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Platelets have been shown to cover a broad range of functions. Besides their role in hemostasis, they have immunological functions and thus participate in the interaction between pathogens and host defense. Platelets have a broad repertoire of receptor molecules that enable them to sense invading pathogens and infection-induced inflammation. Consequently, platelets exert antimicrobial effector mechanisms, but also initiate an intense crosstalk with other arms of the innate and adaptive immunity, including neutrophils, monocytes/macrophages, dendritic cells, B cells and T cells. There is a fragile balance between beneficial antimicrobial effects and detrimental reactions that contribute to the pathogenesis, and many pathogens have developed mechanisms to influence these two outcomes. This review aims to highlight aspects of the interaction strategies between platelets and pathogenic bacteria, viruses, fungi and parasites, in addition to the subsequent networking between platelets and other immune cells, and the relevance of these processes for the pathogenesis of infections.

Helicobacter pylori causes a persistent infection in the human stomach, which can result in chronic gastritis and peptic ulcer disease. Despite an intensive proinflammatory response, the immune system is not able to clear the organism. However, the immune escape mechanisms of this common bacterium are not well understood. We investigated the interaction between H. pylori and human dendritic cells. Dendritic cells (DCs) are potent antigen-presenting cells and important mediators between the innate and acquired immune system. Stimulation of DCs with different concentrations of H. pylori for 8, 24, 48, and 72 h resulted in dose-dependent interleukin-6 (IL-6), IL-8, IL-10 and IL-12 production. Lipopolysaccharide (LPS) from Escherichia coli, a known DC maturation agent, was used as a positive control. The cytokine release after stimulation with LPS was comparable to that induced by H. pylori except for IL-12. After LPS stimulation IL-12 was only moderately released compared to the large amounts of IL-12 induced by H. pylori. We further investigated the potential of H. pylori to induce maturation of DCs. Fluorescence-activated cell sorting analysis of cell surface expression of maturation marker molecules such as CD80, CD83, CD86, and HLA-DR revealed equal upregulation after stimulation with H. pylori or LPS. We found no significant differences between H. pylori seropositive and seronegative donors of DCs with regard to cytokine release and upregulation of surface molecules. These data clearly demonstrate that H. pylori induces a strong activation and maturation of human immature DCs.Helicobacter pylori is a gastric pathogenic gram-negative bacterium that colonizes the gastric mucus layer but does not invade the mucosal epithelium. This bacterial colonization leads to a cellular infiltrate of polymorphonuclear leukocytes, an acute immune response, followed by the migration of macrophages, lymphocytes, and plasma cells in the gastric mucosa, resulting in chronic gastritis. This chronic inflammation does not necessarily produce symptoms but does increase the risk of developing peptic ulcer disease, adenocarcinoma of the distal stomach (antrum and fundus), and primary non-Hodgkin's lymphoma of the stomach (MALTomas) (8,42,43).Although H. pylori induces an immune response involving both the innate and the acquired immune systems, the host is unable to clear the organism from the mucosa, resulting in lifelong infection. This inability to eliminate the bacterium may be due to immune-evasive strategies. Possible mechanisms were investigated, with emphasis on the acquired immune response. Several studies have shown inhibitory effects of H. pylori on cell proliferation (11, 24-26, 60), and the induction of H. pylori-specific regulatory T cells that actively suppress T-cell response have been described (31).Recent studies have investigated possible impairment of antigen presentation. VacA, an H. pylori virulence factor, was reported to interfere with proteolytic processing of tetanus toxoid and was shown to inhibit the Ii-depen...

We compared the activities of antifungal agents against a wide range of yeasts and filamentous fungi. The methodology of the European Committee on Antimicrobial Susceptibility Testing (EUCAST) for yeasts and spore-forming molds was applied; and a total of 349 clinical isolates of Candida spp., other yeast species, Aspergillus spp., and nondermatophyte non-Aspergillus spp. were investigated. The average geometric mean (GM) of the MICs of the various drugs for Candida spp. were as follows: amphotericin B (AMB), 0.55 g/ml; liposomal amphotericin B (l-AMB); 0.35 g/ml; itraconazole (ITC), 0.56 g/ml; voriconazole (VRC), 0.45 g/ml; posaconazole (POS), 0.44 g/ml; and caspofungin (CPF), 0.45 g/ml. The data indicated that the majority of Candida spp. were susceptible to the traditional and new antifungal drugs. For Aspergillus spp., the average GM MICs of AMB, l-AMB, ITC, VRC, POS, and CPF were 1.49 g/ml, 1.44 g/ml, 0.65 g/ml, 0.34 g/ml, 0.25 g/ml, and 0.32 g/ml, respectively. For the various zygomycetes, the average GM MICs of AMB, l-AMB, ITC, and POS were 1.36 g/ml, 1.42 g/ml, 4.37 g/ml, and 1.65 g/ml, respectively. Other yeastlike fungi and molds displayed various patterns of susceptibility. In general, the minimal fungicidal concentrations were 1 to 3 dilutions higher than the corresponding MICs. POS, AMB, and l-AMB showed activities against a broader range of fungi than ITC, VRC, and CPF did. Emerging pathogens such as Saccharomyces cerevisiae and Fusarium solani were not killed by any drug. In summary, the EUCAST data showed that the in vitro susceptibilities of yeasts and filamentous fungi are variable, that susceptibility occurs among and within various genera and species, and that susceptibility depends on the antifungal drug tested. AMB, l-AMB, and POS were active against the majority of pathogens, including species that cause rare and difficult-to-treat infections.