Could problems in the bedroom come from our intestines? A preliminary study of IBS and its impact on female sexuality.

INTRODUCTION: Female sexuality may be affected by many somatic and psychological factors. Somatic conditions have impact on psychological well-being. We assumed that chronic disease like Irritable Bowel Syndrome (IBS), when producing the long-term distress, may greatly influence sexual functioning. AIM: The aim of this study was to determine whether the severity of IBS influences sexual functions of women and take into consideration other factors like Small Intestinal Bacterial Overgrowth (SIBO) comorbidity and duration of IBS. SUBJECTS AND METHODS: Study patients were recruited by contacting IBS patients at Gastroenterology Ward of Clinical University Centre in Katowice. The survey consisted of 3 parts. The first part were socio-demographic questions. The second part was polish translation of Female Sexuality Functions Index (FSFI) questionnaire. The third part consisted of questions about the patient condition, pharmacotherapy and Irritable Bowel Syndrome Severity Score (IBSSS) questionnaire. 307 women were included in the study and completed the questionnaire. 143 participants were diagnosed with IBS. The mean age of participants was 27 (IQR=23-33). 29% of the patients (n=41) had severe, 47% (n=68) moderate and 24% (n=34) mild IBS. RESULTS: The prevalence of sexual dysfunctions was greater in women with IBS (48%) than in healthy control group (23%) (p<0.001). The median of FSFI was: 30.1 (26.3-32.8) for healthy control group, 30 (23.5-32.6) for mild IBS, 26.2 (22.2-31.6) for moderate and 24.4 (20.1-28.9) for severe. CONCLUSION: IBS decreases all domains of women sexual activity. Severity of sexual dysfunctions relate to intensity of IBS symptoms. All physicians treating IBS-patients should take sexual dysfunctions into their clinical consideration.

Toxicity response of silkworm intestine to Bacillus cereus SW7-1 pathogen.

Bacillus cereus is a foodborne pathogen that causes gastrointestinal disease in hosts. The interactions between pathogenic bacteria and silkworms (Bombyx mori L.) involve complex processes. This study aimed to investigate the potential genetic traits of B. cereus SW7-1 and profile the toxicity response of silkworm intestine upon infection by the SW7-1 pathogen. Bacterial genome sequencing and polymerase chain reaction (PCR) detection indicated that B. cereus SW7-1 possesses multiple antibiotic-resistant genes and nine virulence factor genes. Then, silkworm larvae were infected with SW7-1. Comparative transcriptomic analysis revealed that 273 differentially expressed genes (DEGs) with known functions were successfully annotated to the silkworm reference genome. Specifically, 18 DEGs were up-regulated, and 255 DEGs were down-regulated. Compared with the control group, the treated group revealed down-regulated DEGs that are related to stress reactions, immunity, autophagy and apoptosis, DNA replication, ribosomal stress, and carbohydrate metabolism. Quantitative real time PCR analysis showed that many key genes in the Toll pathway, immune deficiency pathway, Janus kinase/signal transducers and activators of transcription pathway, and melanization reaction were up-regulated. Thus, B. cereus SW7-1 pathogen could damage the silkworm intestine, as confirmed by the histological section assay. In addition, SW7-1 can affect the normal physiological functions of intestinal cells. This study contributes toward an improved understanding of the toxicity response of silkworm to the B. cereus pathogen and provides new insights into the molecular mechanisms of the complex interactions between pathogenic microbes and silkworms.

The Microbiota-Gut-Brain Axis.

The importance of the gut-brain axis in maintaining homeostasis has long been appreciated. However, the past 15 yr have seen the emergence of the microbiota (the trillions of microorganisms within and on our bodies) as one of the key regulators of gut-brain function and has led to the appreciation of the importance of a distinct microbiota-gut-brain axis. This axis is gaining ever more traction in fields investigating the biological and physiological basis of psychiatric, neurodevelopmental, age-related, and neurodegenerative disorders. The microbiota and the brain communicate with each other via various routes including the immune system, tryptophan metabolism, the vagus nerve and the enteric nervous system, involving microbial metabolites such as short-chain fatty acids, branched chain amino acids, and peptidoglycans. Many factors can influence microbiota composition in early life, including infection, mode of birth delivery, use of antibiotic medications, the nature of nutritional provision, environmental stressors, and host genetics. At the other extreme of life, microbial diversity diminishes with aging. Stress, in particular, can significantly impact the microbiota-gut-brain axis at all stages of life. Much recent work has implicated the gut microbiota in many conditions including autism, anxiety, obesity, schizophrenia, Parkinson's disease, and Alzheimer's disease. Animal models have been paramount in linking the regulation of fundamental neural processes, such as neurogenesis and myelination, to microbiome activation of microglia. Moreover, translational human studies are ongoing and will greatly enhance the field. Future studies will focus on understanding the mechanisms underlying the microbiota-gut-brain axis and attempt to elucidate microbial-based intervention and therapeutic strategies for neuropsychiatric disorders.

