ovalbumin and Enterocolitis--Pseudomembranous

The immunogenicity of bacterial flagellin has been reported in different studies. By its close interaction with the immune system, the flagellin represents an interesting adjuvant and vaccine candidate. Salmonella Typhimurium flagellin has already been tested as adjuvant to stimulate mucosal immunity. Here, we assessed the ability of Clostridium difficile flagellin FliC to act as a mucosal adjuvant, first combined with ovalbumin as antigen and second with a C. difficile surface protein, the precursor of the S-layer proteins SlpA. Using ovalbumin as antigen, we compared the gut mucosal adjuvanticity of FliC to Salmonella Typhimurium flagellin and cholera toxin. Two routes of immunization were tested in a mouse model: intra-rectal and intra-peritoneal, following which, gut mucosal and systemic antibody responses against ovalbumin (Immunoglobulins G and Immunoglobulins A) were analyzed by Enzyme-Linked Immuno Assay in intestinal contents and in sera. In addition, ovalbumin-specific immunoglobulin producing cells were detected in the intestinal lamina propria by Enzyme-Linked Immunospot. Results showed that FliC as adjuvant for immunization targeting ovalbumin was able to stimulate a gut mucosal and systemic antibody response independently of the immunization route. In order to develop a mucosal vaccine to prevent C. difficile intestinal colonization, we assessed in a mouse model the efficacy of FliC as adjuvant compared with cholera toxin co-administrated with the C. difficile S-layer precursor SlpA as antigen. After challenge, a significant decrease of C. difficile intestinal colonization was observed in immunized groups compared to the control group. Our results showed that C. difficile FliC could be used as adjuvant in mucosal vaccination strategy against C. difficile infections.

Topics: Adjuvants, Immunologic; Animals; Antibodies, Bacterial; Bacterial Proteins; Bacterial Vaccines; Cell Count; Clostridioides difficile; Colony Count, Microbial; Enterocolitis, Pseudomembranous; Female; Flagellin; Immunity; Immunity, Mucosal; Immunization; Immunoglobulin G; Intestinal Mucosa; Membrane Glycoproteins; Mice, Inbred C57BL; Ovalbumin; Rectum; Vaccination

Topics: Animal Feed; Animals; Animals, Newborn; Bacteria; Cell Differentiation; Cortisone; Enterocolitis, Pseudomembranous; Female; Intestinal Absorption; Intestinal Mucosa; Intestine, Small; Liver; Maternal-Fetal Exchange; Ovalbumin; Pregnancy; Prenatal Exposure Delayed Effects; Rats; Rats, Inbred Strains; Stress, Physiological

Cortisone acetate is known to accelerate maturation of the immature intestine. The effect of prenatal administration of cortisone acetate on the morbidity and mortality of necrotizing enterocolitis was examined in a rat pup model. Pregnant rats were administered cortisone acetate, 20 mg/100 g of body weight, or normal saline by daily IP injection from day 18-21 of gestation. Rat pups were taken from the mothers before suckling was initiated, fed a simulated rat milk formula, and subjected to daily ischemic insults to produce an animal model of necrotizing enterocolitis. Both morbidity and the mortality rates were significantly improved with prenatal cortisone treatment. Maturation of the intestinal mucosal barrier was accelerated with the cortisone treatment as measured by decreased serum concentrations of a fed antigen, ovalbumin. Aerobic bacterial colonization of the small intestine and translocation of bacteria to the liver were decreased in the pups pretreated with steroids. These changes observed in a rat model of necrotizing enterocolitis may explain the decreased incidence of necrotizing enterocolitis in human infants born to mothers who received corticosteroids late in gestation.

Topics: Animals; Colony Count, Microbial; Cortisone; Disease Models, Animal; Enterocolitis, Pseudomembranous; Enzyme-Linked Immunosorbent Assay; Female; Humans; Intestinal Mucosa; Maternal-Fetal Exchange; Ovalbumin; Pregnancy; Rats; Rats, Inbred Strains

To evaluate the role of immunologic mechanisms in one specific syndrome of food intolerance in infants, food protein-induced enterocolitis, we measured class-specific serum antibodies to three food proteins, ovalbumin, soy, and cow milk, prior to diagnostic food challenges in 18 infants suspected to have this syndrome. Infants with positive challenge reactions to egg, soy, or cow milk had 5-10 times higher levels of IgA antibody directed against that food than did the infants with negative challenges. Levels of IgG antibody to soy and egg were also significantly higher (greater than 10-fold) in infants with positive challenge responses. There was no significant difference in levels of IgM food antibodies between the two groups. IgA anti-soy antibody levels rose in all 12 infants tested 2-10 weeks after a single soy feeding (challenge). However, IgM anti-soy antibody increased in the five infants who had a negative response to the challenge feeding and decreased in those seven with a positive response. The difference between the two groups was statistically significant (P less than 0.01). Some correlation existed (r = -0.68) between the increase in IgA anti-soy antibody and the decrease in IgM anti-soy antibody for infants with positive soy challenges. Although a pathogenic role for these antibodies is not proven, the findings suggest an altered immunologic response to ingestion of food antigens in infants with food protein-induced enterocolitis.

Topics: Antibodies; Antigens; Dietary Proteins; Enterocolitis, Pseudomembranous; Food Hypersensitivity; Glycine max; Humans; Immunoglobulin G; Immunoglobulin M; Infant; Milk Proteins; Ovalbumin