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Mucosal nasopharyngeal immune responses of horses to protein antigens of Streptococcus equi.

Mucosal nasopharyngeal immunoglobulin A (IgA) and IgG responses to proteins of Streptococcus equi were studied in horses after the experimental production of strangles. S. equi-specific IgA and IgG titers in nasopharyngeal mucus were much higher in samples from animals 1 to 2 weeks after challenge than in samples from control animals. Although IgA was the major immunoglobulin in nasal mucus, there was more antibody activity associated with IgG as measured by radioimmunoassay. Great differences between the specificities of antibodies in nasal mucus and in serum were detected. IgA and IgG of mucus origin recognized only two major proteins with molecular weights of about 41,000 and 46,000 in acid extracts of S. equi and gave no detectable reaction with culture supernatant proteins. Only one protein of about 62,000 molecular weight was recognized in acid extracts of an equine strain of S. zooepidemicus. In contrast, immunoglobulins in serum recognized a great variety of proteins in culture supernatants and acid extracts of S. equi and S. zooepidemicus which did not include those proteins recognized by immunoglobulins in mucus. These findings provide good evidence for the independence of the local and systemic immune responses of the horse to S. equi. Horses rechallenged shortly after recovery from the first infection were resistant to challenge with an inoculum of S. equi 10 times greater than that to which they were originally susceptible. This resistance appeared to be independent of the levels of bactericidal antibody in serum. We therefore suggest that immunity to S. equi infection is mediated by locally produced nasopharyngeal antibodies.

Animals↗

The liquid culture filtrates of Paecilomyces tenuipes (Peck) Samson (=Isaria japonica Yasuda) and Paecilomyces cicadae (Miquel) Samson (=Isaria sinclairii (Berk.) Llond) regulate Th1 and Th2 cytokine response in murine Peyer's patch cells in vitro and ex vivo.

The effects of liquid culture filtrates of medicinal entomogenous fungi, Paecilomyces tenuipes (Peck) Samson (=Isaria japonica Yasuda or Isaria tenuipes) (PTCF) and Paecilomyces cicadae (Miquel) Samson (=Isaria sinclairii (Berk.) Llond) (PCCF), on cytokine productions in cultured Peyer's patches (PP) from C57BL/6J mice were investigated in vitro and ex vivo. In an in vitro experiment, PTCF (100 and 10 microg/ml) enhanced the production of T helper 1 (Th1) cytokines, interleukin (IL)-2 and interferon (IFN)-gamma, in cultured PP cells stimulated with 5 microg/ml concanavalin A (Con A) but did not influence on the production of T helper 2 (Th2) cytokines, IL-4 and IL-5. PTCF also enhanced the production of granulocyte macrophage colony-stimulating factor (GM-CSF) and IL-10 in the cultured PP cells. While, PCCF enhanced the production of IFN-gamma but did not alter the level of IL-2 in the PP cells. In an ex vivo experiment using PP cells removed from the mice after oral treatment of PTCF (10 and 100 mg/kg daily for 7 consecutive days), the production of IL-2 and IFN-gamma were increased in response to Con A. On the other hand, orally treated PCCF (10 mg/kg/day) suppressed IL-2 production but did not change the levels of IFN-gamma and IL-10 in the isolated PP cells. The flow cytometric analysis revealed that the population of CD3(+) cells in the PP cells slightly but significantly increased after oral administration of PCCF. Orally administered PTCF did not change the population of T (CD3(+)), B (CD19(+)), T cell subset (CD4(+)and CD8(+)) and Th1 (IFN-gamma(+)) and Th2 (IL-4(+)). From PTCF, the fraction rich in proteoglycans was separated as active fraction that stimulates Th1 immune response. These results indicate that the mode of action of PTCF and PCCF on mucosal immune response is different and this is contributed to their metabolites. Taken together, there is a possibility of PTCF and PCCF being therapeutic or preventive agents for immune diseases such as cancer, allergy and parasitic disease through activation of mucosal immune response.

