scholarly journals Probiotics Improve Eating Disorders in Mandarin Fish (Siniperca chuatsi) Induced by a Pellet Feed Diet via Stimulating Immunity and Regulating Gut Microbiota

2021 ◽  
Vol 9 (6) ◽  
pp. 1288
Author(s):  
Xiaoli Chen ◽  
Huadong Yi ◽  
Shuang Liu ◽  
Yong Zhang ◽  
Yuqin Su ◽  
...  

Eating disorders are directly or indirectly influenced by gut microbiota and innate immunity. Probiotics have been shown to regulate gut microbiota and stimulate immunity in a variety of species. In this study, three kinds of probiotics, namely, Lactobacillus plantarum, Lactobacillus rhamnosus and Clostridium butyricum, were selected for the experiment. The results showed that the addition of three probiotics at a concentration of 108 colony forming unit/mL to the culture water significantly increased the ratio of the pellet feed recipients and survival rate of mandarin fish (Siniperca chuatsi) under pellet-feed feeding. In addition, the three kinds of probiotics reversed the decrease in serum lysozyme and immunoglobulin M content, the decrease in the activity of antioxidant enzymes glutathione and catalase and the decrease in the expression of the appetite-stimulating regulator agouti gene-related protein of mandarin fish caused by pellet-feed feeding. In terms of intestinal health, the three probiotics reduced the abundance of pathogenic bacteria Aeromonas in the gut microbiota and increased the height of intestinal villi and the thickness of foregut basement membrane of mandarin fish under pellet-feed feeding. In general, the addition of the three probiotics can significantly improve eating disorders of mandarin fish caused by pellet feeding.

2021 ◽  
Vol 2 (4/S) ◽  
pp. 93-100
Author(s):  
Begzod Shokirov ◽  
Yulduz Halimova

Antibiotics are the most common medicines used to treat human infectious diseases. Based on their chemical structure, antibiotics mainly include the following categories: quinolones, β-lactams, macrolides, and aminoglycosides among others. The mechanism of different antibiotics varies, and there are four main mechanisms: inhibition of bacterial cell wall synthesis, interaction with cell membranes, interference with protein synthesis, and inhibition of nucleic acid replication and transcription. Antibiotics can act on pathogenic bacteria. Accordingly, antibiotics can also affect normal bacteria that colonize the human body. The size, structure, and function of the microbiota may change in response to antibiotic treatment. Significant changes in the human gut microbiota may be associated with repeated use of antibiotics [3]; in the following days, these changes were restored. However, little is known about comparing the response of the gut microbiota to antibiotic treatment. Probiotics are beneficial to the host when administered in adequate amounts. Lactobacillus rhamnosus was one of the most common probiotics studied by scientists regarding its culture, function, and metabolism [10]. However, the effect of L. rhamnosus present in the gut microbiota on the host's susceptibility to pathogenic bacteria after taking antibiotics has rarely been discussed. In our current study, rats were given two types of antibiotics, namely vancomycin and ampicillin, and their oral and intestinal microbiota was observed at 3 time points.  The rats were treated with antibiotics or L. rhamnosus, and then infected with Salmonella entericaserovarTyphimurium (S. Typhimurium ) via a gastric tube. Fecal samples were then collected to determine the pathogenic load. Ampicillin and vancomycin act in different antimicrobial spectra and have different absorption in the digestive tract. In addition, the concentration of these antibiotics entering the digestive tract varies; these factors can affect the host microbiota. Thus, this study aimed to compare the effects of these antibiotics on the gut microbiota at normal doses, as well as to evaluate the differences in the results. The gut microbiota underwent dramatic changes during the administration period. Changes in the gut microbiota affected the host's susceptibility to pathogens when infected with bacteria due to changes in resistance to colonization.


2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Sang-Kap Han ◽  
Yeon-Jeong Shin ◽  
Dong-Yeon Lee ◽  
Kyung Min Kim ◽  
Seo-Jin Yang ◽  
...  

