Enhancing gut barrier integrity: Upregulation of tight junction proteins by chitosan oligosaccharide through the ERK1/2 signaling pathway.

OBJECTIVES: This study aimed to explore the protective mechanism of chitosan oligosaccharide (COS) against lipopolysaccharide (LPS)-induced inflammatory responses in IEC-6 cells and dextran sodium sulfate (DSS)-induced colitis in mice. METHODS: The cell inflammation model was constructed by LPS in vitro and enteritis model by DSS in vivo. RESULTS: Following LPS exposure, IEC-6 cell proliferation significantly decreased, epithelial cell integrity was compromised, and TNF-α and IL-1ß levels were increased. However, COS pretreatment reversed these changes. In vivo, DSS-treated mice exhibited evident pathological alterations, including heightened inflammatory levels and significantly decreased expression of tight junction proteins and critical proteins in the Mitogen activated proteins kinase signaling pathway. Nevertheless, COS administration notably reduced inflammatory levels and increased the expression of tight junction proteins and key proteins in the Mitogen activated proteins kinase signaling pathway. CONCLUSIONS: Our findings suggest that COS safeguards gut barrier integrity by upregulating tight junction proteins through the ERK1/2 signaling pathway. Therefore, COS has emerged as a promising candidate for novel drug interventions against inflammatory bowel disease.

Protective Effects of Carbonated Chitosan Montmorillonite on Vomitoxin-Induced Intestinal Inflammation.

Exposure to vomitoxin (DON) can negatively impact the intestinal health of livestock and poultry, leading to compromised nutrient absorption and utilization, resulting in slowed growth and reduced production efficiency. In this study, we synthesized carbonated chitosan montmorillonite intercalation complexes (CCM) through solution precipitation. The successful formation of intercalation complexes was confirmed by examining functional groups and surface features using infrared spectroscopy and scanning electron microscopy. To assess the impact of CCM on DON-infected mice, we established an experimental mouse model of jejunal inflammation induced by DON infection. We analyzed the effects of CCM on blood biochemical and conventional indices, jejunal inflammatory factors, pathological changes, and the expression of proteins in the MAPK pathways in DON-infected mice. Our results indicate that CCM effectively mitigates the adverse effects of DON on growth performance, jejunal injury, and the inflammatory response in mice. CCM supplementation alleviated the negative effects of DON infection on growth performance and reduced intestinal inflammation in mice. Moreover, CCM supplementation successfully inhibited the activation of the mitogen-activated protein kinase (MAPK) signaling pathway induced by DON. These findings suggest that the mitigating effect of CCM on DON-induced inflammatory injury in the murine jejunum is closely linked to the regulation of the MAPK signaling pathway.

Chitosan-gentamicin conjugate attenuates heat stress-induced intestinal barrier injury via the TLR4/STAT6/MYLK signaling pathway: In vitro and in vivo studies.

Heat stress (HS) has a negative impact on animal health. A modified chitosan-gentamicin conjugate (CS-GT) was prepared to investigate its potential protective effects and mechanism of action on heat stress-induced intestinal mucosa injury in IPEC-J2 cells and mouse 3D intestinal organs in a mouse model. CS-GT significantly (P < 0.01) reversed the decline in transmembrane resistance and increased the FITC-dextran permeability of the IPEC-J2 monolayer fusion epithelium caused by heat stress. Heat stress decreased the expression of the tight binding proteins occludin, claudin1, and claudin2. However, pretreatment with CS-GT significantly increased (P < 0.01) the expression of these tight binding proteins. Mechanistically, CS-GT inhibited the activation of the TLR4/STAT6/MYLK signaling pathway induced by heat stress. Molecular docking showed that CS-GT can bind effectively with TLR4. In conclusion, CS-GT alleviates heat stress-induced intestinal mucosal damage both in vitro and in vivo. This effect is mediated, at least partly, by the inhibition of the TLR4/STAT6/MYLK signaling pathway and upregulation of tight junction proteins. These findings suggest that CS-GT may have therapeutic potential in the prevention and treatment of heat stress-related intestinal injury.

Corrigendum: Coral-derived endophytic fungal product, butyrolactone-I, alleviates LPS induced intestinal epithelial cell inflammatory response through TLR4/NF-κB and MAPK signaling pathways: An in vitro and in vivo studies.

