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Division of Endocrinology
Department of Medicine
Centre de recherche clinique Etienne-Le Bel
Centre hospitalier universitaire de Sherbrooke
3001 -12th Avenue North
Sherbrooke, PQ
Canada J1H 5N4 E-mail: andre.carpentier{at}usherbrooke.ca
Division of Geriatrics
Department of Medicine
Centre de recherche clinique Etienne-Le Bel
Centre hospitalier universitaire de Sherbrooke
Sherbrooke, PQ
Canada J1H 5N4
Dear Sir:
We read with great interest the comments of GJ Wanten concerning our recent report (1) of a reduction in circulating T cell activation and proliferation during enhanced intravascular lipolysis with Intralipid and heparin that resulted in a selective increase in plasma linoleate concentrations in healthy humans. We agree with Wanten that our results in healthy subjects cannot be directly extrapolated to the usual intensive-care-unit patients who have severe inflammatory conditions often associated with a severe catabolic state—a state that in itself may alter the immune response. As mentioned by Wanten, the data from the literature are conflicting with respect to the untoward effects of intravenous lipid emulsions on the immune function in humans. Although early studies did not find evidence of an immunosuppressive effect of total parenteral nutrition with Intralipid or other lipid emulsions in the critical or postoperative care setting (2-5), more recent randomized controlled trials found that the administration of an intravenous lipid emulsion with total parenteral nutrition was associated with less T cell proliferation, a higher rate of infection, more prolonged need for mechanical ventilation, and more prolonged stays in the intensive care unit or in the hospital (6, 7). Our findings (1) also confirmed those of several previous studies that showed a reduced reactivity of human peripheral lymphocytes after either in vitro or in vivo exposure to Intralipid or another lipid emulsion composed of long-chain fatty acids (8-10). Thus, we believe that evidence of a role for long-chain fatty acids in the modulation of T cell function is accumulating. Whether this effect and the proposed mechanisms we showed in our study are relevant in pathophysiological states in humans clearly needs more investigation.
Our report did not address the potential role of a selective elevation of plasma linoleate concentrations on the function of circulating monocytes and neutrophils. Neutrophils and monocytes may behave very differently in response to fatty acids than do T lymphocytes. Thus, we agree with Wanten that the effect of long-chain fatty acids shown in one class of white blood cells cannot be extrapolated to other such classes and that more studies are needed to integrate the multiple potential effects of long-chain fatty acids on the immune system in healthy and pathophysiologic states in humans.
ACKNOWLEDGMENTS
The authors had no conflict of interest.
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