The increasing incidence rate of allergic diseases has attracted global attention, and these diseases greatly threaten children′s health. The common pathogenesis of allergic diseases is the specific IgE- or cell-mediated immune response to common inhalant or food allergens. Epidemiological investigation, analysis of fecal flora, and clinical studies all suggest that the development and progression of allergic diseases are closely related to the early disturbance of intestinal flora. Probiotics can regulate intestinal immune response, increase the barrier function of epithelial cells, inhibit the adhesion and colonization of pathogenic bacteria, and thus restore or reconstruct normal intestinal flora. With the increasing understanding of allergic diseases, the effect of probiotics in the prevention and treatment of such diseases will be taken more and more seriously.
Child ; Humans ; Hypersensitivity ; drug therapy ; immunology ; microbiology ; prevention & control ; Intestines ; immunology ; microbiology ; Probiotics ; administration & dosage

BACKGROUNDInflammation is supposed to play a key role in the pathophysiological processes of intestinal ischemia-reperfusion injury (IIRI), and Candida albicans in human gut commonly elevates inflammatory cytokines in intestinal mucosa. This study aimed to explore the effect of C. albicans on IIRI.

METHODSFifty female Wistar rats were divided into five groups according to the status of C. albicans infection and IIRI operation: group blank and sham; group blank and IIRI; group cefoperazone plus IIRI; group C. albicans plus cefoperazone and IIRI (CCI); and group C. albicans plus cefoperazone and sham. The levels of inflammatory factors tumor necrosis factor (TNF)-μ, interleukin (IL)-6, IL-1β, and diamine oxidase (DAO) measured by enzyme-linked immunosorbent assay were used to evaluate the inflammation reactivity as well as the integrity of small intestine. Histological scores were used to assess the mucosal damage, and the C. albicans blood translocation was detected to judge the permeability of intestinal mucosal barrier.

RESULTSThe levels of inflammatory factors TNF-μ, IL-6, and IL-1β in serum and intestine were higher in rats undergone both C. albicans infection and IIRI operation compared with rats in other groups. The levels of DAO (serum: 44.13 ± 4.30 pg/ml, intestine: 346.21 ± 37.03 pg/g) and Chiu scores (3.41 ± 1.09) which reflected intestinal mucosal disruption were highest in group CCI after the operation. The number of C. albicans translocated into blood was most in group CCI ([33.80 ± 6.60] ×102 colony forming unit (CFU)/ml).

CONCLUSIONIntestinal C. albicans infection worsened the IIRI-induced disruption of intestinal mucosal barrier and facilitated the subsequent C. albicans translocation and dissemination.

Amine Oxidase (Copper-Containing) ; metabolism ; Animals ; Anti-Bacterial Agents ; pharmacology ; Candida albicans ; drug effects ; pathogenicity ; Cefoperazone ; pharmacology ; Enzyme-Linked Immunosorbent Assay ; Female ; Interleukin-1beta ; metabolism ; Interleukin-6 ; metabolism ; Intestines ; drug effects ; immunology ; metabolism ; Rats ; Rats, Wistar ; Reperfusion Injury ; immunology ; metabolism ; microbiology

Food allergies, as a type of adverse immune-mediated reactions to ingested food proteins, have become a serious public health issue that harms children and adults health, with increasing incidence year by year. However, without effective therapy for food allergies, doctors-have mostly advised to avoid allergens and provided symptomatic treatment. According to the findings of many studies, allergic diseases are correlated with intestinal barrier function injury, as evidenced by the significant increase in the intestinal permeability among patients with food allergies. In this paper, recent studies on correlations between food allergies and intestinal barrier functions, intestinal barrier function injury mechanisms of allergic foods and food allergy intervention strategies based on intestinal barrier functions were summarized to provide reference for laboratory researches and clinical treatment of food allergic diseases.
Animals ; Food Hypersensitivity ; immunology ; therapy ; Humans ; Intestines ; immunology

OBJECTIVETo explore Chinese medical theory of Fei and Dachang being interior-exteriorly correlated by observing changes of inherent immune response and acquired immune response in the lung tissue and the intestinal tissue of ulcerative colitis (UC) model rats and the intervention of Chinese compounds (CM).