Animals↗

Abnormalities in intestinal mucosal T cells in homosexual populations including those with the lymphadenopathy syndrome and acquired immunodeficiency syndrome.

Enteric infections are common in homosexual men. We have characterized the phenotypic distribution of small intestinal mononuclear cells among healthy homosexual men, homosexual men with lymphadenopathy syndrome, homosexual men with acquired immunodeficiency syndrome (AIDS), and a group of healthy heterosexual men. Total numbers of T lymphocytes in the small intestinal mucosa were significantly decreased in homosexual men with lymphadenopathy syndrome and AIDS. This decrease was most striking among the Leu-3a T-cell subset usually associated with helper/inducer function. The proportion of mucosal T cells reacting with Leu-2a (cytotoxic/suppressor phenotype) and lymphoid cells having the T305 antigen was significantly increased only in AIDS subjects. Both lymphadenopathy syndrome and AIDS subjects had a significant reversal of the normal mucosal helper/suppressor T-cell ratio. Mucosal helper/suppressor T-cell ratios and the distribution of mucosal mononuclear cells were normal in healthy homosexual men, although the same individuals had reversed helper/suppressor ratios among circulating T cells. Enteric infections in healthy homosexual men likely reflect sexual practices, and not a primary abnormality in intestinal mucosal immunity. In contrast, specific abnormalities in intestinal mucosal immunity may contribute to the persistent and opportunistic enteric infections that occur in AIDS.

Acquired Immunodeficiency Syndrome↗

Mucosal IgA elaboration.

Secretory IgA is the main immunoglobulin present along mucosal surfaces. It is elicited best by oral rather than parenteral administration of specific antigens. The role of antigen form on the development of a secretory IgA response is still unclear. IgA protects by preventing attachment of microorganisms or their toxic products to the surface epithelium. A wide variety of regulatory T cells are now known to be of considerable importance in optimizing the secretory IgA response. This regulation is at least partly due to the elaboration of small polypeptide products (lymphokines). These lymphokines have been shown to be key signals during the maturation of IgA precursor B cells to IgA-secreting plasma cells. By studying models of the mucosal immune system which closely approximate the natural mucosal immune response, it should be possible to develop vaccines against many pathogenic microorganisms, their toxic products, and to toxicants and carcinogens within the environment.

Animals↗

Intranasal immunisation with influenza-ISCOM induces strong mucosal as well as systemic antibody and cytotoxic T-lymphocyte responses.

Intranasal administration of vaccines is preferred for induction of mucosal immune responses. In this study, mice were immunised intranasally and subcutaneously with influenza-immuno stimulating complexes (influenza-ISCOM). The intranasal dose was 15-times the subcutaneous dose. All mice dosed with influenza-ISCOMs survived challenge with live virus and comparable serum antibody and splenic cytotoxic T-lymphocyte responses were detected in both groups. Induction of mucosal IgA was significantly higher with intranasal immunisation and was comparable to responses induced with the heat labile enterotoxin of Escherichia coli as adjuvant. These findings demonstrate that intranasal administration of high dose influenza-ISCOM results in potent systemic and mucosal immune responses.

Adjuvants, Immunologic↗

Mucosal responses to parenteral and mucosal vaccines.