Undibacterium piscinae sp. nov., isolated from Korean shiner intestine.

A novel Gram-stain-negative, non-spore-forming, obligate aerobic, motile, rod-shaped, and flagellated bacterium, designated S11R28T, was isolated from the intestinal tract of a Korean shiner, Coreoleuciscus splendidus. Based on 16S rRNA gene sequences, strain S11R28T was identified as member of the genus Undibacterium in class Betaproteobacteria, and was closely related to Undibacterium parvum DSM 23061T (98.49 %). The isolate grew at 4-25 °C, pH 6-9, with 0 % (w/v) NaCl, and grew optimally at 20 °C, pH 8, in the absence of NaCl. The main cellular fatty acids were C16 : 0 and summed features 3 (C16 : 1ω7c and/or C16 : 1ω6c). The strain possessed diphosphatidylglycerol, phosphatidylglycerol, and phosphatidylethanolamine as predominant polar lipids, and ubiquinone Q-8 as a respiratory quinone. The polyamine profile composed of 2-hydroxyputrescine, spermidine, putrescine, and benzoic acid. A genomic DNA G+C content was 51.4 mol%. The average nucleotide identity between strains S11R28T and U. parvum DSM 23061T was 78.66 %. Thus, Undibacterium piscinae can be considered a novel species within the genus Undibacterium with the type strain S11R28T (=KCTC 62668T=JCM 33224T).

Alterations of the Brain Proteome and Gut Microbiota in d-Galactose-Induced Brain-Aging Mice with Krill Oil Supplementation.

Brain aging is commonly associated with neurodegenerative disorders, but the ameliorative effect of krill oil and the underlying mechanism remain unclear. In this study, the components of krill oil were measured, and the antiaging effects of krill oil were investigated in mice with d-galactose (d-gal)-induced brain aging via proteomics and gut microbiota analysis. Krill oil treatment decreased the expression of truncated dopamine- and cAMP-regulated phosphoproteins and proteins involved in the calcium signaling pathway. In addition, the concentrations of dopamine were increased in the serum (p < 0.05) and brain (p > 0.05) due to the enhanced expressions of tyrosine-3-monooxygenase and aromatic l-amino acid decarboxylase. Moreover, krill oil alleviated gut microbiota dysbiosis, decreased the abundance of bacteria that consume the precursor tyrosine, and increased the abundance of Lactobacillus spp. and short-chain fatty acid producers. This study revealed the beneficial effect of krill oil against d-gal-induced brain aging and clarified the underlying mechanism through proteomics and gut microbiota analysis.

Intestinal microbiota and colorectal cancer: changes in the intestinal microenvironment and their relation to the disease.

Tools that predict the risk of colorectal cancer are important for early diagnosis, given the high mortality rate for this cancer. The composition of the intestinal microbiota is now considered to be a risk factor for the development of colorectal cancer. This discovery has motivated a growing number of studies to identify the micro-organisms responsible for the onset and/or progression of colorectal cancer. With this in mind, this review discusses the relationship between the composition of the intestinal microbiota and colorectal cancer risk. Prospective and case-control studies indicate that the intestinal microbiota of individuals with colorectal cancer usually contains a greater proportion of bacteria responsible for gastrointestinal tract inflammatory diseases, as well as bacteria that produce toxins and carcinogenic metabolites. In contrast, there tends to be a reduced presence of butyric acid-producing bacteria, probiotic bacteria and potentially probiotic bacteria. Despite these differences, the onset and development of colorectal cancer cannot be attributed to a specific micro-organism. Thus, studies focused on the formation of the intestinal microbiota and factors that modulate its composition are important for the development of approaches for colorectal cancer prevention.

Microbiome Signatures Associated With Steatohepatitis and Moderate to Severe Fibrosis in Children With Nonalcoholic Fatty Liver Disease.

