• Thacianna Barreto Da Costa, Natália Gomes De Morais, Joana Maria Bezerra De Lira, Thays Miranda De Almeida, Suênia Da Cunha Gonçalves-De-Albuquerque, Pereira Valéria Rêgo Alves VR Department of Immunology, Aggeu Magalhães Research Center, Oswaldo Cruz Foundation, Campus Federal University of Pernambuco, Recife, Brazil., Milena De Paiva Cavalcanti, and Célia Maria Machado Barbosa De Castro.
• Department of Tropical Medicine, Federal University of Pernambuco, Recife, Brazil. thaciannabc@gmail.com.
• Eur J Nutr. 2017 Mar 1; 56 (2): 693-704.

PurposeTo investigate the effects of neonatal malnutrition followed by nutritional replacement on the signaling mechanisms developed by the inflammasome complex by analyzing the expression of the targeted TLR2, TLR4, NLRP3, caspase-1 and release of IL-1β and IL-18 by alveolar macrophages infected in vitro with Candida albicans.MethodsMale Wistar rats (n = 24), 90-120 days, were suckled by mothers whose diet during lactation contained 17 % protein in the nourish group and 8 % protein in the malnourished group. After weaning, both groups were fed a normal protein diet. Macrophages were obtained after tracheostomy, through the collection of bronchoalveolar lavage fluid. The quantification of the expression levels of targets (TLR2, TLR4, NLRP3 and caspase-1) was performed by real-time RT-PCR. Production of cytokines was performed by ELISA.ResultsThe malnourished animals during lactation showed reduced body weight from the fifth day of life, remaining until adulthood. Further, the model applied malnutrition induced a lower expression of TLR4 and caspase-1. The quantification of the TLR2 and NLRP3, as well as the release of IL-1β and IL-18, was not different between groups of animals nourished and malnourished. The system challenged with Candida albicans showed high expression levels of all targets in the study.ConclusionsThe tests demonstrate nutritional restriction during critical periods of development, although nutritional supplementation may compromise defense patterns in adulthood in a timely manner, preserving distinct signaling mechanism, so that the individual does not become widely vulnerable to infections by opportunistic pathogens.

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