Lentinan administration alleviates diarrhea of rotavirus-infected weaned pigs via regulating intestinal immunity

Background:Lentinan(LNT)may regulate many important physiological functions of human and animals.This study aimed to verify whether LNT administration could relieve diarrhea via improving gut immunity in rotavirus(RV)-challenged weaned pigs.Methods:Twenty-eight weaned pigs were randomly fed 2 diets containing 0 or 84 mg/kg LNT product for 19 d(n=14).RV infection was executed on d 15.After extracting polysaccharides from LNT product,its major monosaccharides were analyzed.Then,LNT polysaccharide was used to administrate RV-infected IPEC-J2 cells.Results:Dietary LNT supplementation supported normal function of piglets even when infected with RV,as reflected by reduced growth performance loss and diarrhea prevalence,and maintained gut immunity(P<0.05).The polysaccharide was isolated from LNT product,which molecular weight was 5303 Da,and major monosaccharides included glucose,arabinose and galactose.In RV-infected IPEC-J2 cells,this polysaccharide significantly increased cell viability(P<0.05),and significantly increased anti-virus immunity via regulating pattern recognition receptors and host defense peptides(P<0.05).Conclusion:Those results suggest that LNT administration increases the piglets’resistance to RV-induced stress,likely by supporting intestinal immunity.

The development and role of microbialhost interactions in gut mucosal immune development

At birth the piglet＇s immune system is immature and it is dependent upon passive maternal protection until weaning.The piglet＇s mucosal immune system develops over the first few weeks but has not reached maturity at weaning ages which are common on commercial farms. At weaning piglets are presented with a vast and diverse range of microbial and dietary/environmental antigens. Their ability to distinguish between antigens and mount a protective response to potential pathogens and to develop tolerance to dietary antigens is critical to their survival and failure to do so is reflected in the high incidence of morbidity and mortality in the post-weaning period. A growing recognition that the widespread use of antibiotics to control infection during this critical period should be controlled has led to detailed studies of those factors which drive the development of the mucosal immune system, the role of gut microbiota in driving this process, the origin of the bacteria that colonise the young piglet＇s intestine and the impact of rearing environment. This review briefly describes how the mucosal immune system is equipped to respond ＂appropriately＂ to antigenic challenge and the programmed sequence by which it develops. The results of studies on the critical interplay between the host immune system and gut microbiota are discussed along with the effects of rearing environment. By comparing these with results from human studies on the development of allergies in children, an approach to promote an earlier maturation of the piglet immune system to resist the challenges of weaning are outlined.

Role of the gut microbiota in inflammatory bowel disease pathogenesis: What have we learnt in the past 10 years?

Our understanding of the microbial involvement in inflammatory bowel disease (IBD) pathogenesis has increased exponentially over the past decade. The development of newer molecular tools for the global assessment of the gut microbiome and the identification of nucleotide-binding oligomerization domain-containing protein 2 in 2001 and other susceptibility genes for Crohn&#x02019;s disease in particular has led to better understanding of the aetiopathogenesis of IBD. The microbial studies have elaborated the normal composition of the gut microbiome and its perturbations in the setting of IBD. This altered microbiome or &#x0201c;dysbiosis&#x0201d; is a key player in the protracted course of inflammation in IBD. Numerous genome-wide association studies have identified further genes involved in gastrointestinal innate immunity (including polymorphisms in genes involved in autophagy: ATG16L1 and IGRM), which have helped elucidate the relationship of the local innate immunity with the adjacent luminal bacteria. These developments have also spurred the search for specific pathogens which may have a role in the metamorphosis of the gut microbiome from a symbiotic entity to a putative pathogenic one. Here we review advances in our understanding of microbial involvement in IBD pathogenesis over the past 10 years and offer insight into how this will shape our therapeutic management of the disease in the coming years.

Novel metabolic and physiological functions of branched chain amino acids: a review

It is widely known that branched chain amino acids（BCAA） are not only elementary components for building muscle tissue but also participate in increasing protein synthesis in animals and humans. BCAA（isoleucine, leucine and valine） regulate many key signaling pathways, the most classic of which is the activation of the m TOR signaling pathway. This signaling pathway connects many diverse physiological and metabolic roles. Recent years have witnessed many striking developments in determining the novel functions of BCAA including：（1） Insufficient or excessive levels of BCAA in the diet enhances lipolysis.（2） BCAA, especially isoleucine, play a major role in enhancing glucose consumption and utilization by up-regulating intestinal and muscular glucose transporters.（3）Supplementation of leucine in the diet enhances meat quality in finishing pigs.（4） BCAA are beneficial for mammary health, milk quality and embryo growth.（5） BCAA enhance intestinal development, intestinal amino acid transportation and mucin production.（6） BCAA participate in up-regulating innate and adaptive immune responses.In addition, abnormally elevated BCAA levels in the blood（decreased BCAA catabolism） are a good biomarker for the early detection of obesity, diabetes and other metabolic diseases. This review will provide some insights into these novel metabolic and physiological functions of BCAA.

Chronic heat stress induces the disorder of gut transport and immune function associated with endoplasmic reticulum stress in growing pigs

Although high temperatures influence gut health,data on underlying mechanisms remains scant.Using a pig model,this study performed a global analysis on how chronic heat stress affects the transport and immune function of the gut through transcriptome,proteome,microbial diversity and flow cytometry.A total of 27 pigs with similar body weights were assigned into 3 groups,control(Con)group(23℃),chronic heat stressed(HS)group(33°C),and pair-fed(PF)group,in a controlled environment for 21 days.Our results showed that pigs in the HS group had reduced growth performance and diminished height of ileal villi(P<0.01).Transcriptome and proteome analyses demonstrated notable modification of expression of nutrients and ion transport-related transporters and gut mechanical barrier-related genes by chronic heart stress(P<0.05),suggesting damage of transport functions and the gut barrier.Chronic heat stress-induced endoplasmic reticulum stress also increased the synthesis of misfolded proteins,leading to upregulation of misfolded protein degradation and synthesis,as well as vesicle transport disorder(P<0.05).Energy supply processes were enhanced in the mitochondrion(P<0.05)to maintain biological processes with high energy demands.Furthermore,chronic heat stress activated complement cascade response-related genes and proteins in the gut mucosa(P<0.05).Our flow cytometry assays showed that the proportion of gut lymphocytes(CD4^(+)T cells,T cells,B cells in Peyer’s patch lymphocytes and CD4^(+)CD25^(+)T cells in intraepithelial lymphocytes)were significantly altered in the HS group pigs(P<0.05).In addition,the occurrence of gut microbial dysbiosis in the HS group pigs was characterized by increased potential pathogens(e.g.,Asteroleplasma,Shuttleworthia,Mycoplasma)and suppression of beneficial bacteria(e.g.,Coprococcus and Aeriscardovia),which are associated with gut immune function.Altogether,our data demonstrated that chronic heat stress induced gut transport and immune function disorder associated with endoplasmic reticulum stress in growing pigs.