BACKGROUND & AIMS: The intestinal microbiome might affect the development and severity of nonalcoholic fatty liver disease (NAFLD). We analyzed microbiomes of children with and without NAFLD. METHODS: We performed a prospective, observational, cross-sectional study of 87 children (age range, 8-17 years) with biopsy-proven NAFLD and 37 children with obesity without NAFLD (controls). Fecal samples were collected and microbiome composition and functions were assessed using 16S ribosomal RNA amplicon sequencing and metagenomic shotgun sequencing. Microbial taxa were identified using zero-inflated negative binomial modeling. Genes contributing to bacterial pathways were identified using gene set enrichment analysis. RESULTS: Fecal microbiomes of children with NAFLD had lower α-diversity than those of control children (3.32 vs 3.52, P = .016). Fecal microbiomes from children with nonalcoholic steatohepatitis (NASH) had the lowest α-diversity (control, 3.52; NAFLD, 3.36; borderline NASH, 3.37; NASH, 2.97; P = .001). High abundance of Prevotella copri was associated with more severe fibrosis (P = .036). Genes for lipopolysaccharide biosynthesis were enriched in microbiomes from children with NASH (P < .001). Classification and regression tree model with level of alanine aminotransferase and relative abundance of the lipopolysaccharide pathway gene encoding 3-deoxy-d-manno-octulosonate 8-phosphate-phosphatase identified patients with NASH with an area under the receiver operating characteristic curve value of 0.92. Genes involved in flagellar assembly were enriched in the fecal microbiomes of patients with moderate to severe fibrosis (P < .001). Classification and regression tree models based on level of alanine aminotransferase and abundance of genes encoding flagellar biosynthesis protein had good accuracy for identifying case children with moderate to severe fibrosis (area under the receiver operating characteristic curve, 0.87). CONCLUSIONS: In an analysis of fecal microbiomes of children with NAFLD, we associated NAFLD and NASH with intestinal dysbiosis. NAFLD and its severity were associated with greater abundance of genes encoding inflammatory bacterial products. Alterations to the intestinal microbiome might contribute to the pathogenesis of NAFLD and be used as markers of disease or severity.

Cohaesibacter intestini sp. nov., isolated from the intestine of abalone, Haliotis discus hannai.

A Gram-stain-negative, rod-shaped and facultative anaerobic strain named YE-B6T was isolated from the intestine of abalone, Haliotis discus hannai. The reactions of oxidase and catalase were both positive. Strain YE-B6T could grow at 10-37 °C (optimum, 28-33 °C), at pH 7-9 (optimum, pH 7) and in salinity of 0-8 % NaCl (w/v; optimum, 2 %). The 16S rRNA gene sequence of strain YE-B6T had maximum sequence similarities to Cohaesibacter celericrescens H1304T (98.0 %), Cohaesibacter marisflavi DQHS21T (97.4 %), Cohaesibacter haloalkalitolerans JC131T (97.4 %) and Cohaesibacter gelatinilyticus CL-GR15T (97.3 %). Results of phylogenetic analysis showed that it was affiliated to the genus Cohaesibacter within the order Rhizobiales in the Alphaproteobacteria. The respiratory quinone of strain YE-B6T was Q-10. The cellular fatty acids mainly comprised C18 : 1 ω7c and summed feature 3 (C16 : 1ω6c and/or C16 : 1ω7c). The polar lipid profile consisted of diphosphatidylglycerol, phosphatidylcholine, phosphatidylethanolamine, phosphatidylglycerol, phosphatidylmonomethylethanolamine, two unidentified aminolipids, two unidentified polar lipids and one unidentified phospholipid. The G+C content of strain YE-B6T was 55.6 mol%. Based on its genotypic, physiological and biochemical characteristics, strain YE-B6T represented a novel species within the genus Cohaesibacter, for which the name Cohaesibacterintestini sp. nov. is proposed. The type strain of the new species is YE-B6T (=MCCC 1A13131T=KCTC 62716T).

Effects of ß-Cyclodextrin and Hydroxypropyl-ß-Cyclodextrin Inclusions on the Degradation of Magnolol by Intestinal Bacteria.

