Publications by authors named "K Schmolke"

Secondary heterologous dengue infection is a risk factor for severe disease manifestations because of the immune-enhancement phenomenon. Succeeding clinical infections are seldom reported, and the clinical course of tertiary and quaternary dengue infections is not clear. Cuba represents a unique environment to study tertiary/quaternary dengue infections in a population with known clinical and serologic dengue markers and no dengue endemicity.

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Dengue virus has become endemic in most tropical urban areas throughout the world, and DHF has appeared concomitantly with this expansion. The intensity of dengue virus replication during the early stages of infection could determine clinical outcomes; therefore, it is important to understand the impact of dengue virus infection on the earliest immune defense against microbial infection, which also strongly regulates the adaptive immune responses. This study was aimed at evaluating the expression of the CC-chemokines MIP-1α/CCL3 and MCP-1/CCL2 in peripheral blood leukocytes using an ex vivo model resembling dengue infection in vivo, in subjects with a well characterized dengue immune background, due to the exceptional Cuban epidemiological situation in dengue.

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Increased serum levels of cytokines released by cells of the immune response have been detected in patients suffering from dengue disease. Likewise, secondary infections by a different dengue virus serotype result in a highest risk of development of the severe dengue disease. Both findings suggest that the memory immune response is one of the key players in the pathogenesis of this disease.

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Mannose-binding lectin (MBL) mediates important functions within the innate immune system, and its deficiency was associated with infectious complications. However, in adults without concomitant immunodeficiency the clinical relevance of MBL deficiency remains controversial. We analyzed the distribution of MBL deficiency and its association with concomitant immunodeficiency in 228 adult Caucasian patients with a history of recurrent and/or severe infections.

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Background: We have recently shown that ischemic stroke causes a stress-mediator-induced long-lasting immunodepressive state in mice.

Methods: Using head magnetic resonance imaging and standardized immunoassays, we prospectively investigated whether poststroke immunodepression is also seen in humans.

Results: Compared to healthy volunteers (n = 30), a rapid depression of lymphocyte counts and a functional deactivation of monocytes and T helper type 1 cells was observed in acute stroke patients (SP; n = 40).

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