METHODSSeventy rats were randomly divided into 5 groups, i.e., the normal control group (n = 10), the model group (n = 15), the treatment 1 group (n = 15, treated from Fei), the treatment 2 group (n = 15, treated from the intestine), and the Western medicine (WM) group [n = 15, treated with Sulfasalazine (SASP). Except those in the normal control group, the UC rat model was prepared by allergizing colon mucosa combined with TNBS-alcohol (50%) enema, and then intervened by medication (treated with CM complex prescription of treatment from lung, CM complex prescription of treatment from intestine, and SASP). After intragastric administration for 4 weeks, rats were sacrificed and samples taken. The expression of tumor necrosis factor α (TNF-α) and IL-8 contents in the lung tissue, the intestinal tissue, and the serum were detected by radioimmunoassay. Serum MedCAM-1 contents were detected using ELISA. Changes of the expression of Toll-like receptor 4 (TLR4), nuclear factor κB (NF-κB), neutrophil migration inhibition factor (MIF), mucosal addressin cell adhesion molecule-1 (MadCAM-1) mRNA in the lung tissue and the intestinal tissue were detected by real time PCR.

RESULTSCompared with the normal control group, the expression levels of TNF-α, TLR4 mRNA, IL-8, MIF mR- NA, and MadCAM-1 mRNA obviously increased in the model group (P < 0.01). Compared with the model group, the expression levels of TNF-α, TLR4 mRNA, IL-8, MIF mRNA, and MadCAM-1 mRNA obviously decreased in the treatment 1 and 2 groups (P < 0.01). The expression of MadCAM-1 mRNA in the intestinal tissue was obviously higher in the model group than in the normal control group (P < 0.01), while the expressions of TNF-α and NF-κB mRNA was obviously lower in the model group than in the normal control group (P < 0.05, P < 0.01). Compared with the model group, the expression of MadCAM-1 mRNA all significantly deceased in each treatment group (P < 0.05, P < 0.01). Serum TNF-α contents were higher in the model group than in the normal control group (P < 0.05). Compared with the model group, serum TNF-α contents could be lowered in the treatment 1 and 2 groups (P < 0.05, P < 0.01).

CONCLUSIONSThe main mechanisms of the intestinal injury in this UC model might be related with activation of acquired immune response, accompanied with lowered functions of inherent immune response. The main mechanisms of the lung injury in this UC model might be related acquired immune response and inherent immune response. Treatment from Fei and treatment from Dachang both could obviously improve the immunodissonance of Fei and Dachang, indicating the special relation between the lung tissue and the intestinal tissue, thus providing experimental evidence for Chinese medical theory of Fei and Dachang being interior-exteriorly correlated.

Aleurites ; Animals ; Colitis, Ulcerative ; drug therapy ; immunology ; Drugs, Chinese Herbal ; therapeutic use ; Enema ; Interleukin-8 ; metabolism ; Intestinal Mucosa ; immunology ; Intestines ; immunology ; Lung ; immunology ; Lung Injury ; NF-kappa B ; metabolism ; RNA, Messenger ; Rats ; Tumor Necrosis Factor-alpha ; metabolism

BACKGROUNDUlcerative colitis (UC) is associated with differential expression of genes involved in inflammation and tissue remodeling, including FOXO3a, which encodes a transcription factor known to promote inflammation in several tissues. However, FOXO3a expression in tissues affected by UC has not been examined. This study investigated the effects of FOXO3a on UC pathogenesis.