Most human pathogens are acquired through mucosal portals of entry, and replicate in the mucosal tissues. Subsequently, the infecting agent may invade the blood stream and produce disease at distant systemic sites. However, a large number of pathogenic organisms are limited to development of disease only at the site of initial mucosal replication. Studies carried out with naturally acquired infections and mucosally delivered vaccines have provided strong evidence for the existence of a common mucosal immune system in the organized lymphoid follicles in respiratory and intestinal epithelium, and in the mucosa of genital tract, mammary glands, conjunctiva, upper airways, and the middle ear cavity. Mucosal application of live attenuated oral poliovaccine (OPV), rubella virus vaccine (RA 27/3), adenoviruses, influenza A virus, rotavirus, salmonella, and cholera vaccines have demonstrated consistent development of secretory IgA, serum antibody, and cellular immune responses. Mucosal immunization appears to result in preferential expression of several integrins and cell adhesion molecules associated with homing of lymphocytes to mucosal sites of immunization. Induction of mucosal immune responses often result in specific protection against reinfection challenge and against illness. Replicating agents introduced via the parenteral route also result in the development of mucosal responses and protection against systemic illness. Parenteral immunization with non-replicating agents often fails to induce specific mucosal responses. Such immunization, however, is quite effective in mounting high levels of serum antibody with development of protection against systemic illness. Parenteral vaccines, such as enhanced potency inactivated polio vaccine (eIPV), Haemophilus influenzae type B (HIB), hepatitis B virus (HBV), and other non-mucosal vaccines, have been highly effective in preventing systemic disease during subsequent exposure to natural infection. Recent evidence has shown that parenteral immunization can also be quite effective in inducing varying degrees of functional mucosal antibody responses as detected by ELISA and less frequently by neutralization. Systemic illnesses such as poliomyelitis and Haemophilus influenzae meningitis and community circulation of these agents has been eliminated or significantly limited in many parts of the world with the exclusive use of inactivated vaccines. Based on these observations, it is suggested that development of serum immunological responses are effective in the prevention of systemic disease regardless of the types of vaccines or route of their administration. However, induction of pathogen-specific antibody or cellular immunity at the mucosal sites is best elicited by mucosal application of the antigen.

Antibodies, Viral↗

Vaccination against enteric bacterial diseases.

We review evidence that the systemic and mucosal immune systems of the body are compartmentalized. The development of immunity against an antigen at one mucosal surface may lead to the appearance of that immunity at other mucosal surfaces. In order to attain good protective immunity against a bacterial enteropathogen, it may be necessary to induce such immunity through the mucosal immune system of the gut. Earlier attempts to elicit protective immunity against bacterial enteropathogens by parenteral vaccination are reviewed. The modern approach involves oral administration of antigen. Such antigen may consist of killed bacteria or--more effectively--live, attenuated bacteria bearing antigens of interest. Such bacteria may be enteropathogens attenuated by mutation, either general or site-directed, or hybrid strains in which a bacterial carrier expresses an antigenic determinant of interest from cloned DNA. While good progress has been made in the comprehension of the requirements for effective vaccination against enteropathogenic bacteria, future work will produce more effective carrier strains than are currently available.

Administration, Oral↗

Coincidence of different structures of mucosa-associated lymphoid tissue (MALT) in the respiratory tract of children: no indications for enhanced mucosal immunostimulation in sudden infant death syndrome (SIDS).

Mucosa-associated lymphoid tissue (MALT) is the principal inductive site for mucosal immune responses that are capable of T and B cell responses and antigen-specific responses. In previous independent studies different structures of MALT, e.g. bronchus-, larynx- and nose-associated lymphoid tissue (BALT, LALT, NALT) have been described separately in various frequencies in the human respiratory tract over life spans. Because upper respiratory tract infections are common in infants, dysregulations of mucosal immune responses might be seriously involved in the aetiology of sudden infant death syndrome (SIDS). In the present study the coincidental occurrence of the three different MALT structures in the respiratory tract within the same patients were studied, and cases of SIDS and children who had died from different traumatic and natural causes of death (non-SIDS) were compared. First, the frequency of BALT and LALT in 46 children (35 SIDS, 11 non-SIDS) with or without NALT were examined. A tendency was found of a coincidence of respiratory MALT structures. In 50 additional cases of infant death (30 SIDS, 20 non-SIDS) from the multi-centric German Study on Sudden Infant Death Syndrome (GeSID) where death had occurred in the first year of life, the coincidence was evaluated. A coincidental occurrence of BALT, LALT and NALT or BALT and LALT (each about 30%) was found in both groups, whereby the coincidence in SIDS and the control patients did not differ. Interestingly, the children with coincidental MALT were strikingly older, supporting the hypothesis of respiratory MALT formation via environmental stimulation over time.

