ovalbumin and Atrophy

Age-related thymic atrophy results in reduced output of naïve conventional T (Tcon) cells. However, its impact on regulatory T (Treg) cells is insufficiently understood. Given evidence that thymic Treg (tTreg) cell generation is enhanced in the aged, atrophy thymus and that the aged periphery accumulates peripheral Treg (pTreg) cells, we asked why these Treg cells are unable to effectively attenuate increased autoreactivity-induced chronic inflammation in the elderly. We designed a mock-self-antigen chimera mouse model, in which membrane-bound ovalbumin (mOVA) transgenic mice, bearing a FoxN1-floxed gene for induction of conditional thymic atrophy, received OVA-specific (OT-II) T-cell receptor (TCR) transgenic progenitor cells. The chimeric mice with thymic atrophy exhibited a significant decrease in OVA-specific tTreg and pTreg cells but not polyclonal (pan)-Treg cells. These OVA-specific pTreg cells were significantly less able to suppress OVA-specific stimulation-induced proliferation in vitro and exhibited lower FoxP3 expression. Additionally, we conducted preliminary TCR repertoire diversity sequencing for Treg cells among recent thymic emigrants (RTEs) from Rag

Topics: Aged; Aging; Animals; Atrophy; Autoantigens; Autoimmune Diseases; Clonal Selection, Antigen-Mediated; Clone Cells; Humans; Immunomodulation; Inflammation; Mice; Mice, Transgenic; Ovalbumin; Receptors, Antigen, T-Cell; T-Cell Antigen Receptor Specificity; T-Lymphocytes, Regulatory; Thymus Gland; Transplantation Chimera

The immunomodulatory effects of the ethanol extract of Gynostemma pentaphyllum (GP-EX) were examined in electric footshock (EFS)-stressed mice. The mice were orally administered various doses of GP-EX for 7 days before exposure to EFS (duration: 3 min, interval: 10 s, intensity: 2 mA) once a day from day 8 for 14 days with continuous daily feeding of GP-EX. Oral administration of GP-EX to mice prevented EFS stress-induced immunosuppression as determined by the lymphoid organ (thymus and spleen) weight and cellularity. In addition, oral administration of GP-EX restored EFS-suppressed functional properties of mature lymphocytes in terms of concanavalin A-induced proliferation of splenocytes and lipopolysaccharide-induced cytokine production (TNF-α, IL-1β). Furthermore, we found that mice that were orally administered with GP-EX generated much more potent ovalbumin-specific cytotoxic T lymphocyte responses upon intravenous ovalbumin injection compared to the untreated controls. These results demonstrate that oral administration of the ethanol extract of Gynostemma pentaphyllum could increase host defense in immunocompromised situations such as stress-induced immunosuppression.

Topics: Animals; Atrophy; Cell Proliferation; Cytokines; Electroshock; Gynostemma; Immunosuppression Therapy; Lipopolysaccharides; Mice; Ovalbumin; Plant Extracts; Spleen; Stress, Physiological; T-Lymphocytes, Cytotoxic; Thymus Gland

Pigs reared commercially indoors are exposed to air heavily contaminated with particulate and gaseous pollutants. Epidemiological surveys have shown an association between the levels of these pollutants and the severity of lesions associated with the upper respiratory tract disease of swine atrophic rhinitis. This study investigated the role of aerial pollutants in the etiology of atrophic rhinitis induced by Pasteurella multocida. Forty, 1-week-old Large White piglets were weaned and divided into eight groups designated A to H. The groups were housed in Rochester exposure chambers and continuously exposed to the following pollutants: ovalbumin (groups A and B), ammonia (groups C and D), ovalbumin plus ammonia (groups E and F), and unpolluted air (groups G and H). The concentrations of pollutants used were 20 mg m-3 total mass and 5 mg m-3 respirable mass for ovalbumin dust and 50 ppm for ammonia. One week after exposure commenced, the pigs in groups A, C, E, and G were infected with P. multocida type D by intranasal inoculation. After 4 weeks of exposure to pollutants, the pigs were killed and the extent of turbinate atrophy was assessed with a morphometric index (MI). Control pigs kept in clean air and not inoculated with P. multocida (group H) had normal turbinate morphology with a mean MI of 41.12% (standard deviation [SD], +/- 1. 59%). In contrast, exposure to pollutants in the absence of P. multocida (groups B, D, and F) induced mild turbinate atrophy with mean MIs of 49.65% (SD, +/-1.96%), 51.04% (SD, +/-2.06%), and 49.88% (SD, +/-3.51%), respectively. A similar level of atrophy was also evoked by inoculation with P. multocida in the absence of pollutants (group G), giving a mean MI of 50.77% (SD, +/-2.07%). However, when P. multocida inoculation was combined with pollutant exposure (groups A, C, and E) moderate to severe turbinate atrophy occurred with mean MIs of 64.93% (SD, +/-4.64%), 59.18% (SD, +/-2.79%), and 73.30% (SD, +/-3.19%), respectively. The severity of atrophy was greatest in pigs exposed simultaneously to dust and ammonia. At the end of the exposure period, higher numbers of P. multocida bacteria were isolated from the tonsils than from the nasal membrane, per gram of tissue. The severity of turbinate atrophy in inoculated pigs was proportional to the number of P. multocida bacteria isolated from tonsils (r2 = 0.909, P < 0.05) and nasal membrane (r2 = 0.628, P < 0.05). These findings indicate that aerial pollutants contribute to the