Cyclodextrin (CD) inclusions are generally used to increase the solubility of poorly soluble drugs. In this study, magnolol (MAG) was used as a model drug for exploring the effects of CD on the degradation of pharmaceutical drugs by intestinal microflora. MAG/ß-cyclodextrin (ß-CD) and MAG/hydroxypropyl-ß-CD (HP-ß-CD) inclusion complexes were successfully prepared by the saturated aqueous solution and freeze-drying methods, respectively. Structural characterisation along with analyses of solubility, residual water content and drug content of the inclusion complexes was performed. The intestinal microflora of male rats was used to study MAG degradation in vitro. At three concentrations, the degradation of both the inclusion complexes was slower than that of the MAG monomer, MAG and CD mixtures and the MAG-poloxamer 188 micelle. There were no statistically significant differences in the degradation of the MAG/ß-CD and MAG/HP-ß-CD inclusion complexes. A simulation first-order equation of the degradation parameters revealed that the degradation of the inclusion complexes was slower and pronounced, judging by slope. The experimental findings were verified by molecular docking for predicting the stable molecular structure of the inclusion complexes. In conclusion, the inclusion complexes partially protected MAG from degradation by the intestinal bacteria.

Mikrobiota und Reizdarmsyndrom ­ eine kritische Bestandsaufnahme. / [Microbiota and irritable bowel syndrome: A critical inventory].

This narrative review critically explores the role of the gut microbiota in functional bowel disorders of IBS-type. Starting with changes in the microbiota composition and diversity, as they have been often found in correlative IBS studies, it raises the question of cause and consequence, of sensitivity and specificity of findings in comparison to other diseases, and of the scientific and clinical options to manipulate the microbiota. This includes a discussion of pre- and probiotics and antibiotics as well as the role of nutrition and the microbiota exchange with fecal microbiota transfer (FMT). For IBS, most of these strategies have not been found to be successful therapies. This may be due to the heterogeneity of the disease itself, but eventually also due to the concepts of microbiological research, e. g., the term dysbiosis, or in methodological differences of the molecular-genetic research that are not visible in the published papers. Future studies should aim to identify those factors that may explain and predict the response to such therapies.

Intestinal infection triggers Parkinson's disease-like symptoms in Pink1-/- mice.

Parkinson's disease is a neurodegenerative disorder with motor symptoms linked to the loss of dopaminergic neurons in the substantia nigra compacta. Although the mechanisms that trigger the loss of dopaminergic neurons are unclear, mitochondrial dysfunction and inflammation are thought to have key roles1,2. An early-onset form of Parkinson's disease is associated with mutations in the PINK1 kinase and PRKN ubiquitin ligase genes3. PINK1 and Parkin (encoded by PRKN) are involved in the clearance of damaged mitochondria in cultured cells4, but recent evidence obtained using knockout and knockin mouse models have led to contradictory results regarding the contributions of PINK1 and Parkin to mitophagy in vivo5-8. It has previously been shown that PINK1 and Parkin have a key role in adaptive immunity by repressing presentation of mitochondrial antigens9, which suggests that autoimmune mechanisms participate in the aetiology of Parkinson's disease. Here we show that intestinal infection with Gram-negative bacteria in Pink1-/- mice engages mitochondrial antigen presentation and autoimmune mechanisms that elicit the establishment of cytotoxic mitochondria-specific CD8+ T cells in the periphery and in the brain. Notably, these mice show a sharp decrease in the density of dopaminergic axonal varicosities in the striatum and are affected by motor impairment that is reversed after treatment with L-DOPA. These data support the idea that PINK1 is a repressor of the immune system, and provide a pathophysiological model in which intestinal infection acts as a triggering event in Parkinson's disease, which highlights the relevance of the gut-brain axis in the disease10.

Omics Analyses of Gut Microbiota in a Circadian Rhythm Disorder Mouse Model Fed with Oolong Tea Polyphenols.

Microbiome has been revealed as a key element involved in maintaining the circadian rhythms. Oolong tea polyphenols (OTP) has been shown to have potential prebiotic activity. Therefore, this study focused on the regulation mechanisms of OTP on host circadian rhythms. After 8 weeks of OTP administration, a large expansion in the relative abundance of Bacteroidetes with a decrease in Firmicutes was observed, which reflected the positive modulatory effect of OTP on gut flora. In addition, Kyoto Encyclopedia of Genes and Genomes pathways of ATP-binding cassette transporters, two-component system, and the biosynthesis of amino acids enriched the most differentially expressed genes after OTP treatment. Of the differentially expressed proteins identified, most were related to metabolism, genetic information processing, and environmental information processing. It underscores the ability of OTP to regulate circadian rhythm by enhancing beneficial intestinal microbiota and affecting metabolic pathways, contributing to the improvement of host microecology.