Bronchi↗

Intestinal and systemic humoral immunological events in the susceptible Balb/C mouse strain after oral administration of Echinococcus multilocularis eggs.

The aim of the study was to investigate the systemic and, for the first time, the intestinal humoral events in the susceptible Balb/C mouse strain after oral administration of Echinococcus multilocularis eggs. Thirty-one mice were divided into three groups; W-2, W-8 and control group. Each mouse of the W-2 and W-8 groups was orally infected with 1,500 E. multilocularis eggs, two weeks and eight weeks before sacrifice respectively. Control group mice received phosphate buffer saline. Measurement of anti-E. multilocularis and non-specific IgG, IgA and IgM, and of a transudation marker, albumin, were performed in serum and intestinal washings by a time-resolved immunofluorometric assay. These results were complemented by microscopic examination of the intestinal mucosa. This infection model is well-suited to the study of mucosal immunity during alveolar echinococcosis. It showed a major specific intestinal response in the early stage of the disease whereas the systemic response predominated later in the disease. Histopathological studies and calculation of the relative coefficient of excretion of Ig also confirmed that the presence of the parasite, even during a short period, was responsible for a local immunological and inflammatory response and for a change in mucosal permeability. Mucosal immunity could thus play a role in tolerance induction against E. multilocularis that could be a prerequisite for the subsequent development of the larvae in the liver, and for the occurrence of the parasitic disease, alveolar echinococcosis.

Animals↗

Intestinal B cell hyperactivity in AIDS is controlled by highly active antiretroviral therapy.

BACKGROUND: It is well documented that highly active antiretroviral therapy (HAART) restores systemic immunity to human immunodeficiency virus (HIV) but the effect of this treatment on the mucosal immune system is less clear. AIMS: Because future preventive or therapeutic vaccines against HIV may be administered by the mucosal route, we wished to evaluate the effect of HAART on the activation level and homeostasis of the intestinal B cell system. PATIENTS AND METHODS: Duodenal biopsy specimens were collected consecutively from infection prone HIV positive adults (n = 31), mostly with advanced AIDS. In situ two colour immunofluorescence staining was performed to quantify mucosal immunoglobulin (Ig) class and subclass producing immunocytes (plasmablasts and plasma cells). RESULTS: HIV positive patients had, on average, duodenal proportions of IgA (74.6%), IgM (19.5%), and IgG (3.4%) immunocytes similar to median values recorded in 11 HIV seronegative healthy controls but the total immunocyte number per mucosal section length unit (500 microm) was significantly increased in patients (median 175 v 120 cells/unit; p<0.008), mainly comprised of IgA (p<0.02) and IgG1 (median 81.8% of total IgG; p<0.02) isotypes. Patients receiving a successful HAART regimen tended to normalise their IgG1 proportion and showed significantly lower total duodenal IgA immunocyte number than those receiving no or insufficient antiretroviral treatment (p<0.005). CONCLUSION: Our study demonstrated that advanced AIDS patients hyperactivate their intestinal B cell system. HAART could significantly reverse this perturbation, suggesting restored ability of the mucosal immune system to control intestinal infections.

Acquired Immunodeficiency Syndrome↗

Is there a role of food allergy in irritable bowel syndrome and functional dyspepsia? A systematic review.

