Nutrition and phagocyte intracellular signal transduction

Autor: Shigeo Ikeda, Hideaki Saito, Woodae Kang
Rok vydání: 2003
Předmět:
Zdroj: International Congress Series. 1255:61-64
ISSN: 0531-5131
Popis: Malnutrition contributes to increased morbidity and mortality through reduced phagocyte function. Dietary restriction impairs neutrophil migration through reduced cytokine and chemokine production by macrophages. Dietary restriction also decreased neutrophil phagocytosis. Intracellular signal transduction is responsible for cytokine/chemokine production and migration and phagocytosis of phagocytes. This article focuses on effects of nutrition on the intracellular signaling of phagocytes. Either tyrosine kinase inhibition or extracellular signal-regulated kinase (ERK) inhibition decreased survival of ad labium, but not for diet-restricted mice in the cercal ligation and puncture model. Peritoneal cells harvested from diet-restricted mice could not increase tyrosine phosphorylation in response to N-formyl-methionyl-leucyl-phenylalanine (fMLP) stimulation. Laser scanning of cytometers revealed that tyrosine phosphorylation is mainly localized in the cytoplasm of the resident macrophages. ERK was activated in peritoneal exudative cells (PECs) from ad libitum mice after fMLP stimulation, whereas the cells of diet-restricted animals did not show any increase in ERK phosphorylation. Dietary restriction impaired tumor necrosis factor alpha (TNF-α)-induced nuclear factor kappa B (NFκB) activation in the peritoneal resident cells (PRCs). Refeeding for only 1 day recovered the impaired NFκB activation. In conclusion, deranged tyrosine phosphorylation, ERK activation and NFκB activation of phagocytes by diet restriction, at least in part, account for the impaired host defense during malnutrition. Detailed information concerning the molecular mechanisms involved in regulation of host defense by malnutrition may help to develop new strategies for nutritional support.
Databáze: OpenAIRE
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