METHODSFOXO3a expression, in 23 patients with UC and in HT29 cells treated with tumor necrosis factor-α (TNF-α) for various durations, was detected by quantitative real-time polymerase chain reaction and Western blotting analysis. Enzyme-linked immunosorbent assay was used to quantify interleukin (IL)-8 expression in FOXO3a-silenced HT29 cells treated with TNF-α for various durations.

RESULTSThe messenger RNA and protein expression of FOXO3a were significantly lower in UC tissues than those in normal subjects (P < 0.01). TNF-α treatment for 0, 0.5, 1, 6, and 24 h induced FOXO3 degradation in HT29 cells. FOXO3a silencing increased IL-8 levels in HT29 cells treated with TNF-α for 6 h (P < 0.05).

CONCLUSIONFOXO3a may play an important role in the intestinal inflammation of patients with UC.

Adult ; Blotting, Western ; Colitis, Ulcerative ; immunology ; metabolism ; pathology ; Enzyme-Linked Immunosorbent Assay ; Female ; Forkhead Box Protein O3 ; genetics ; metabolism ; HT29 Cells ; Humans ; Inflammation ; immunology ; metabolism ; pathology ; Interleukin-8 ; metabolism ; Intestines ; immunology ; metabolism ; pathology ; Male ; Middle Aged ; Real-Time Polymerase Chain Reaction ; Tumor Necrosis Factor-alpha ; metabolism

BACKGROUNDDiarrhea is a common clinical feature of ulcerative colitis resulting from unbalanced intestinal fluid and salt absorption and secretion. The Cl(-)/HCO3(-) exchanger SLC26A3 is strongly expressed in the mid-distal colon and plays an essential role in colonic Cl(-) absorption and HCO3(-) secretion. Slc26a3 expression is up-regulated by lysophosphatidic acid (LPA) in vitro. Our study was designed to investigate the effects of LPA on SLC26A3 expression and the diarrheal phenotype in a mouse colitis model.

METHODSColitis was induced in C57BL/6 mice by adding 4% of dextran sodium sulfate (DSS) to the drinking water. The mice were assigned to LPA treatment DSS group, phosphate-buffered saline (PBS) treatment DSS group, DSS only group and untreated mice with a completely randomized design. Diarrhea severity was evaluated by measuring mice weight, disease activity index (DAI), stool water content and macroscopic evaluation of colonic damage. The effect of LPA treatment on Slc26a3 mRNA level and protein expression in the different groups of mice was investigated by quantitative PCR and Western blotting.

RESULTSAll mice treated with DSS lost weight, but the onset and severity of weight loss was attenuated in the LPA treatment DSS group. The increases in stool water content and the macroscopic inflammation score in LPA treatment DSS group were significantly lower compared to DSS control group or PBS treatment DSS group ((18.89±8.67)% vs. (28.97±6.95)% or (29.48±6.71)%, P = 0.049, P = 0.041, respectively and 2.67±0.81 vs. 4.5±0.83 or 4.5±0.54, P = 0.020, P = 0.006, respectively), as well as the increase in DAI (P = 0.004, P = 0.008, respectively). LPA enema resulted in higher Slc26a3 mRNA and protein expression levels compared to PBS-treated and untreated DSS colitis mice.

CONCLUSIONLPA increases Slc26a3 expression in the inflamed intestine and reduces diarrhea severity in DSS-induced colitis, suggesting LPA might be a therapeutic strategy in the treatment of colitis associated diarrhea.

Animals ; Antiporters ; genetics ; metabolism ; Colitis ; chemically induced ; drug therapy ; Colon ; immunology ; metabolism ; Dextran Sulfate ; pharmacology ; Dextrans ; pharmacology ; Diarrhea ; drug therapy ; metabolism ; Female ; Immunoblotting ; Intestines ; drug effects ; metabolism ; Lysophospholipids ; therapeutic use ; Mice ; Mice, Inbred C57BL

OBJECTIVETo discuss the effect of matrine on nitric oxide (NO) and asymmetric methylarginine (ADMA) metabolism pathways in serum and tissues of mice with lipopolysaccharide (LPS) -induced intestine tissue inflammation.