A significant proportion of adults believe they suffer from food allergy, and 20-65% of patients with irritable bowel syndrome (IBS) attribute their symptoms to something in food that activates an abnormal response. This systematic review evaluates the role of food allergy in aetiology and management of these disorders. Activation of gastrointestinal mucosal immune system may be one of the causative factors in the pathogenesis of functional dyspepsia and IBS. This activation may result from effects of bacterial infection or other luminal factors including commensal microbial flora and food antigens. Some studies have reported on the role of food allergy in IBS; only one epidemiological study on functional dyspepsia and food allergy has been published. The mechanism by which food activates mucosal immune system is uncertain, but food specific IgE and IgG4 appeared to mediate the hypersensitivity reaction in a subgroup of IBS patients. Exclusion diets based on skin prick test, RAST for IgE or IgG4, hypoallergic diet and clinical trials with oral disodium cromoglycate have been conducted, and some success has been reported in a subset of IBS patients. Further well-controlled studies are needed to establish whether food allergy plays a role in the pathophysiology of functional dyspepsia and IBS.

Adult↗

Cholera toxin adjuvant greatly promotes antigen priming of T cells.

Cholera toxin (CT) given perorally is a powerful mucosal immunogen and adjuvant. Information that explains the adjuvant effect of CT may be used for the development of more effective oral vaccines and might also contribute to our understanding of the mechanisms involved in regulating mucosal immunity. The present study was undertaken to investigate if CT administered together with keyhole limpet hemocyanin (KLH) would act to promote or inhibit priming of KLH-specific T cells and whether the adjuvant effect of CT is restricted to mucosal immune responses or is a generalized phenomenon due to direct immunomodulating effects of CT. We found that CT adjuvant greatly augmented the effectiveness of a single oral priming immunization with KLH: re-challenge with KLH in vitro 1 week following immunization gave several-fold stronger proliferation in KLH-specific spleen, mesenteric lymph node, Peyer's patch and gut lamina propria T cells from KLH + CT adjuvant as opposed to KLH only-treated mice. Moreover, several-fold stronger cytokine production, i.e. interleukin (IL)-2, IL-4, IL-5, IL-6, IL-10 and interferon-gamma accompanied the enhanced proliferative response of T cells from CT adjuvant-treated mice. The adjuvant effect of CT was not restricted to mucosal immune responses but was evident also following a single parenteral immunization with KLH + CT. Limiting dilution analysis revealed that CT adjuvant promoted a 20- to 40-fold increase in the frequency of primed KLH-specific T cells. Phenotypic and functional analyses clearly demonstrated that CT adjuvant primarily enhanced priming of CD4+ rather than CD8+ T cells and the pattern of lymphokine secretion disclosed that CT most probably promoted antigen priming of both Th1 and Th2 type of CD4+ T precursor cells.

Adjuvants, Immunologic↗

Influence of the gastrointestinal microbiota on development of the immune system in young animals.

The gastrointestinal tract (GIT) of adult mammals is colonized by a complex and dynamic community of microorganisms. Most protection against potential pathogens occurs via a mucosal immune system involving mechanisms of innate immunity as well as a secondary lymphoid organ, the gut-associated lymphoid tissue (GALT). However, the bacterial community also supports its host against invasion by potential pathogens, by a mechanism called 'colonization resistance'. Young animals need time to develop both a complex bacterial community and their immature GIT immune system, and until such developments have taken place, they are vulnerable to the presence of potential pathogens in their GIT. Initial protection against invading pathogens is provided by milk and colostrum, which contain antibodies and other bioactive components. At weaning, with the introduction of solid food and deprivation of the mother's milk, the young must also cope with a rapidly changing microbiota. The colonizing microbiota not only provides colonization resistance to potentially pathogenic bacteria. It also has a major role in the development of the intestinal immune system, both in terms of GALT development and mucosal immunity, and the induction of oral tolerance. Studies using gnotobiotic animal models have revealed that the presence of even limited numbers of the indigenous microbiota may influence the GIT immune system. Regulation of the composition of the GIT microbiota, e.g. by the use of pre- and probiotics, offers the possibility to influence the development of mucosal, and also systemic immunity.

Animals↗

Recovery of gut-associated lymphoid tissue and upper respiratory tract immunity after parenteral nutrition.

