Feeding a diet containing a fructooligosaccharide mix can enhance Salmonella vaccine efficacy in mice.

Fructooligosaccharides (FOS) are considered prebiotics because of their ability to promote growth of specific beneficial gut bacteria, such as bifidobacteria. Some studies reported potential immune-modulating properties. The aim of this study was to investigate the effect of FOS:inulin mix on murine response to Salmonella vaccine and evaluate the relevance toward protection against Salmonella infection.

Supplementation of food with Enterococcus faecium (SF68) stimulates immune functions in young dogs.

The gut microflora play a crucial role in several physiologic functions of the host, including maturation of the gut-associated lymphoid tissues during the first months of life. Oral administration of probiotic lactic acid bacteria (LAB) modulates the immune system of humans and some laboratory animals. This effect has never been examined in dogs; therefore, our aim was to study the capacity of a probiotic LAB to stimulate immune functions in young dogs.

Divergent patterns of colonization and immune response elicited from two intestinal Lactobacillus strains that display similar properties in vitro.

Lactobacilli derived from the endogenous flora of normal donors are being increasingly used as probiotics in functional foods and as vaccine carriers. However, a variety of studies done with distinct strains of lactobacilli has suggested heterogeneous and strain-specific effects. To dissect this heterogeneity at the immunological level, we selected two strains of lactobacilli that displayed similar properties in vitro and studied their impact on mucosal and systemic B-cell responses in monoxenic mice.

Novel probiotics for the management of allergic inflammation.

Several pathologies of the gastrointestinal tract, particularly food allergy, are due to an exaggerated and imbalanced response of the gut mucosal immune system. The intestinal microflora is an important constituent of the gut mucosal barrier against food allergens and there is increasing evidence that one important acquired factor predisposing to food allergy in infants is the gut microflora. Indeed, the balance of bifidobacteria versus Clostridia in the neonatal flora appears to determine the allergic status in infants.

Suppression of specific and bystander IgE responses in a mouse model of oral sensitization to beta-lactoglobulin.

Background: Mechanisms of systemic IgE suppression by oral tolerance have been extensively studied, but less is known about oral tolerance induction in mice challenged at mucosal sites. We have previously shown in systemically challenged mice that high-dose tolerance suppressed specific but not bystander IgE. In an attempt to mimic oral tolerance in food-allergic patients, we have investigated how IgE suppression could be induced in mice sensitized orally against beta-lactoglobulin (BLG).

Induction by a lactic acid bacterium of a population of CD4(+) T cells with low proliferative capacity that produce transforming growth factor beta and interleukin-10.

We investigated whether certain strains of lactic acid bacteria (LAB) could antagonize specific T-helper functions in vitro and thus have the potential to prevent inflammatory intestinal immunopathologies. All strains tested induced various levels of both interleukin-12 (IL-12) and IL-10 in murine splenocytes. In particular, Lactobacillus paracasei (strain NCC2461) induced the highest levels of these cytokines.

Interferon gamma signaling alters the function of T helper type 1 cells.

One mechanism regulating the ability of different subsets of T helper (Th) cells to respond to cytokines is the differential expression of cytokine receptors. For example, Th2 cells express both chains of the interferon gamma receptor (IFN-gammaR), whereas Th1 cells do not express the second chain of the IFN-gammaR (IFN-gammaR2) and are therefore unresponsive to IFN-gamma. To determine whether the regulation of IFN-gammaR2 expression, and therefore IFN-gamma responsiveness, is important for the differentiation of naive CD4(+) T cells into Th1 cells or for Th1 effector function, we generated mice in which transgenic (TG) expression of IFN-gammaR2 is controlled by the CD2 promoter and enhancer.

The induction of a protective response in Leishmania major-infected BALB/c mice with anti-CD40 mAb.

A protective immune response to the intracellular parasite Leishmania major requires the development of a Th1 CD4+ T cell phenotype. We demonstrate herein that BALB/c mice, which normally develop a susceptible Th2 response to L. major infection, are protected when co-injected with an agonistic anti-murine CD40 mAb.

A role for B cells in the development of T cell helper function in a malaria infection in mice.