[This corrects the article DOI: 10.3389/fnut.2021.748118.].

One-dimensional N-doped carbon nanofibers produced by pre-oxide treatment for effective lithium storage.

Amorphous carbon materials have been confirmed as attractive anode materials for lithium-ion batteries. Herein, an effective strategy to fabricate amorphous carbon materials at low temperature under air atmosphere is proposed. As demonstrated, one-dimensional nitrogen-doping carbon nanofibers were obtained through simple electrospinning technology, following low-temperature heat treatment. Meanwhile, the nitrogen-doping concentration can be regulated by the heating temperature, which can further introduce different levels of adsorption sites on the surface of carbon and enhance the electronic conductivity. Based on experimental investigation, carbon nanofibers with a high nitrogen doping concentration of 18.1 at% achieved an outstanding cycling durability (194.0 mA h g-1 at 2.0 A g-1 after 2000 cycles).

Chitosan oligosaccharide improves the mucosal immunity of small intestine through activating SIgA production in mice: Proteomic analysis.

Chitosan oligosaccharide (COS) plays a vital role in improving the host system and mucosal immune function. So far, the impact of COS on mucosal immune response in the early stage of oral administration is not well understood. Herein, the distribution of COS after oral gavage and the protein expression changes related to innate immune by tandem mass tag (TMT)-based proteomic analysis were investigated. The results revealed that COS was mainly distributed in the stomach, duodenum, and kidney and increased the number of monocytes and lymphocytes in peripheral blood. A total of 21,677 proteins and 7,483 protein groups were identified. Among them, 338 significant differentially expressed proteins were screened, including 205 upregulated and 133 downregulated. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis showed that the intestinal immune network for the IgA production pathway was activated, pIgR, MHCI, MHCII, Itgb2, Itgb7, and B2m were significantly increased (P < 0.05). Furthermore, the expression of the above molecular genes was detected by enzyme-linked immunosorbent assay (ELISA), western blotting, and quantitative real-time PCR. We found that the expressions of IgA, MHCII, TGF-ß1, IL-6, and pIgR were significantly increased (P < 0.05) 1 h after exposure to COS. The protein and mRNA expression of pIgR and MHCI were significantly increased (P < 0.05) at 0.5 h, while the AID protein level was significantly increased (P < 0.05) 1.5 h after COS exposure. The expression of MHCII and H2-Q10 was significantly increased (P < 0.05) by 1 h and 2 h post-exposure to COS. In conclusion, oral administration of COS can significantly enhance intestinal mucosal immunity in mice by activating the SIgA secretion pathway. These results suggest that COS can be used as an oral vaccine or drug adjuvant for small intestinal mucosa.

Effect of Immune Stress on Growth Performance and Immune Functions of Livestock: Mechanisms and Prevention.

Immune stress markedly affects the immune function and growth performance of livestock, including poultry, resulting in financial loss to farmers. It can lead to decreased feed intake, reduced growth, and intestinal disorders. Studies have shown that pathogen-induced immune stress is mostly related to TLR4-related inflammatory signal pathway activation, excessive inflammatory cytokine release, oxidative stress, hormonal disorders, cell apoptosis, and intestinal microbial disorders. This paper reviews the occurrence of immune stress in livestock, its impact on immune function and growth performance, and strategies for immune stress prevention.

A Comprehensive Analysis of the Colonic Flora Diversity, Short Chain Fatty Acid Metabolism, Transcripts, and Biochemical Indexes in Heat-Stressed Pigs.

