Obesity is associated with increased visceral adipose tissue (VAT) neutrophils and a distinct bacterial community. A study shows that microbiome-depleted mice gavaged with stool from obese individuals on a high-fat diet (HFD) show increased VAT neutrophils, suggesting donor microbiome and recipient diet influence VAT neutrophilia. Obese individuals have higher circulating insulin, leptin, triglycerides, and lower adiponectin, with higher levels of zonulin and LPS binding protein (LBP), indicating increased intestinal permeability and bacterial presence. VAT from obese individuals contains more neutrophils, which are associated with insulin resistance and pro-inflammatory gene expression. Neutrophils in VAT are distinct from peripheral blood (PB) neutrophils, with unique gene expression patterns related to inflammation, chemotaxis, and extracellular matrix production. VAT neutrophils may be a therapeutic target for obesity-related complications, including insulin resistance and colon cancer. The study also found that VAT neutrophils are distinct from other activated neutrophil states, with a unique expression signature. A custom-signature tool identified VAT-like neutrophils in diverse tissues, including colon cancer, where their abundance correlated with overall survival. The findings suggest that VAT neutrophils may play a role in both metabolic disease and obesity-related cancer progression. The study highlights the role of gut microbiota in VAT inflammation, with bacteria from the gastrointestinal tract contributing to neutrophil recruitment. The results indicate that HFD increases gut permeability, allowing bacterial translocation to VAT, which may drive inflammation and insulin resistance. VAT neutrophils are functionally distinct from PB neutrophils, with increased expression of chemokines, extracellular matrix components, and pro-inflammatory genes. The study provides evidence that VAT neutrophils are a key player in obesity-related inflammation and may be a target for therapeutic interventions.Obesity is associated with increased visceral adipose tissue (VAT) neutrophils and a distinct bacterial community. A study shows that microbiome-depleted mice gavaged with stool from obese individuals on a high-fat diet (HFD) show increased VAT neutrophils, suggesting donor microbiome and recipient diet influence VAT neutrophilia. Obese individuals have higher circulating insulin, leptin, triglycerides, and lower adiponectin, with higher levels of zonulin and LPS binding protein (LBP), indicating increased intestinal permeability and bacterial presence. VAT from obese individuals contains more neutrophils, which are associated with insulin resistance and pro-inflammatory gene expression. Neutrophils in VAT are distinct from peripheral blood (PB) neutrophils, with unique gene expression patterns related to inflammation, chemotaxis, and extracellular matrix production. VAT neutrophils may be a therapeutic target for obesity-related complications, including insulin resistance and colon cancer. The study also found that VAT neutrophils are distinct from other activated neutrophil states, with a unique expression signature. A custom-signature tool identified VAT-like neutrophils in diverse tissues, including colon cancer, where their abundance correlated with overall survival. The findings suggest that VAT neutrophils may play a role in both metabolic disease and obesity-related cancer progression. The study highlights the role of gut microbiota in VAT inflammation, with bacteria from the gastrointestinal tract contributing to neutrophil recruitment. The results indicate that HFD increases gut permeability, allowing bacterial translocation to VAT, which may drive inflammation and insulin resistance. VAT neutrophils are functionally distinct from PB neutrophils, with increased expression of chemokines, extracellular matrix components, and pro-inflammatory genes. The study provides evidence that VAT neutrophils are a key player in obesity-related inflammation and may be a target for therapeutic interventions.