OBJECTIVE: The authors characterize the recovery of parenteral nutrition-induced changes in gut-associated lymphoid tissue (GALT) and upper respiratory tract immunity with enteral nutrition and provide further information defining the effects of enteral feeding on mucosal immunity. SUMMARY BACKGROUND DATA: The small intestine plays a prominent role in development and maintenance of mucosal immunity, both intestinal and extraintestinal, primarily through immunoglobulin A (IgA)-mediated mechanisms. Prior research has shown that mice fed total parenteral nutrition (TPN) have reduced GALT T and B cells, the cells responsible for IgA production, as well as impaired upper respiratory tract immunity to viral challenge of previously immunized animals. The recovery of TPN-induced changes in GALT and upper respiratory tract immunity after enteral refeeding is studied. METHODS: Male institute of Cancer Research mice received 5 days of TPN followed by 0 to 4 days of chow. Small intestinal GALT was characterized by flow cytometry. In a second experiment, animals were immunized intranasally with moused-adapted influenza virus. Three weeks later, one group received a 5-day course of TPN followed by enteral refeeding for 5 days. A second group received TPN alone. Both groups were challenged with intranasal virus and killed 40 hours postchallenge to determine viral shedding from the upper respiratory tract. RESULTS: Animals fed TPN only had significantly fewer GALT lymphocytes compared with those chow-fed control subjects. Peyer's patch counts increased after a single day of refeeding, returning to normal levels by 48 hours. Lamina propria counts remained significantly depressed after 24 hours of refeeding, but also returned to normal after 48 hours of refeeding. The T-cell and B-cell populations mimicked total cell patterns. Lamina propria CD4+/CD8+ ratio returned to normal only after 72 hours of refeeding. None of the 9 animals refed enterally for 5 days were positive for viral shedding, compared with 8 of 12 matched TPN-fed animals. CONCLUSIONS: Enteral refeeding after TPN is associated with rapid repletion of GALT cellularity, initially within Peyer's patches and subsequently within the lamina propria. Refeeding corrects the impairment of IgA-mediated upper respiratory tract antiviral immunity occurring with TPN administration. This work further enhances the authors' knowledge of the underlying immunologic differences influenced by routes of nutrition.

Animals↗

Role of the glycocalyx in regulating access of microparticles to apical plasma membranes of intestinal epithelial cells: implications for microbial attachment and oral vaccine targeting.

Transepithelial transport of antigens and pathogens across the epithelial barrier by M cells may be a prerequisite for induction of mucosal immunity in the intestine. Efficient transport of antigens and pathogens requires adherence to M cell apical surfaces. Coupling of antigen-containing particles to the pentameric binding subunit of cholera toxin (CTB) has been proposed as a means for increasing antigen uptake because the CTB receptor, ganglioside GM1, is a glycolipid present in apical membranes of all intestinal epithelial cells. To test the accessibility of enterocyte and M cell membrane glycolipids to ligands in the size ranges of viruses, bacteria, and particulate mucosal vaccines, we analyzed binding of CTB probes of different sizes to rabbit Peyer's patch epithelium. Soluble CTB-fluorescein isothiocyanate (diameter 6.4 nm) bound to apical membranes of all epithelial cells. CTB coupled to 14 nm colloidal gold (final diameter, 28.8 nm) failed to adhere to enterocytes but did adhere to M cells. CTB-coated, fluorescent microparticles (final diameter, 1.13 microns) failed to adhere to enterocytes or M cells in vivo or to well-differentiated Caco-2 intestinal epithelial cells in vitro. However, these particles bound specifically to GM1 on BALB/c 3T3 fibroblasts in vitro and to undifferentiated Caco-2 cells that lacked brush borders and glycocalyx. Measurements of glycocalyx thickness by electron microscopy suggested that a relatively thin (20 nm) glycocalyx was sufficient to prevent access of 1-micron microparticles to glycolipid receptors. Thus, the barrier function of the intestinal epithelial cell glycocalyx may be important in limiting microbial adherence to membrane glycolipids, and in CTB-mediated targeting of vaccines to M cells and the mucosal immune system.