Topics: Air Pollution, Indoor; Ammonia; Animals; Atrophy; Dust; Eating; Female; Ovalbumin; Palatine Tonsil; Pasteurella multocida; Rhinitis, Atrophic; Swine; Swine Diseases; Turbinates

Morphologic and immunologic changes in the gut mucosa of food-hypersensitive mice, from a study model generated by feeding ovalbumin (OVA) to female BALB/c mice after intraperitoneal injection of cyclophosphamide (CY), were investigated in an effort to clarify the mechanisms of food-sensitive enteropathy. Villous atrophy, crypt hyperplasia, and increased numbers of intraepithelial lymphocytes (IEL) were confirmed in the antigen-challenged OVA-sensitive mice as seen in food-sensitive enteropathy in humans, whereas no significant morphologic changes were observed in the nontreated control group or groups treated with OVA or CY alone. IEL and lamina propria lymphocytes (LPL) were isolated from the intestinal mucosa before and after the antigen challenge, and surface markers were analyzed by FACScan. After the antigen challenge, the numbers of CD8+ cells increased among the IEL, and the occurrence of both CD4+ and CD8+ cells increased among the LPL. The numbers of Thy-1+ cells and TCR- alpha/beta + cells increased among both the IEL and LPL, and LFA-1 expression was enhanced in both of these lymphocyte populations. The proliferative response of IEL and LPL to OVA increased in a dose-dependent manner after the antigen challenge in the OVA-sensitive mouse model. These results indicate that IEL and LPL, possibly those that have migrated from peripheral blood, are activated by orally administered antigens and cause mucosal damage in the food-sensitive enteropathy.

Topics: Animals; Antigens; Atrophy; Disease Models, Animal; Female; Food Hypersensitivity; Hyperplasia; In Vitro Techniques; Intestinal Diseases; Intestinal Mucosa; Jejunum; Lymphocyte Activation; Mice; Mice, Inbred BALB C; Ovalbumin; T-Lymphocyte Subsets

The purpose of the research was to observe the influence of the bacterial infection and inhalation vapours on the histologic picture of bronchi and lungs in the course on the experimental asthma induced in guinea pigs. The animals were divided into 6 groups. The animals were immunized by ovalbumin. Group I was control and was subjected to inhalations of physiologic salt solutions. Group II was immunized by the soluble of ovalbumin intraperitoneally and was inhaled with the solution of ovalbumin. Group III was subjected only to inhalation of the ovalbumin. Group IV was inhaled with the solution of formalin alternately. Group V experienced only formalin inhalations. Group VI was infected with Pseudomonas aeruginosa strain and inhaled with the solution of ovalbumin. On the histologic examination of the lung tissue the authors found the atrophy of the lymphatic system, the hypertrophy of the mucous membrane and muscular coat of the bronchi, the accumulation of large amount of mucus in their lumen and the exfoliation of the bronchial epithelium.

Topics: Animals; Asthma; Atrophy; Bronchi; Bronchial Spasm; Epithelium; Formaldehyde; Guinea Pigs; Hypertrophy; Lung; Male; Mucous Membrane; Ovalbumin; Pseudomonas Infections