, Samuel A.; Brocker, Chad; Gainullina, Anastasiia; Hornburg, Daniel; Horng, Sam; Maier, Bárbara; Cravedi, Paolo; LeRoith, Derek; Gonzalez, Frank J.; Meissner, Felix; Ochando, Jordi; Rahman, Adeeb; Chipuk, Jerry E.; Artyomov, Maxim N.; Frenette, Paul S.; Piccio, Laura; Berres, Marie‐Luise; Mérad, Miriam

doi:10.1016/j.cell.2019.07.050

Cited by 273 publications

(204 citation statements)

References 62 publications

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“…We would argue that this is also a clinically-relevant problem that people on KD face, and thus is an important aspect of the model. It should also be noted that previous studies describing the impact of nutrient restriction on immune system function indicate that restrictions induce lymphopenia (11)(12)(13)(14)(15), which is opposite to our findings that 7 days of KD increased γδ T cell numbers in the lungs and adipose tissue (1, 4). Furthermore, as described above in relation to protein, if our phenotype were driven by differences in relative amounts of various macronutrients and/or micronutrients (based on Kcal composition), one might expect long-term feeding to potentiate our γδ T cell phenotype.…”

contrasting

confidence: 99%

Authors’ Response to Reply: Ketogenic diet activates protective γδ T cell responses against influenza virus infection

Goldberg¹,

Iwasaki²,

Dixit³

2020

Preprint

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We are glad for the broad interest and readership our recent publication “Ketogenic diet activates protective γδ T cell responses against influenza virus infection” has received. The goal of our study was to understand how the immune system might be involved in mediating the surprising protection against lethal influenza A virus infection we observed when we fed mice a ketogenic diet (KD) for one week. What made our findings particularly intriguing is that robust protective changes were occurring in the lungs, the site of influenza infection and, importantly, not a tissue traditionally considered in manipulations of systemic metabolism, and that these protective changes were γδ T cell-dependent. Amidst this enthusiasm, Bass et al. have raised concern about the control diets used in our experiments, specifically with regards to the protein, fiber, and micronutrient content. We welcome critical feedback and appreciate the opportunity to respond to these criticisms.

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contrasting

confidence: 99%

Authors’ Response to Reply: Ketogenic diet activates protective γδ T cell responses against influenza virus infection

Goldberg¹,

Iwasaki²,

Dixit³

2020

Preprint

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“…Prior studies have indicated that CR inhibited critical pathways involved in cytokine and chemokine signaling to reduce the level of circulating pro-in ammatory cytokines, such as TNFα, IL-6, and IL-1β [53][54][55][56][57][58]. Healthy individuals undergoing short-term CR have been shown to have reduced monocyte metabolic and in ammatory activity and a drastic decrease in circulating and organ monocyte numbers [59,60]. The recruitment of in ammatory cells in tissues and airway induced by intake of high fat or high caloric diet could be reversed by CR [61,62].…”

Section: Discussionmentioning

confidence: 99%

Caloric restriction attenuates C57BL/6J mouse lung injury and extra-pulmonary toxicity induced by real ambient particulate matter exposure

Chen

et al. 2020

Preprint

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Background: Caloric restriction (CR) is known to improve health and extend lifespan in human beings. The effects of CR on adverse health outcomes in response to particulate matter (PM) exposure and the underlying mechanisms have yet to be defined.Results: Male C57BL/6J mice were fed with a CR diet or ad libitum (AL) and exposed to PM for 4 weeks in a real-ambient PM exposure system located at Shijiazhuang, China, with a daily mean concentration (95.77 μg/m³) of PM2.5. Compared to AL-fed mice, CR-fed mice showed attenuated PM-induced pulmonary injury and extra-pulmonary toxicity characterized by reduction in oxidative stress, DNA damage and inflammation. RNA sequence analysis revealed that several pulmonary pathways that were involved in production of reactive oxygen species (ROS), cytokine production, and inflammatory cell activation were inactivated, while those mediating antioxidant generation and DNA repair were activated in CR-fed mice upon PM exposure. In addition, transcriptome analysis of murine livers revealed that CR led to induction of xenobiotic metabolism and detoxification pathways, corroborated by increased levels of urinary metabolites of polycyclic aromatic hydrocarbons (PAHs) and decreased cytotoxicity measured in an ex vivo assay.Conclusion: These novel results demonstrate, for the first time, that CR in mice confers resistance against pulmonary injuries and extra-pulmonary toxicity induced by PM exposure. CR led to activation of xenobiotic metabolism and enhanced detoxification of PM-bound chemicals. These findings provide evidence that dietary intervention may afford therapeutic means to reduce the health risk associated with PM exposure.

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“…Recently, a very elegant study has shown that fasting increases AMP-activated protein kinase levels (AMPK), modulates the metabolic activity of monocytes, including a decrease in OXPHOS, and reduces the steady state levels of CCL2, thus precluding monocytes from leaving the bone marrow (BM). Of note, by doing so, fasting improves the phenotype of mice undergoing experimental autoimmune encephalomyelitis (EAE) without altering the immune response to bacterial infections [42]. Calorie restriction and CR mimetics modulate inflammaging, neuroinflammation and gut permeability.…”

Section: Anti-inflammatory Effects Of Calorie Restrictionmentioning

confidence: 99%

“…As illustrated below, CR induces autophagosome formation, mitophagy and rises cellular levels of nicotinamide adenine dinucleotide (NAD + ), improving autophagy function and mitochondrial fitness. Interestingly, CR protocols have shown potent anti-inflammatory properties [42]. In light of the findings regarding the beneficial effects of CR diets, several efforts have been made in generating and characterizing new compounds, known as CR mimetics, that mimic the effects of CR without the evident unpleasant consequences of food intake restriction (Figure 2).…”

mentioning

confidence: 99%

Control of Inflammation by Calorie Restriction Mimetics: On the Crossroad of Autophagy and Mitochondria

Gabandé‐Rodríguez

Heras

Mittelbrunn

2019

Cells

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Mitochondrial metabolism and autophagy are two of the most metabolically active cellular processes, playing a crucial role in regulating organism longevity. In fact, both mitochondrial dysfunction or autophagy decline compromise cellular homeostasis and induce inflammation. Calorie restriction (CR) is the oldest strategy known to promote healthspan, and a plethora of CR mimetics have been used to emulate its beneficial effects. Herein, we discuss how CR and CR mimetics, by modulating mitochondrial metabolism or autophagic flux, prevent inflammatory processes, protect the intestinal barrier function, and dampen both inflammaging and neuroinflammation. We outline the effects of some compounds classically known as modulators of autophagy and mitochondrial function, such as NAD+ precursors, metformin, spermidine, rapamycin, and resveratrol, on the control of the inflammatory cascade and how these anti-inflammatory properties could be involved in their ability to increase resilience to age-associated diseases.

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Dietary Intake Regulates the Circulating Inflammatory Monocyte Pool

Cited by 273 publications

References 62 publications

Authors’ Response to Reply: Ketogenic diet activates protective γδ T cell responses against influenza virus infection

Authors’ Response to Reply: Ketogenic diet activates protective γδ T cell responses against influenza virus infection

Caloric restriction attenuates C57BL/6J mouse lung injury and extra-pulmonary toxicity induced by real ambient particulate matter exposure

Control of Inflammation by Calorie Restriction Mimetics: On the Crossroad of Autophagy and Mitochondria

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