Effect of Long-Term Intake of Dietary Titanium Dioxide Nanoparticles on Intestine Inflammation in Mice.

Early stage exposure of foodborne substances, such as brightening agent titanium dioxide nanoparticles (TiO2 NPs), can cause long-term effects in adulthood. We aimed to explore the potential adverse effect of long-term dietary intake of TiO2 NPs. After feeding for 2-3 months from weaning, TiO2 NPs-exposed mice showed lower body weight and induced intestinal inflammation. However, this phenomenon was not observed in gut microbiota-removed mice. TiO2 NPs exposure rarely affected the diversity of microbial communities, but significantly decreased the abundance of several probiotic taxa including Bifidobacterium and Lactobacillus. Additionally, TiO2 NPs aggravated DSS-induced chronic colitis and immune response in vivo, and reduced the population of CD4+T cells, regulatory T cells, and macrophages in mesenteric lymph nodes. Therefore, dietary TiO2 NPs could interfere with the balance of immune system and dynamic of gut microbiome, which may result in low-grade intestinal inflammation and aggravated immunological response to external stimulus, thus introducing potential health risk.

Fermentation capacities of fructan- and pectin-rich by-products and purified fractions via an in vitro piglet faecal model.

BACKGROUND: Dietary strategies such as the inclusion of prebiotics have been suggested for modulating intestinal microbiota. In piglets, this strategy could result in a reduction of post-weaning-associated disorders and the use of antibiotics. To date, mainly purified fractions have been tested for their prebiotic effects at weaning while trials of potential health-promoting effects of products and corresponding by-products remain rare. In this study, fructan- and pectin-based ingredients have been tested in a two-step in vitro model for their fermentation kinetics as well as for their short-chain fatty acid production and microbiota profiles in fermentation broth as indicators for their prebiotic activity. RESULTS: Chicory root, in contrast to chicory pulp, exhibited an extensive and rapid fermentation similar to inulin and oligofructose, although butyrate levels of root and pulp did not reach those of the purified fractions. Chicory pulp showed higher relative levels of Lactobacillus spp., Bifidobacterium spp., Clostridium cluster IV and butyryl-CoA:acetate-CoA transferase gene abundance compared to chicory root. Sugar beet pulp, orange and citrus by-products displayed extensive gas fermentation patterns, equivalent to those of purified pectin, and revealed an elevated butyrate production compared to purified pectin. Moreover, several orange and citrus by-products displayed significantly higher relative levels of Bifidobacterium spp. in comparison to purified pectin. CONCLUSIONS: Chicory root and pulp as well as orange and citrus by-products appear to be promising ingredients for piglet diets for modulating intestinal fermentation for health purposes. © 2019 Society of Chemical Industry.

Frequency of Escherichia coli virotypes in calf diarrhea and intestinal morphologic changes associated with these virotypes or other diarrheagenic pathogens.

Calf diarrhea is a common cause of pre-weaning morbidity and mortality in cattle operations. We evaluated the role of Escherichia coli by assessing the frequency of genes encoding virulence factors (virotypes) in E. coli from feces or intestinal contents, and the association of these virotypes or other diarrheagenic pathogens with intestinal morphologic changes in calves with or without diarrhea. E. coli was isolated from 408 feces and 105 intestines of calves with diarrhea and compared to those isolated from 635 feces and 100 intestines of calves without diarrhea, from 2002 to 2016. Virotype EAST1:F17, in combination with minor virotypes, was the most commonly detected type, but without differences in frequency between the 2 groups of calves. No significant intestinal morphologic changes were observed with the different E. coli virotypes in either group of calves, except for bacterial attachment to enterocytes for virotype STa:F5, which was detected only in calves with diarrhea. These observations suggest that E. coli, excluding virotype STa:F5, is not a significant diarrhea-causing agent in calves. However, the intestinal lesions observed in ~82% of calves with diarrhea were attributed to other diarrheagenic pathogens that include bovine coronavirus, Clostridium perfringens, Cryptosporidium spp., Eimeria spp., rotavirus, and Salmonella spp.

Weaned piglets: another factor to be considered for the control of Salmonella infection in breeding pig farms.