METHODKunming mice were randomly divided into five groups: the normal control group, the LPS group and matrine (80, 40, 20 mg x kg(-1) x d(-1)) groups. The mice were intragastrically administered with drugs for 3 d (distilled water of the same volume for the normal control group and the LPS group). One hour after the last intragastrical administration, normal saline or LPS (1 mg x kg(-1)) were intraperitoneally injected. Twelve hours later, serum and tissues were collected to determine NO and ADMA levels and observe the pathological changes of intestinal tissues. The Western blot method was adopted to detect the protein expressions of arginine methyltransferases 1 (PRMT1) and dimethylarginine dimethylaminohydrolase 2 (DDAH2) in intestinal tissues.

RESULTCompared with the model group, matrine (80, 40, 20 mg x kg(-1) x d(-1)) groups showed lower NO content in serum and tissues, higher ADMA level in serum and increased PRMT1 expression in intestinal tissues, but without effect on DDAH2 expression.

CONCLUSIONMatrine could inhibit LPS-induced intestine tissue inflammation in mice. Its action mechanism is related to the decreased NO content in serum and tissues and increased ADMA level in serum and PRMT1 expression in intestinal tissues.

Alkaloids ; administration & dosage ; Animals ; Arginine ; analogs & derivatives ; blood ; metabolism ; Humans ; Inflammation ; Intestinal Diseases ; drug therapy ; enzymology ; immunology ; metabolism ; Intestines ; drug effects ; enzymology ; immunology ; metabolism ; Lipopolysaccharides ; adverse effects ; Male ; Mice ; Nitric Oxide ; blood ; metabolism ; Protein-Arginine N-Methyltransferases ; genetics ; metabolism ; Quinolizines ; administration & dosage

The incidence and prevalence of inflammatory bowel diseases (IBDs) including ulcerative colitis and Crohn disease are rapidly increasing in Western countries and in developed Asian countries. Although biologic agents targeting the immune system have been effective in patients with IBD, cessation of treatment leads to relapse in the majority of patients, suggesting that intrinsic immune dysregulation is an effect, not a cause, of IBD. Dramatic changes in the environment, resulting in the dysregulated composition of intestinal microbiota or dysbiosis, may be associated with the fundamental causes of IBD. Japan now has upgraded water supply and sewerage systems, as well as dietary habits and antibiotic overuse that are similar to such features found in developed Western countries. The purpose of this review article was to describe the association of diet, particularly Japanese food and microbiota, with IBD.
Animals ; *Asian Continental Ancestry Group ; Diet/*ethnology ; Evidence-Based Medicine ; Food Habits/ethnology ; Humans ; Incidence ; Inflammatory Bowel Diseases/diagnosis/diet therapy/*ethnology/immunology/*microbiology ; Intestines/immunology/*microbiology ; Japan/epidemiology ; *Microbiota ; Prevalence ; Probiotics/therapeutic use ; Prognosis ; Risk Factors

Animals ; Graft vs Host Disease ; immunology ; metabolism ; Intestines ; immunology ; pathology ; Lymph Nodes ; cytology ; Lymphocyte Activation ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; T-Lymphocytes ; immunology ; metabolism

Animals ; Anti-Bacterial Agents ; administration & dosage ; Escherichia coli ; Female ; Galactosylceramides ; immunology ; Gastric Mucosa ; pathology ; Gastritis, Atrophic ; pathology ; Helicobacter Infections ; complications ; drug therapy ; Helicobacter pylori ; pathogenicity ; Humans ; Inflammation ; pathology ; Intestines ; microbiology ; Levofloxacin ; Lymphocyte Activation ; Male ; Natural Killer T-Cells ; microbiology ; Ofloxacin ; administration & dosage ; Sphingomonas ; Stomach ; pathology