Similar to cytokines above, quantitation revealed that vaccinatio

Similar to cytokines above, quantitation revealed that vaccinations did not increase the levels of salivary mucin expression, with, if anything, a decrease in mucin expression relative to infected, non-vaccinated mice (Fig. 4). Vaccination strategies against H. pylori have thus far proven inadequate this website due to their typical inability to reliably produce complete protection. The development

of a truly effective vaccine against H. pylori is severely hindered by our lack of understanding of host mechanisms involved in protective immunity against this infection. In this study we followed on from a previous observation by Shirai et al. which indicated that vaccine-mediated protection against H. pylori requires salivary glands, but for which a mechanism was lacking [11]. As the majority of H. pylori reside in mucus lining the gastric mucosa where they are exposed to secreted mucins, we theorized that mucin secretion by salivary Sirolimus datasheet glands could explain this observation. However, we found no evidence to suggest that vaccination produces any increase in immune response in the salivary glands. Cytokine and mucin expression levels were actually lower

in vaccinated/challenged mice compared with infected or uninfected controls, which in fact demonstrates an inverse correlation with the effector stage of protection. Shirai et al. concluded that salivary glands were important in the induction of protective

immunity, as sialoadenectomy 上海皓元 prior to vaccination against H. pylori removed vaccine efficacy [11]. However, they also found that salivary glands were important for long-term maintenance of vaccine-induced protection. The current study was not designed to evaluate the role of mucins in the initial induction of protective immunity, as we envisage that secreted salivary mucins are unlikely to play a role in immune induction. Hence a theoretical role for mucins in vaccine-mediated induction of protection against H. pylori cannot be completely ruled out by this study, although the mechanism by which this may occur is unclear. Rather, by their nature, we hypothesized that secreted salivary mucins may play an important role in the effector/maintenance stage of this protection; the data presented in this study argue against this theory. Another major product of salivary glands is immunoglobulin A (IgA) which is the main antibody isotype secreted into the gastrointestinal tract. The increased protein levels found in the salivary glands of vaccinated mice in this study correlated with an increase in IgA production which is completely consistent with current dogma regarding mucosal immune response to gastrointestinal vaccination and infection. This is further supported by Shirai et al., who showed that sialoadenectomized mice had less than half the levels of gastric and fecal IgA than did control animals [11].

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