B cell knockout mice are unable to clear a primary erythrocytic infection of Plasmodium chabaudi chabaudi. However, the early acute infection is controlled to some extent, giving rise to a chronic relapsing parasitemia that can be reduced either by drug treatment or by adoptive transfer of B cells. Similar to mice rendered B-cell deficient by lifelong treatment with anti-mu antibodies, B cell knockout mice (muMT) retain a predominant CD4+ Th1-like response to malarial antigens throughout a primary infection.

Altered erythrocytes and a leaky block in B-cell development in CD24/HSA-deficient mice.

The heat stable antigen (HSA, or murine CD24) is a glycosyl phosphatidylinositol-linked surface glycoprotein expressed on immature cells of most, if not all, major hematopoietic lineages, as well as in developing neural and epithelial cells. It has been widely used to stage the maturation of B and T lymphocytes because it is strongly induced and then repressed again during their maturation. Terminally differentiated lymphocytes, as well as most myeloid lineages, are negative for HSA.

Early production of IL-4 and induction of Th2 responses in the lymph node originate from an MHC class I-independent CD4+NK1.1- T cell population.

Splenic CD4+NK1.1+ T cells have been shown to secrete large and transient amounts of IL-4 mRNA 90 min after i.v.

Gene-targeted mice lacking B cells are unable to eliminate a blood stage malaria infection.

Mice deficient of mature B cells due to a targeted disruption of the transmembrane exon of the Ig mu-chain gene (mu-MT mice) can reduce a primary acute infection with the malaria parasite Plasmodium chabaudi chabaudi (AS strain) to low levels but are unable to eliminate parasites and instead develop chronic relapsing parasitemias. This model of B cell deficiency confirms previous findings using anti-mu-treated mice that B cells are required for final parasite clearance. Injection of B cells from immune donors into chronically infected mu-MT mice enabled them to clear their infection within 1 wk.

A proline-rich TGF-beta-responsive transcriptional activator interacts with histone H3.

The molecular mechanisms involved in the regulation of gene expression by transforming growth factor-beta (TGF-beta) have been analyzed. We show that TGF-beta specifically induces the activity of the proline-rich trans-activation domain of CTF-1, a member of the CTF/NF-I family of transcription factors. A TGF-beta-responsive domain (TRD) in the proline-rich transcriptional activation sequence of CTF-1 was shown to mediate TGF-beta induction in NIH-3T3 cells.

The immune response to Plasmodium chabaudi malaria in interleukin-4-deficient mice.

Interleukin(IL)-4 promotes the development of T helper (TH)2 cells, induces immunoglobulin class switching to IgG1 and is thought to be essential for switching to IgE. During a primary infection with the erythrocytic stages of Plasmodium chabaudi chabaudi, TH1 and TH2 cells specific for the parasite appear sequentially as infection progresses. To dissect the possible role of TH2 responses at the later stages of infection, mice with a targetted disruption of the IL-4 gene were infected with P.

A dual role for B cells in Plasmodium chabaudi chabaudi (AS) infection?

CD4+ T cells are necessary for a protective immune response against the erythrocytic stages of the malaria parasite Plasmodium chabaudi chabaudi AS. B cells are not required for control of early acute parasitaemias, but appear to be important for final clearance of the infection, most probably by producing specific antibodies against the parasite. However, immune sera and immune IgG are unable to replace the protective capacity of B cells in adoptive transfer of immunity to P.

The roles of cytokines produced in the immune response to the erythrocytic stages of mouse malarias.

This review describes the role of cytokines produced by CD4+ T cells and macrophages in response to the erythrocytic stages of P. chabaudi chabaudi and other malaria infections in mice. Since virtually all compartments of the immune system are activated during the response against malaria, the variety of cytokines produced during infection is considerable.

Altered response of CD4+ T cell subsets to Plasmodium chabaudi chabaudi in B cell-deficient mice.

Mice depleted of B cells from birth by treatment with anti-mu antibodies can control but not clear an infection with the malaria parasite Plasmodium chabaudi chabaudi (AS). Splenic CD4+ T cells from these mice were unable to mount a significant Th2 response to the parasite in vitro as shown by much lower precursor frequencies of Th cells for antibody production and of IL-4-producing cells compared with the response of control-treated mice. CD4+ T cells of the anti-mu-treated mice which respond to antigens of P.