pylori [11] While removal of the salivary glands from these anim

pylori [11]. While removal of the salivary glands from these animals also resulted in a large decrease in total IgA levels in their gastric mucosa and feces [11], numerous

studies using antibody-deficient mice have shown that immunoglobulins are not required for H. pylori vaccine efficacy [5, 12, 13]. Thus any failure of vaccinations in sialoadenectomised mice would not be due to a loss of antibody secretion into the gastrointestinal tract. However, the actual explanation for the observation made by Shirai et al. remains unknown. Another important product of salivary glands are the secretory mucins. Previously, we have hypothesized that the effector stage of vaccine-induced protection against H. pylori may be mediated by the production of mucins [14]. Mucins comprise a family of heavily glycosylated glycoproteins that are either cell surface expressed or secreted, where they can constitute a major component find more of mucus. Such mucins form an intrinsic part of Bafilomycin A1 mouse the barrier system lining the gastrointestinal tract that protects against bacterial infection [15]. We have previously demonstrated that the cell surface gastric mucin Muc1/MUC1 (mouse/human) plays a critical role in regulating the inflammatory response to H. pylori infection, and also restricts the ability of these bacteria to attach to the epithelial cell surface by acting as a releasable decoy [16, 17]. Importantly, mucin secretion can

be regulated by the 上海皓元 acquired immune response including CD4+ T helper cells [18, 19], and therefore may potentially be influenced by memory responses to previous infections, or even vaccinations. We therefore

theorized that if salivary glands play a role in vaccine-mediated protection against H. pylori this could be implemented by the migration of adaptor T helper cells into the salivary glands, and modifications in the production of salivary mucins. To examine this possibility, we examined the effect of vaccination and H. pylori infection on the expression of cytokines and mucins in murine salivary glands. Helicobacter pylori strain SS1 [20] was grown on horse blood agar plates [Blood Agar Base No. 2, 2.5 μg/mL Amphotericin B (Sigma, St Louis, MO, USA) and Skirrow's Selective Supplements (Oxoid, Basingstoke, UK) and 5% horse blood (Biolab, Melbourne, Vic, Australia)] in an anaerobic jar with a microaerophilic gas generating kit (Oxoid) for 2 days at 37 °C. For infection of mice, bacteria were subcultured into brain heart infusion broth (BHI; Oxoid) containing 0.02% Amphostat and 5% horse serum (Sigma) and grown in microaerophilic conditions for 24 hours at 37 °C. Animal experimentation was performed under institutional guidelines and with approval from the University of Melbourne Animal Ethics Committee. Groups of age-matched, female C57BL/6 mice were dosed orogastrically with 100 μL of either 1, PBS (unvaccinated); or 2, 100 μg H. pylori SS1 lysate plus 10 μg cholera toxin (Sigma) (vaccinated).

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