The effects of diclazuril on the bursa of Fabricius (BF) structure and secretory IgA (SIgA) expression in chickens infected with Eimeria tenella were examined. The morphology of the BF was observed by hematoxylin and eosin staining, while ultrastructural changes were monitored by transmission electron microscopy. E. tenella infection caused the BF cell volumes to decrease, irregularly arranged, as well as, enlargement of the intercellular space. Diclazuril treatment alleviated the physical signs of damages associated with E. tenella infection. The SIgA expression in BF was analyzed by immunohistochemistry technique. The SIgA expression increased significantly by 350.4% (P<0.01) after E. tenella infection compared to the normal control group. With the treatment of diclazuril, the SIgA was relatively fewer in the cortex, and the expression level was significantly decreased by 46.7% (P<0.01) compared with the infected and untreated group. In conclusion, E. tenella infection in chickens induced obvious harmful changes in BF morphological structure and stimulated the expression of SIgA in the BF. Diclazuril treatment effectively alleviated the morphological changes. This result demonstrates a method to develop an immunological strategy in coccidiosis control.
Animals ; Bursa of Fabricius/anatomy & histology/*parasitology ; Chickens ; Coccidiosis/drug therapy/metabolism/parasitology/*veterinary ; Coccidiostats/administration & dosage/*adverse effects ; Eimeria tenella/*physiology ; Female ; Immunoglobulin A, Secretory/*genetics/metabolism ; Male ; Nitriles/administration & dosage/*adverse effects ; Poultry Diseases/*drug therapy/genetics/metabolism/parasitology ; Triazines/administration & dosage/*adverse effects

OBJECTIVETo valuate the intestinal mucosal secretary IgA (sIgA) responses to the ovalbumin-induced allergy in mice, to provide some clues for the exploration of mechanisms and therapeutic methods in the children's food allergy.

METHODSFemale BALB/c mice aged 6 weeks fed on the ovalbulmin-free diet, were randomly divided into 2 groups with 8 mice in each. The mice in group Ch were sensitized with ovalbumin (OVA) intraperitoneal injection two times and challenged intragastrically 3 times. Two days after the last challenge with oral OVA, the mice were sacrificed and the samples were collected. The mice in group Ns were given intraperitoneal and intragastrical normal saline as control. The levels of total IgA and OVA-specific IgA in the intestinal mucus of the mice were determined by ELISA; the immunohistochemical methods were adopted to observe IgA(+) plasmacytes in lamina propria (LP) and surface membrane IgA (smIgA)(+) lymphocytes in peyer's patch (PP); the IL-4 mRNA expression in LP was assessed by RT-PCR. The IL-4 mRNA expression in PP was evaluated by in situ hybridization.

RESULTSAfter the mice in Ch group were sensitized and challenged with OVA, the levels of the total IgA and the OVA-specific IgA in mucus remarkably increased (P < 0.01 respectively), the amounts of the IgA(+) plasmacytes in LP and the smIgA(+) lymphocytes in PP significantly increased (P < 0.01 respectively); a significantly positive correlation was found among the total IgA levels, the OVA-specific IgA levels, the IgA(+) plasmacyte counts in LP and the smIgA(+) lymphocyte counts in PP (P < 0.01 respectively); the mRNA expressions of IL-4 in LP and in PP were significantly augmented (P < 0.01 respectively); significantly positive correlations were found either between the IL-4 mRNA expression and the IgA(+) plasmacyte counts in LP (P < 0.01) or between the IL-4 mRNA expression and the smIgA(+) lymphocyte counts in PP (P < 0.01).

CONCLUSIONSThe intestinal mucosal sIgA responses are abnormally augmented in the ovalbumine-induced allergic mice, which may be partly due to the increased expression of IL-4 mRNA in gut.

Animals ; Disease Models, Animal ; Enzyme-Linked Immunosorbent Assay ; Female ; Food Hypersensitivity ; immunology ; Immunoglobulin A, Secretory ; metabolism ; Immunohistochemistry ; Interleukin-4 ; genetics ; metabolism ; Intestinal Mucosa ; immunology ; metabolism ; Mice ; Mice, Inbred BALB C ; Ovalbumin ; administration & dosage ; immunology ; Peyer's Patches ; immunology ; RNA, Messenger ; metabolism ; Random Allocation

OBJECTIVETo investigate the effect of total alkaloids of Sophora alopecuroides (TASA) on dextran sulfate sodium (DSS)-induced colitis in mice.

METHODSChronic experimental colitis was induced by administration of 4 cycles of 4% DSS. Fifty mice were randomly distributed into 4 groups (normal, DSS, DSS/high-dose TASA, and DSS/low-dose TASA groups) by a random number table with body weight stratification. Mice in the normal group (n=11) and DSS-induced colitis control group (n=15) received control treatment of 20 mL/kg distilled water; DSS plus TASA high- and low-dose groups (n=12 each) were treated with TASA solution (20 mL/kg) at the doses of 60 mg/kg and 30 mg/kg, respectively. The severity of colitis was assessed on the basis of clinical signs, colon length, and histology scores. Moreover, secretory immunoglobulin A (sIgA) and haptoglobin (HP) were analyzed by enzyme linked immunosorbent assay; intercellular adhesion molecule 1 (ICAM-1) and macrophage-migration inhibitory factor (MIF) gene expressions were analyzed by quantitative reverse transcriptase realtime polymerase chain reaction (qRT-PCR) using SYBA green I; and nuclear factor κ B (NF-κ B) expression and activation and p65 interaction with the promoter of ICAM-1 gene were assessed by Western blotting and chromatin immunoprecipitation assay.

RESULTSTASA administration significantly attenuated the damage and substantially reduced HP elevation and maintained the level of cecum sIgA. TASA inhibited the ICAM-1 gene expression and had no effect on MIF gene expression. Also, TASA was able to reduce phospho-I κ B α (p-I κ B α) protein expression; however, it had no effect on the activation of I κ B kinase α (IKK α) and inhibitor of NF-κ B α (I κ B α). Moreover, TASA inhibited the p65 recruitment to the ICAM-1 gene promoter.

CONCLUSIONSTASA had a protective effect on DSS-induced colitis. Such effect may be associated with its inhibition of NF-κ B activation and blockade of NF-κ B-regulated transcription activation of proinflammatory mediator gene.

Alkaloids ; pharmacology ; therapeutic use ; Animals ; Cecum ; drug effects ; metabolism ; pathology ; Colitis ; chemically induced ; drug therapy ; pathology ; prevention & control ; Colon ; pathology ; ultrastructure ; Dextran Sulfate ; Down-Regulation ; drug effects ; Female ; Haptoglobins ; metabolism ; I-kappa B Proteins ; metabolism ; Immunoglobulin A, Secretory ; metabolism ; Intercellular Adhesion Molecule-1 ; genetics ; metabolism ; Intestinal Mucosa ; drug effects ; pathology ; ultrastructure ; Macrophage Migration-Inhibitory Factors ; genetics ; metabolism ; Mice ; Mice, Inbred C57BL ; NF-KappaB Inhibitor alpha ; Phosphorylation ; drug effects ; Phytotherapy ; Promoter Regions, Genetic ; genetics ; Protective Agents ; pharmacology ; therapeutic use ; Protein Binding ; drug effects ; Signal Transduction ; drug effects ; Sophora ; chemistry ; Transcription Factor RelA ; metabolism