The basic premise of vaccinology is to achieve strong protective immunity against defined infectious agents by a vaccine mimicking the effects of natural primary exposure to a pathogen. Because an exposure of humans and animals to microbes occurs mostly through mucosal surfaces, targeting the mucosa seems a rational and efficient vaccination strategy. Many experimental and clinical data confirmed that mucosal immunization offers many advantages over widely used in human and veterinary medicine subcutaneous or intramuscular immunization. In the present article selected aspects regarding mucosal vaccination are discussed. The structure and function of mucosaassociated lymphoid tissue (MALT), comprised of four main mucosal compartments forming a structural and functional unity as well as pivotal cellular MALT components (dendritic and M cells) were briefly characterized. Particular attention was focused on the mode of simple but efficacious delivery of vaccine antigens to mucosal surfaces. A few trials to generate potential mucosal vaccines against toxoplasmosis introduced by nasal or oral routes to experimental animals are also presented.
Even though there is no general agreement as to the mechanism of gastric mucosal protection, the consensus is that the initial brunt of luminal insults falls on the mucus layer which constitutes the only identifiable physical barrier between the gastric lumen and the mucosal surface. The continuous renewal and resilient nature of this layer efficiently counters peptic erosion of the gel, assures its viscoelastic and permselective properties, and provides a milieu for containment of the diffusing luminal acid by mucosal bicarbonate. Disturbances in this delicate balance lead to the impairment of the protective function of mucus resulting in gastric disease. Indeed, the weakening of gastric mucosal defense is intimately associated with the diminished viscoelastic qualities of mucus, decrease in hydrogen ion retardation capacity, and the extensive proteolysis of its mucin component. Although until recently the disintegration of the mucus coat was attributed exclusively to the enhanced activity of intragastric pepsin, our studies provided strong argument that a bacterial factor, namely infection by Helicobacter pylori, through the action of its protease and. lipase enzymes also is highly detrimental to the integrity of gastric mucus. Hence, agents capable of interfering with the pathogenic activity of this bacteria are becoming the drugs of choice in peptic ulcer therapy.
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