Heat stressed pigs show typical characteristics of inflammatory bowel disease (IBD). However, little is known about the pathogenesis of heat stress (HS)-induced IBD in pigs. In this study, we determined the effects of HS on colon morphology, intestinal microbiota diversity, transcriptome genes (transcripts), and short chain fatty acids (SCFAs) metabolism in pigs. In addition, the correlation among these parameters was analyzed by weighted gene co-expression network analysis. Results showed that the liver and kidney functions related to blood biochemical indexes were partially changed in pigs under HS. Furthermore, the levels of diamine oxidase and D-lactic acid were significantly increased, whereas the levels of secretory immunoglobulin A were decreased. The integrity of colonic tissue was damaged under HS, as bleeding, lymphatic infiltration, and villi injury were observed. The concentrations of SCFAs in the colon, such as acetic acid and butyric acid, were decreased significantly. In addition, the composition of colon microbiota, such as decrease in Lactobacillus johnsonii, Lactobacillus reuteri and increase in Clostridium sensu stricto 1 of day 7 and 14 while under HS. These changes were associated with changes in the concentration of SCFAs and biochemical indexes above mentioned. Differentially expressed genes were enriched in the nucleotide-binding oligomerization domain-like receptor signaling pathway, Th17 cell differentiation, and IBD pathway, which were also associated with the changes in SCFAs. Thus, the structure, diversity of intestinal microorganisms, and changes in the levels of SCFAs in colon of heat stressed pigs changed significantly, contributing to the activation of immune response and inflammatory signal pathways and causing abnormal physiological and biochemical indexes and intestinal mucosal damage. These results highlight the interconnections between intestinal microbiota, SCFAs, and immune response and their role in the pathogenesis of stress induced IBD therapy.

Coral-Derived Endophytic Fungal Product, Butyrolactone-I, Alleviates Lps Induced Intestinal Epithelial Cell Inflammatory Response Through TLR4/NF-κB and MAPK Signaling Pathways: An in vitro and in vivo Studies.

Herein, we assessed the anti-inflammatory and intestinal barrier protective effects of butyrolactone-I (BTL-1), derived from the coral-derived endophytic fungus (Aspergillus terreus), using the LPS-induced IPEC-J2 inflammation model and the DSS-induced IBD model in mice. In IPEC-J2 cells, pretreatment with BTL-I significantly inhibited TLR4/NF-κB signaling pathway and JNK phosphorylation, resulting in the decrease of IL-1ß and IL-6 expression. Interestingly, BTL-1 pretreatment activated the phosphorylation of ERK and P38, which significantly enhanced the expression of TNF-α. Meanwhile, BTL-1 pretreatment upregulated tight junction protein expression (ZO-1, occludin, and claudin-1) and maintained intestinal barrier and intestinal permeability integrity. In mice, BTL-1 significantly alleviated the intestinal inflammatory response induced by DSS, inhibited TLR4/NF-κB signaling pathway, and MAPK signaling pathway, thus reducing the production of IL-1, IL-6, and TNF-α. Further, the expression of tight junction proteins (ZO-1, occludin, and claudin-1) was upregulated in BTL-1 administrated mice. Therefore, it has been suggested that butyrolactone-I alleviates inflammatory responses in LPS-stimulated IPEC-J2 and DSS-induced murine colitis by TLR4/NF-κB and MAPK signal pathway. Thereby, BTL-1 might potentially be used as an ocean drug to prevent intestinal bowel disease.

The aging population in China: Subjective well-being of empty nesters in rural eastern China.

In this article, we explore the subjective well-being of empty nesters who lived in rural eastern China (N = 967). The Memorial University of Newfoundland Scale of Happiness is used to measure subjective well-being. The results indicate that Memorial University of Newfoundland Scale of Happiness is appropriate for empty nesters in rural China due to its reliability and validity. Generally, male empty nesters report greater subjective well-being scores than females. Negative factors include low levels of education, being a widow or widower, or being unmarried. It is argued that the empty nesters' incapability to access adequate social service and home care leads to their poor subjective well-being.

China's Air Quality and Respiratory Disease Mortality Based on the Spatial Panel Model.

Background: Air pollution has become an important factor restricting China's economic development and has subsequently brought a series of social problems, including the impact of air pollution on the health of residents, which is a topical issue in China. Methods: Taking into account this spatial imbalance, the paper is based on the spatial panel data model PM2.5. Respiratory disease mortality in 31 Chinese provinces from 2004 to 2008 is taken as the main variable to study the spatial effect and impact of air quality and respiratory disease mortality on a large scale. Results: It was found that there is a spatial correlation between the mortality of respiratory diseases in Chinese provinces. The spatial correlation can be explained by the spatial effect of PM2.5 pollutions in the control of other variables. Conclusions: Compared with the traditional non-spatial model, the spatial model is better for describing the spatial relationship between variables, ensuring the conclusions are scientific and can measure the spatial effect between variables.