Field studies on Salmonella infection in suckling piglets are scarce due to the intrinsic difficulties of collecting proper samples (i.e. tonsils or mesenteric lymph nodes), and most of them rely on the analysis of rectal swabs that limit their accuracy. We used 495 slaughtered 4-weeks-old male piglets intended for human consumption from 5 Salmonella-seropositive breeding farms to collect gastrointestinal packages and perform a thorough detection of Salmonella on mesenteric lymph nodes and intestinal content. The overall prevalence of both infection and shedding was high (≈ 36%) indicating that piglets played an active role in Salmonella maintenance in the farms. Major serotypes found in piglets included 4,[5],12:i: (35.4%), Rissen (17.1%), Derby (10.9%) and Bovismorbificans (10.3%). In most of the infected animals (72.8%) the same serotype was found in mesenteric lymph nodes and feces. Significant higher ELISA OD% values were found in meat juice samples from non-infected piglets compared to infected ones (median OD% of 12.0 and 17.3, respectively; P = 0.002) suggesting some protective effect of sow's colostrum. Salmonella was also isolated from feces from weaned sows contemporary of the slaughtered piglets, and 89% of the serotypes identified in sows were also detected in piglets. Pulsed field gel electrophoresis analyses showed that 75% of the piglet isolates that were compared to those of sows were related to them, suggesting the circulation of Salmonella strains between sows and piglets. It appears that improving piglet colostrum intake along with the reduction of the shedding in sows may favor the control of Salmonella infection in breeding farms.

Isolation and characterization of a novel temperate bacteriophage from gut-associated Escherichia within black soldier fly larvae (Hermetia illucens L. [Diptera: Stratiomyidae]).

To gain insight into the presence and nature of prophages in the black soldier fly (BSF; Hermetia illucens L. [Diptera: Stratiomyidae]) gut, we isolated and characterized a novel, temperate Escherichia bacteriophage designated vB_EcoS_PHB10 (PHB10). Electron microscopy analysis revealed that phage PHB10 has a long, flexible, non-contractile tail and belongs to the family Siphoviridae. The phage was found to be stable over a wide range of temperatures (4-37 °C) and pH values (pH 5-9), and it lysed two out of 13 Escherichia strains tested. The genome of PHB10 contains genes encoding a putative transcriptional regulator and an integrase, and it shows a high degree of similarity to a region of the Enterobacter cloacae MBRL1077 genome. Induction experiments revealed that phage PHB10 could be induced by different gut substrates, suggesting that diet might be a potential regulator of lytic/lysogenic switches in commensal lysogens.

Effect of pre- and post-weaning dietary supplementation with arginine and glutamine on rabbit performance and intestinal health.

BACKGROUND: The purpose of the present study was to assess if the exposure to glutamine (Gln), arginine (Arg) or their combination from pregnancy, through the maternal diet, to a post weaning supplemented diet, can stimulate litter performance, gut development and immune function. To this end does and their litters were fed the same basal diet no supplemented (control C), or supplemented with 0.4% Gln, 0.4% Arg, or 0.4 Gln + 0.4 Arg. Rabbits were weaned at 25 d of age and fed the same experimental diet as their mothers for 10 additional days (35 d of age). Bacterial translocation to mesenteric lymph nodes (MLN) at 6 d of age and intestinal histology, enzymatic activity, phenotypical and functional analysis of intraepithelial lymphocytes (IEL) from the appendix were determined at 6, 25 and 35 d of age. RESULTS: No significant differences on animal performance or mortality rates were observed among dietary treatments. However, kits from rabbit does supplemented with Gln tended (P ≤ 0.10) to reduce the translocation of total number of both aerobic and facultative anaerobic bacteria to the MLN. Also, rabbits fed the Gln supplemented diets maintained intestinal villous height at weaning compared to the non-supplemented diets (P < 0.05). The proportions of CD45+CD4+ and CD45+CD8+ IEL in the appendix were not affected by dietary means. However, in rabbits IEL at weaning dietary Gln significantly upregulated IL-2 and downregulated IL-6 expression. CONCLUSIONS: Despite a lack of effect on performance and mortality the inclusion of 0.4% Gln has a positive effect by maintaining intestinal villous height and modulating the cytokine profile at weaning. The supplementation with Arg or Arg + Gln at the selected doses in this study did not exert positive effects on rabbit intestinal health.