The DOI matches its Crossref record; 16 of the 16 references it cites were found in a registry or an index.
Neutrophils transiently infiltrate intra-abdominal fat early in the course of high-fat feeding
Open accessAbstract
Chronic inflammation of adipose tissue in obesity is by now an established phenomenon, but the initiating event(s) of the inflammatory cascade are still unknown. We hypothesized that neutrophil infiltration into adipose tissue may precede macrophage infiltration as in classical immune responses. Here we demonstrate that early (3 and 7 days) after initiating high-fat feeding of C57BL/6J mice, neutrophils transiently infiltrate the parenchyma of intra-abdominal adipose tissue. Mean periepdidymal fat myeloperoxidase expression (representing neutrophils) was significantly increased 3.5-fold (P < 0.01) and 2.9-fold (P < 0.03), at days 3 and 7 compared with day 0. Immunohistochemistry analysis demonstrated a physical binding between neutrophils and adipocytes, which was supported by in vitro adherence assay: mouse peritoneal neutrophils adhered to a monolayer of 3T3-L1 mouse adipocytes, in a manner dependent on their activation state, 41.9 +/- 3.7% or 29.5 +/- 2%, by PMA or the IL-8 analog CXCL1 (KC), respectively, compared with 24.8 +/- 1.5% in unstimulated neutrophils, respectively. The degree of surface exposure of CD11b (Mac-1) corresponded to the percentage of adhered neutrophils. The adherence was prevented by preincubating neutrophils or adipocytes with anti-CD11b or anti-ICAM-1 antibodies. Furthermore, immunoprecipitation of CD11b from lysates of a mixed neutrophil-adipocyte cell population resulted in coimmunoprecipitation of ICAM-1, indicating that the interaction is mediated by neutrophil CD11b and adipocyte ICAM-1.
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Obesity is associated with macrophage accumulation in adipose tissue
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Obesity-induced inflammatory changes in adipose tissue
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CCR2 modulates inflammatory and metabolic effects of high-fat feeding
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Absence of an Effect of Liposuction on Insulin Action and Risk Factors for Coronary Heart Disease
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Cited by
Mechanisms of Insulin Action and Insulin Resistance
Petersen, M. C., & Shulman, G. I. (2018) · Physiological Reviews · doi:10.1152/physrev.00063.2017 · Cited by 3,028
Macrophages, inflammation, and insulin resistance
Olefsky, J. M., & Glass, C. K. (2010) · Annual Review of Physiology · doi:10.1146/annurev-physiol-021909-135846 · Cited by 2,733
Adipose tissue inflammation and metabolic dysfunction in obesity
Kawai, T., Autieri, M. V., & Scalia, R. (2021) · American Journal of Physiology-Cell Physiology · doi:10.1152/ajpcell.00379.2020 · Cited by 1,947
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Adipose Tissue Remodeling: Its Role in Energy Metabolism and Metabolic Disorders
Choe, S. S., Huh, J. Y., Hwang, I. J., Kim, J. I., & Kim, J. B. (2016) · Frontiers in Endocrinology · doi:10.3389/fendo.2016.00030 · Cited by 1,206
Metadata
- Authors
- Elgazar-Carmon, V., Rudich, A., Hadad, N., & Levy, R.
- Venue
- Journal of Lipid Research
- Publisher
- Elsevier BV
- Published
- 2008-09
- Volume
- 49
- Issue
- 9
- Pages
- 1894-1903
- ISSN
- 0022-2275 (ISSN-L)
- OpenAlex
- W2125220665
- Cited by
- 487
- References
- 16
- FWCI
- 8.32
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Elgazar-Carmon, V., Rudich, A., Hadad, N., & Levy, R. (2008). Neutrophils transiently infiltrate intra-abdominal fat early in the course of high-fat feeding. Journal of Lipid Research. https://doi.org/10.1194/jlr.m800132-jlr200
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
