Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2003) 5 P74

BES2003 Poster Presentations Cytokines and Growth Factors (9 abstracts)

Leptin enhances expression of CD11b by human neutrophils through TNF-alpha

H Zarkesh-Esfahani , AG Pockley , PG Hellewell , AP Weetman & RJM Ross

Division of Clinical Sciences (North), Sheffield University, Sheffield, UK.

Background: Leptin, the satiety hormone that is produced by adipose tissue appears to act as a link between nutritional status and immune function, and it has been shown to elicit a number of immunoregulatory effects, including the promotion of T cell proliferative responses, and the elicitation of pro-inflammatory cytokines from T cells and monocytes. Given that leptin deficiency is associated with an increased susceptibility to infection, and that polymorphonuclear neutrophils (PMNs) play a major role in innate immunity and host defence against infection, this study evaluated the influence of leptin on PMN activation status. Methods: The presence of leptin receptors on human PMNs was determined using RT-PCR, and its effects on PMN activation status, on the basis of CD11b expression, was evaluated using flow cytometry. Results: In contrast to monocytes which express both the short and long forms of the leptin receptor (Ob-Ra and Ob-Rb respectively), PMNs expressed only Ob-Ra. Leptin induced the expression of CD11b, an early marker of PMN activation, in whole blood after 90 minutes (p<0.01), yet it had no effect on purified PMNs, even those primed by sub-maximal doses of TNF-alpha or PMA. The kinetics of leptin-induced activation was consistent with an indirect effect mediated by TNF-alpha release from monocytes, and 70% of the leptin stimulatory effect on PMNs could be blocked by a TNF antagonist. In conclusion, although leptin activates PMNs, it does so indirectly via TNF-alpha release from monocytes. These findings provide an additional link between the obesity-derived hormone leptin, innate immune function and infectious disease.

Volume 5

22nd Joint Meeting of the British Endocrine Societies

British Endocrine Societies 

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