The World Health Organization recommends exclusive breastfeeding until 6 months followed by introduction of iron-rich complementary foods (CFs). The aim of this study was to determine the impact of different iron-rich CFs on infant gut inflammation and microbiota. Eighty-seven exclusively breastfed infants were randomly assigned to receive one of the following as their first CF: iron-fortified cereal (Cer), iron-fortified cereal with fruit (Cer + Fr), or meat (M). Urine and stool samples were collected to assess reactive oxygen species (ROS) generation, gut microbiota and inflammation. Fecal iron differed across feeding groups (p < 0.001); levels were highest in the Cer group and lowest in M group. A significant increase of fecal ROS formation (p < 0.002) after the introduction of CFs was observed, but did not differ across feeding groups. Fecal calprotectin increased within all groups after the introduction of CFs (p = 0.004). Gut microbiota richness increased after introduction of M or Cer + Fr. Regardless of feeding group, Coriobacteriaceae were positively correlated with ROS and Staphylococcaceae were negatively correlated with calprotectin. Choice of first CF may influence gut inflammation and microbiota, potentially due to variations in iron absorption from different foods. Further research is warranted to fully characterize these associations and to establish implications for infant health. This study was registered in the ClinicalTrial.gov registry (Identifier No. NCT01790542 ). This study was registered in the ClinicalTrial.gov registry under the name “Assessment of Complementary Feeding of Canadian Infants” (Identifier No. NCT01790542 ) February 6, 2013.
14 February 2006 in Molecular and Cellular Biochemistry
β-glucan is considered as an effective immunostimulant because of its binding capacity to different receptors on leukocytes leading to the stimulation of immune responses including bactericidal activity, cytokine productivity, and survival fit ability at cellular levels. In response to immune cell surface receptors, β-glucan stimulates to release cytokines and chemokines. It has been found that these signaling proteins eventually stimulate the immunocompetent cells in fish such as monocytes, macrophages, and neutrophils for killing pathogens by phagocytosis, oxidative burst, and cytotoxic killing activities. They also procreate immunological memories and specific antibodies through activation of T and B lymphocytes. Researchers have proved that β-glucan can modulate some important biochemical (serum hemoglobin, serum protein, and total hemocyte count) and immunological (lysozyme activity, phagocytic activity, oxidative burst activity, and phenoloxidase activity) properties providing more competent immune profile for treating fish and aquatic organisms. β-glucan-supplemented fish showed limited sensitivity of genes involved in acute inflammatory reactions. Findings have shown that β-glucan exerts a positive impact on fish and aquatic organisms’ immunity, enhancing their disease resistance by increasing functional and decreasing deleterious responses. This review focuses on the basic bump of β-glucan on fish and shellfish immunity and recent information on the uses of β-glucan in progressive aquaculture.
Polyunsaturated fatty acids (PUFAs) exhibit beneficial biological functions in carcinogenic processes. We examined the effects of PUFAs in the acid and phospholipid forms on three colon cancer cell lines (HT-29, Caco-2, and DLD-1). Docosahexaenoic acid (DHA) and eicosapentaenoic (EPA) in both acid and phospholipid forms showed growth inhibition effects on experimental colon cancer cell lines. But these PUFAs had the strongest growth-inhibitory effect on HT-29 than Caco-2 and DLD-1. Combined application of PUFAs and sodium butyrate (NaBt) increased the growth inhibition. Growth inhibition was apparently caused by increased lipid peroxidation. DHA or EPA in combination with NaBt significantly increased caspase-3 activity compared to control. DHA and DHA-rich phosphatidylcholine decreased Bcl-2 level in HT-29 and Caco-2 cells.