Abstract Background Gut microbiota closely communicate in the immune system to maintain a balanced immune homeostasis in the gastrointestinal tract of the host. Oral administration of probiotics modulates gut microbiota composition. In the present study, we isolated Lactobacillus rhamnosus HDB1258, which induced tumor necrosis factor (TNF)-α and interleukin (IL)-10 expression in macrophages, from the feces of breastfeeding infants and examined how HDB1258 could regulate the homeostatic immune response in mice with or without lipopolysaccharide (LPS)-induced systemic inflammation. Results Oral administration of HDB1258 significantly increased splenic NK cell cytotoxicity, peritoneal macrophage phagocytosis, splenic and colonic TNF-α expression, TNF-α to IL-10 expression ratio, and fecal IgA level in control mice, while Th1 and Treg cell differentiation was not affected in the spleen. However, HDB1258 treatment significantly suppressed peritoneal macrophage phagocytosis and blood prostaglandin E2 level in mice with LPS-induced systemic inflammation. Its treatment increased LPS-suppressed ratios of Treg to Th1 cell population, Foxp3 to T-bet expression, and IL-10 to TNF-α expression. Oral administration of HDB1258 significantly decreased LPS-induced colon shortening, myeloperoxidase activity and NF-κB+/CD11c+ cell population in the colon, while the ratio of IL-10 to TNF-α expression increased. Moreover, HDB1258 treatment shifted gut microbiota composition in mice with and without LPS-induced systemic inflammation: it increased the Cyanobacteria and PAC000664_g (belonging to Bacteroidetes) populations and reduced Deferribacteres and EU622763_s group (belonging to Bacteroidetes) populations. In particular, PAC001066_g and PAC001072_s populations were negatively correlated with the ratio of IL-10 to TNF-α expression in the colon, while the PAC001070_s group population was positively correlated. Conclusions Oral administered HDB1258 may enhance the immune response by activating innate immunity including to macrophage phagocytosis and NK cell cytotoxicity in the healthy host and suppress systemic inflammation in the host with inflammation by the modulation of gut microbiota and IL-10 to TNF-α expression ratio in immune cells.


2021 ◽  
Vol 22 (13) ◽  
pp. 6921
Author(s):  
Norihisa Nishimura ◽  
Kosuke Kaji ◽  
Koh Kitagawa ◽  
Yasuhiko Sawada ◽  
Masanori Furukawa ◽  
...  

Recent studies have suggested that an alteration in the gut microbiota and their products, particularly endotoxins derived from Gram-negative bacteria, may play a major role in the pathogenesis of liver diseases. Gut dysbiosis caused by a high-fat diet and alcohol consumption induces increased intestinal permeability, which means higher translocation of bacteria and their products and components, including endotoxins, the so-called “leaky gut”. Clinical studies have found that plasma endotoxin levels are elevated in patients with chronic liver diseases, including alcoholic liver disease and nonalcoholic liver disease. A decrease in commensal nonpathogenic bacteria including Ruminococaceae and Lactobacillus and an overgrowth of pathogenic bacteria such as Bacteroidaceae and Enterobacteriaceae are observed in cirrhotic patients. The decreased diversity of the gut microbiota in cirrhotic patients before liver transplantation is also related to a higher incidence of post-transplant infections and cognitive impairment. The exposure to endotoxins activates macrophages via Toll-like receptor 4 (TLR4), leading to a greater production of proinflammatory cytokines and chemokines including tumor necrosis factor-alpha, interleukin (IL)-6, and IL-8, which play key roles in the progression of liver diseases. TLR4 is a major receptor activated by the binding of endotoxins in macrophages, and its downstream signal induces proinflammatory cytokines. The expression of TLR4 is also observed in nonimmune cells in the liver, such as hepatic stellate cells, which play a crucial role in the progression of liver fibrosis that develops into hepatocarcinogenesis, suggesting the importance of the interaction between endotoxemia and TLR4 signaling as a target for preventing liver disease progression. In this review, we summarize the findings for the role of gut-derived endotoxemia underlying the progression of liver pathogenesis.


2019 ◽  
Vol 10 (5) ◽  
pp. 2935-2946 ◽  
Author(s):  
Rongkang Hu ◽  
Feng Zeng ◽  
Linxiu Wu ◽  
Xuzhi Wan ◽  
Yongfang Chen ◽  
...  

Carrot juice fermented with Lactobacillus rhamnosus GG, enriched with free phenolics, organic acids and short-chain fatty acid, has the potential to ameliorate type 2 diabetes, in part through modulating specific gut microbiota and regulating the mRNA and protein expressions levels involved in glucose metabolism.


2010 ◽  
Vol 13 (2) ◽  
pp. 151-162 ◽  
Author(s):  
Guoqiang Zhang ◽  
Wuying Chu ◽  
Songnian Hu ◽  
Tao Meng ◽  
Linlin Pan ◽  
...  

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