Melatonin is a ubiquitous hormone found in various organisms and highly affects the function of immune cells. In this review, we summarize the current understanding of the significance of melatonin in macrophage biology and the beneficial effects of melatonin in macrophage‐associated diseases. Enzymes associated with synthesis of melatonin, as well as membrane receptors for melatonin, are found in macrophages. Indeed, melatonin influences the phenotype polarization of macrophages. Mechanistically, the roles of melatonin in macrophages are related to several cellular signaling pathways, such as NF‐κB, STATs, and NLRP3/caspase‐1. Notably, miRNAs (eg, miR‐155/‐34a/‐23a), cellular metabolic pathways (eg, α‐KG, HIF‐1α, and ROS), and mitochondrial dynamics and mitophagy are also involved. Thus, melatonin modulates the development and progression of various macrophage‐associated diseases, such as cancer and rheumatoid arthritis. This review provides a better understanding about the importance of melatonin in macrophage biology and macrophage‐associated diseases.

BackgroundOchratoxin A (OTA) is a widespread mycotoxin and induces liver inflammation to human and various species of animals. The intestinal microbiota has critical importance in liver inflammation; however, it remains to know whether intestinal microbiota mediates the liver inflammation induced by OTA. Here, we treated ducklings with oral gavage of OTA (235 μg/kg body weight) for 2 weeks. Then, the microbiota in the cecum and liver were analyzed with 16S rRNA sequencing, and the inflammation in the liver was analyzed. To explore the role of intestinal microbiota in OTA-induced liver inflammation, intestinal microbiota was cleared with antibiotics and fecal microbiota transplantation was conducted.ResultsHere, we find that OTA treatment in ducks altered the intestinal microbiota composition and structure [e.g., increasing the relative abundance of lipopolysaccharides (LPS)-producing Bacteroides], and induced the accumulation of LPS and inflammation in the liver. Intriguingly, in antibiotic-treated ducks, OTA failed to induce these alterations in the liver. Notably, with the fecal microbiota transplantation (FMT) program, in which ducks were colonized with intestinal microbiota from control or OTA-treated ducks, we elucidated the involvement of intestinal microbiota, especially Bacteroides, in liver inflammation induced by OTA.ConclusionsThese results highlight the role of gut microbiota in OTA-induced liver inflammation and open a new window for novel preventative or therapeutic intervention for mycotoxicosis.

Obesity is a nutritional disorder resulting from a chronic imbalance between energy intake and expenditure. This disease is characterized by inflammation in multiple cell types, including macrophages. M1 macrophage responses are correlated with the progression of obesity or diabetes; therefore, strategies that induce repolarization of macrophages from an M1 to an M2 phenotype may be promising for the prevention of obesity- or diabetes-associated pathology. Glutamine (the most abundant amino acid in the plasma of humans and many other mammals including rats) is effective in inducing polarization of M2 macrophages through the glutamine–UDP-N-acetylglucosamine pathway and α-ketoglutarate produced via glutaminolysis, whereas succinate synthesized via glutamine-dependent anerplerosis or the γ-aminobutyric acid shunt promotes polarization of M1 macrophages. Interestingly, patients with obesity or diabetes show altered glutamine metabolism, including decreases in glutamine and α-ketoglutarate concentrations in serum but increases in succinate concentrations. Thus, manipulation of macrophage polarization through glutamine metabolism may provide a potential target for prevention of obesity- or diabetes-associated pathology.

BackgroundEnterotoxigenic Escherichia coli (ETEC) causes diarrhea in humans, cows, and pigs. The gut microbiota underlies pathology of several infectious diseases yet the role of the gut microbiota in the pathogenesis of ETEC-induced diarrhea is unknown.ResultsBy using an ETEC induced diarrheal model in piglet, we profiled the jejunal and fecal microbiota using metagenomics and 16S rRNA sequencing. A jejunal microbiota transplantation experiment was conducted to determine the role of the gut microbiota in ETEC-induced diarrhea. ETEC-induced diarrhea influenced the structure and function of gut microbiota. Diarrheal piglets had lower Bacteroidetes: Firmicutes ratio and microbiota diversity in the jejunum and feces, and lower percentage of Prevotella in the feces, but higher Lactococcus in the jejunum and higher Escherichia-Shigella in the feces. The transplantation of the jejunal microbiota from diarrheal piglets to uninfected piglets leaded to diarrhea after transplantation. Microbiota transplantation experiments also supported the notion that dysbiosis of gut microbiota is involved in the immune responses in ETEC-induced diarrhea.ConclusionWe conclude that ETEC infection influences the gut microbiota and the dysbiosis of gut microbiota after ETEC infection mediates the immune responses in ETEC infection.Electronic supplementary materialThe online version of this article (10.1186/s12917-018-1704-9) contains supplementary material, which is available to authorized users.

BackgroundIntestinal stem cells can be differentiated into absorptive enterocytes and secretory cells, including Paneth cells, goblet cells, and enteroendocrine cells. Glutamine is a primary metabolic fuel of small intestinal enterocytes and is essential for the viability and growth of intestinal cells.ObjectiveWhether glutamine supplementation affects the differentiation of intestinal stem cells is unknown.DesignThree-week-old ICR (Institute of Cancer Research) male mice were divided randomly into two groups: 1) mice receiving a basal diet and normal drinking water and 2) mice receiving a basal diet and drinking water supplemented with glutamine. After 2 weeks, the mice were sacrificed to collect the ileum for analysis.ResultsThe study found that glutamine supplementation in weanling mice decreases the crypt depth in the ileum, leading to higher ratio of villus to crypt in the ileum, but promotes cell proliferation of intestinal cells and mRNA expression of Lgr5 (leucine-rich repeat-containing g-protein coupled receptor5) in the ileum. Glutamine has no effect on the number of Paneth cells and goblet cells, and the expression of markers for absorptive enterocytes, Paneth cells, goblet cells, and enteroendocrine cells.ConclusionThese findings reveal the beneficial effects of dietary glutamine supplementation to improve intestinal morphology in weanling mammals.

Bacteria, viruses, protozoa, and fungi establish a complex ecosystem in the gut. Like other microbiota, gut mycobiota plays an indispensable role in modulating intestinal physiology. Notably, the most striking characteristics of intestinal fungi are their extraintestinal functions. Here, we provide a comprehensive review of the importance of gut fungi in the regulation of intestinal, pulmonary, hepatic, renal, pancreatic, and brain functions, and we present possible opportunities for the application of gut mycobiota to alleviate/treat human diseases.

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Pasteurella multocida causes a variety of infectious diseases in various species of mammals and birds, resulting in enormous economic loss to the modern livestock and poultry industry. However, the mechanism of host-pathogen interaction is unclear. Here, we found that l-serine levels were significantly decreased in murine lungs infected with P. multocida.