F1----parental bone marrow chimeras between CBA and B10 mice were used to show that even after 1 year follicular dendritic cells (FDC), also termed dendritic reticular cells, are not derived from bone marrow stem cells. However clusters of cells wrapped in the dendritic processes of FDC, isolated by enzyme digestion of the spleen contain B cells originating from donor marrow. This implies that evidence for the presence of antigens such as Ia-like detected by others (Gerdes, J. and Stein, H., Clin. Exp. Immunol. 1982. 48: 348) by immunohistology in or on FDC clusters should be interpreted with caution. Deposition of immune complexes on mouse spleen FDC depends upon the presence of a radio- and cyclophosphamide-sensitive population of cells, although FDC themselves are resistant to such treatments. After whole body irradiation the capacity to localize fluorescein isothiocyanate-labeled aggregated human gamma globulin can be restored by normal or T-deprived spleen cells, but restoration requires an interval of more than 1 though less than 5 days. These findings are compatible with the evidence of Gray et al., Eur. J. Immunol. 1984. 14: 47, that in the rat immune complexes are transported to FDC by a sessile population of marginal zone lymphocytes, as first suggested by Brown et al., Immunology 1973. 24: 955.

Gastrointestinal health is influenced by the functional genes and metabolites generated by the human microbiome. As the volume of current biomedical and translational research indicates, the importance and impact of this ecosystem of microorganisms, especially those comprising the gut microbiome on human health, has become increasingly apparent. Changes to the gut microbiome are associated with inflammatory bowel disease (IBD), which is characterized by persistent intestinal inflammation. Furthermore, the lifetime dietary choices of their host may positively or negatively affect both the gut microbiome and its impact on IBD. As such, “anti-inflammatory” dietary supplements, their impact, and mechanisms in restoring gut microbiota homeostasis during IBD is an area of intensive research. Dietary supplementation may represent an important adjuvant treatment avenue for limiting intestinal inflammation in IBD. Overall, this review addresses the development of the gut microbiome, the significance of the gut microbiome in IBD, and the use of dietary supplements such as vitamin D, fish oil, and resveratrol in the mitigation of IBD-associated gut dysbiosis and intestinal inflammation.

Chronic alcohol use has been attributed to the development of malnutrition. This is in part due to the inhibitory effect of ethanol on the absorption of vital nutrients, including glucose, amino acids, lipids, water, vitamins, and minerals within the small intestine. Recent advances in research, along with new cutting-edge technologies, have advanced our understanding of the mechanism of ethanol’s effect on intestinal nutrient absorption at the brush border membrane (BBM) of the small intestine. However, further studies are needed to delineate how ethanol consumption could have an impact on altered nutrient absorption under various disease conditions. Current research has elucidated the relationship of alcohol consumption on glucose, glutamine, vitamins B1 (thiamine), B2 (riboflavin), B9 (folate), C (ascorbic acid), selenium, iron, and zinc absorption within the small intestine. We conducted systematic computerized searches in PubMed using the following keywords: (1) “Alcohol effects on nutrient transport”; (2) “Alcohol mediated malabsorption of nutrients”; (3) “Alcohol effects on small intestinal nutrient transport”; and (4) “Alcohol mediated malabsorption of nutrients in small intestine”. We included the relevant studies in this review. The main objective of this review is to marshal and analyze previously published research articles and discuss, in-depth, the understanding of ethanol’s effect in modulating absorption of vital macro and micronutrients in health and disease conditions. This could ultimately provide great insights in the development of new therapeutic strategies to combat malnutrition associated with alcohol consumption.

During obesity, diabetes and hypertension inevitably coexist and cause innumerable health disparities. In the obesity, diabetes, and hypertension triad (ODHT), deregulation of glucose and NaCl homeostasis, respectively, causes diabetes and hypertension. In the mammalian intestine, glucose is primarily absorbed by Naglucose cotransport 1 (SGLT1) and coupled NaCl by the dual operation of Na‐H exchange 3 (NHE3) and Cl‐HCO3 [down‐regulated in adenoma (DRA) or putative anion transporter 1 (PAT1)] exchange in the brush border membrane (BBM) of villus cells. The basolateral membrane (BLM) Na/K‐ATPase provides the favorable transcellular Na gradient for BBM SGLT1 and NHE3. How these multiple, distinct transport processes may be affected in ODHT is unclear. Here, we show the novel and broad regulation by Na/K‐ATPase of glucose and NaCl absorption in ODHT in multiple species (mice, rats, and humans). In vivo, during obesity inhibition of villus‐cell BLM, Na/K‐ATPase led to compensatory stimulation of BBM SGLT1 and DRA or PAT1, whereas NHE3 was unaffected. Supporting this new cellular adaptive mechanism, direct silencing of BLM Na/K‐ATPase in intestinal epithelial cells resulted in selective stimulation of BBM SGLT1 and DRA or PAT1 but not NHE3. These changes will lead to an increase in glucose absorption, maintenance of traditional coupled NaCl absorption, and a de novo increase in NaCl absorption from the novel coupling of stimulated SGLT1 with DRA or PAT1. Thus, these novel observations provide the pathophysiologic basis for the deregulation of glucose and NaCl homeostasis of diabetes and hypertension, respectively, during obesity. These observations may lead to more efficacious treatment for obesity‐associated diabetes and hypertension.—Palaniappan, B., Arthur, S., Sundaram, V. L., Butts, M., Sundaram, S., Mani, K., Singh, S., Nepal, N., Sundaram, U. Inhibition of intestinal villus cell Na/K‐ATPase mediates altered glucose and NaCl absorption in obesity‐associated diabetes and hypertension. FASEB J. 33, 9323–9333 (2019). http://www.fasebj.org

To examine the effects of activated neutrophils (PMNs) on Na(+)-K(+)-ATPase, phorbol 12-myristate 13-acetate (PMA)-stimulated PMNs were incubated with canine renal cortical basolateral membrane (BLM), and BLM ouabain-sensitive Na(+)-K(+)-ATPase activity was subsequently quantified. Na(+)-K(+)-ATPase activity decreased to 40.0 +/- 8.7% (SE) of control in the presence of activated PMNs, from 0.89 +/- 0.12 to 0.34 +/- 0.05 mumol Pi.mg protein-1.min-1. This inhibition coincided with a decrease in the apparent Michaelis constant (Km) for ATP from 0.18 +/- 0.02 to 0.05 +/- 0.01 mM. Inclusion of catalase (CAT) and superoxide dismutase (SOD) in the BLM/PMN/PMA incubation mixture resulted in partial preservation of enzyme activity, with an increase to 57.0 +/- 4.6% of control with CAT alone and to 70.0 +/- 5.3% with both CAT and SOD. SOD alone had no protective effect. Neither the myeloperoxidase inhibitor azide nor the hypochlorous acid scavenger L-methionine preserved enzyme activity. Hydroxyl radical scavengers and iron chelators were also ineffective in attenuating Na(+)-K(+)-ATPase inhibition by activated PMNs. These results indicate that activated PMNs mediate a decrease in BLM Na(+)-K(+)-ATPase activity characterized by a reduction in maximum velocity and Km for ATP that appears to be mediated in part by reactive oxygen metabolites.

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