Gut microbiota modulates weight gain in mice after discontinued smoke exposure.

Cigarette smoking constitutes a leading global cause of morbidity and preventable death, and most active smokers report a desire or recent attempt to quit. Smoking-cessation-induced weight gain (SCWG; 4.5 kg reported to be gained on average per 6-12 months, >10 kg year in 13% of those who stopped smoking) constitutes a major obstacle to smoking abstinence, even under stable or restricted caloric intake.

Persistent microbiome alterations modulate the rate of post-dieting weight regain.

In tackling the obesity pandemic, considerable efforts are devoted to the development of effective weight reduction strategies, yet many dieting individuals fail to maintain a long-term weight reduction, and instead undergo excessive weight regain cycles. The mechanisms driving recurrent post-dieting obesity remain largely elusive. Here we identify an intestinal microbiome signature that persists after successful dieting of obese mice and contributes to faster weight regain and metabolic aberrations upon re-exposure to obesity-promoting conditions.

The gut microbiome in human immunodeficiency virus infection.

HIV/AIDS causes severe dysfunction of the immune system through CD4+ T cell depletion, leading to dysregulation of both the adaptive and innate immune arms. A primary target for viral infection is the gastrointestinal tract, which is a reservoir of CD4+ T cells. In addition to being a major immune hub, the human gastrointestinal tract harbors trillions of commensal microorganisms, the microbiota, which have recently been shown to play critical roles in health.

Integration of Innate Immune Signaling.

The last decades of research in innate immunology have revealed a multitude of sensing receptors that evaluate the presence of microorganisms or cellular damage in tissues. In the context of a complex tissue, many such sensing events occur simultaneously. Thus, the downstream pathways need to be integrated to launch an appropriate cellular response, to tailor the magnitude of the reaction to the inciting event, and to terminate it in a manner that avoids immunopathology.