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Adipokines, Inflammation, and Metabolic Diseases · Journal article
Journal of Leukocyte Biology · August 6, 2026
Encouraging direction, but not yet definitive.
This comparative study demonstrates that neutrophils from individuals with obesity exhibit selective impairment in bacterial killing of Pseudomonas aeruginosa and Klebsiella quasipneumoniae despite enhanced activation markers and intact phagocytosis. The findings support a mechanistic link between obesity-induced neutrophil dysfunction and increased infection susceptibility, though clinical correlation and larger sample characterization are needed.
Comparative cross-sectional study with ex vivo functional assays. Individuals with obesity and individuals with normal weight; specific inclusion/exclusion criteria, age range, sex distribution, and recruitment setting not specified. Intervention: Neutrophils from individuals with obesity. Compared with: Neutrophils from individuals with normal weight.
Neutrophils from individuals with obesity showed higher membrane expression of CD66b, CD11b, CD15, CD14, CD18, and CD182, correlating with higher BMI PMA-induced respiratory burst was greater in neutrophils from individuals with obesity than those without obesity Phagocytosis and PMA-induced NETosis were comparable between obesity and normal weight groups
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These findings suggest obesity-associated impairment in pathogen-specific antimicrobial killing may contribute to elevated infection risk in obese individuals. The selective nature of the killing defect (preserved against S. aureus, impaired against Gram-negative species) warrants investigation of obesity-specific mechanistic vulnerabilities and potential clinical stratification.
A well-designed comparative study of neutrophil function in obesity versus normal weight controls, reporting pathogen-specific killing deficits with mechanistic phenotyping, but limited by modest sample size and lack of clinical outcome data.
As stated by the source record.
These findings suggest obesity-associated impairment in pathogen-specific antimicrobial killing may contribute to elevated infection risk in obese individuals. The selective nature of the killing defect (preserved against S. aureus, impaired against Gram-negative species) warrants investigation of obesity-specific mechanistic vulnerabilities and potential clinical stratification.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
What is missing. This record has no reported figures. That is a gap in the analysis, not a judgement about the study.
Obesity is a disease associated with an increased risk of various medical complications, including cardiovascular problems, diabetes, and infectious diseases. The higher incidence of infections in individuals with obesity is likely due to impaired immune functions. Neutrophils deploy microbicidal functions. However, it is unclear whether neutrophils in individuals with obesity function effectively against infections. To evaluate whether neutrophils in obesity have dysfunctional antimicrobial functions, neutrophils from individuals with normal weight and from individuals with obesity were isolated, and their phenotype and microbicidal functions were assessed. Neutrophils from individuals with obesity showed higher expression of CD66b, CD11b, CD15, CD14, CD18, and CD182 on their membranes. The higher expression of these molecules correlated with higher BMI, suggesting that obesity is associated with neutrophil activation. Accordingly, the PMA-induced respiratory burst in neutrophils from individuals with obesity was greater than in those from individuals without obesity. But, phagocytosis and PMA-induced NETosis were comparable between neutrophils from individuals with or without obesity, implying that neutrophil functions are not impaired by obesity. However, NET formation of neutrophils from individuals with obesity was selectively reduced in response to Staphylococcus aureus. Nevertheless, the actual killing of these bacteria was similar between neutrophils from individuals with or without obesity. In contrast, neutrophils from individuals with obesity exhibited impaired killing of Pseudomonas aeruginosa and of Klebsiella quasipneumoniae. Together, these findings suggest that obesity induces neutrophil activation but disrupts pathogen-specific antimicrobial mechanisms of neutrophils. This deficiency in pathogen clearance could explain the increased susceptibility to infections observed in individuals with obesity.
Taken from the source record, never inferred. Follow any of these and new work involving them reaches your briefing.