3T3 Cells↗

Organizing a mucosal defense.

Gastrointestinal associated lymphoid tissue can be divided into loosely organized effector sites, which include the lamina propria and intraepithelial lymphocytes, and more organized structures, such as mesenteric lymph nodes (LNs), Peyer's patches (PPs), isolated lymphoid follicles, and cryptopatches (CPs). These organized structures in the gastrointestinal tract have been hypothesized to play the role of primary lymphoid organ, supporting the extrathymic development of T lymphocytes (CPs), secondary lymphoid organs involved in the induction of the mucosal immune response (PPs), and tertiary lymphoid structures whose function is still under debate (isolated lymphoid follicles). The most widely studied lymphoid structure found in the small intestine is the PP. PPs are secondary lymphoid structures, and their development and function have been extensively investigated. However, single lymphoid aggregates resembling PPs have been also described in humans and in the murine small intestines. These isolated lymphoid follicles have both germinal centers and an overlying follicle-associated epithelium, suggesting that they also can function as inductive sites for the mucosal immune response. This review compares and contrasts the development and function of the four main organized gastrointestinal lymphoid tissues: CPs, isolated lymphoid follicles, PPs, and mesenteric LNs.

Animals↗

Human immunity to rotavirus.

Rotaviruses are the most important cause of severe gastro-enteritis in infants and young children. However, the determinants of protective immunity are poorly understood. Human immunity to rotavirus can be acquired passively or actively. It may be humoral or cell-mediated, protective or non-protective, homotypic or heterotypic and mucosal or systemic, or any combination of these. Mucosal immunity is protective against rotavirus illness, but not against infection, whereas systemic immunity reflects exposure, but probably has little if any role in protection. Both local and cell-mediated immunity are likely to be important in protection. However, there is no agreement as to a reliable surrogate marker of small intestinal protective immunity, and little is known about small intestinal cell-mediated immunity in man, especially infants. Passive mucosal immunity, but not systemic immunity, may contribute to protection in breast-fed infants, and in those at increased risk of serious illness who have been given oral immunoglobulin, either as prophylaxis or therapeutically. Animal and adult studies may have only limited relevance to those who are at greatest risk of serious illness. However, it is probably from such studies that hypotheses about small intestinal cell-mediated immunity in the protection of infants against rotavirus infection in man remain unclear, and this continues to hinder vaccine research.

Animals↗

Immunological effects of yogurt addition to a re-nutrition diet in a malnutrition experimental model.

The therapeutic and preventive effects of yogurt and lactic acid bacteria on diseases such as cancer, infection and gastrointestinal disorders are well ocumented. The aim of this research was to study the effects of different doses of yogurt addition after milk re-nutrition diet, on the recovery of the intestinal barrier and mucosal immune function. Experiments were performed on groups of mice, malnourished and re-nourished with milk during 7 d, and mice with diet supplemented with yogurt for 2, 5 and 7 consecutive d. Nutritional parameters such as weight gain, serum total protein, and the number of IgA, IgM and IgG B cells of the small intestine were determined. We also quantified intraepithelial leukocytes, mastocytes and goblet cells, and performed structural and ultrastructural studies on the small intestine. We observed that 5 d of yogurt feeding was the optimal dose for improving gut barrier function and mucosal immune system in a malnutrition model. This effect was not observed with milk re-nutrition. Although the results were better for 5 d of yogurt, addition for 7 d also showed beneficial effects. Yogurt feeding in our model did not impair any gut functions. These results suggest that yogurt addition after a re-nutrition diet gives better recovery of intestinal function than the re-nutrition diet usually recommended. Although these results were obtained in an animal model, they indicate that consumption of yogurt by malnourished children might accelerate the restoration of gut function.

Animals↗