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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK; Malden, USA : Munksgaard International Publishers
    Experimental dermatology 13 (2004), S. 0 
    ISSN: 1600-0625
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract:  Wound healing in healthy individuals proceeds at an optimal rate. However, in patients, with – e.g.– locally impaired blood flow or diabetes, chronic wounds develop and often become infected. Chronic wounds mean a low quality of life for the afflicted patients, not to mention enormous costs. Rather than using recombinant growth factors to accelerate wound healing, we employed the toll-like receptor agonist macrophage-activating lipopeptide-2 (MALP-2) to improve the healing of full-thickness excision skin wounds in an animal model with obese, diabetic mice. A gene array experiment suggested that MALP-2 stimulates the release of various mediators involved in wound healing. Further data to be presented in this study will show (i) that MALP-2 is capable of stimulating the appearance of the monocyte chemoattractant protein-1 at the wound site, (ii) that this leads to increased leucocyte and, in particular, macrophage infiltration and (iii) that MALP-2-treated wounds closed 2 weeks earlier than vehicle-treated controls. MALP-2, thus, appears to stimulate the early inflammatory process needed to set in motion the ensuing consecutive natural steps of wound healing resulting in wound closure.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-8798
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary.  Seroconversion from HBeAg to αHBe of persons chronically infected by HBV is usually associated with a transient exacerbation of liver disease and subsequent normalization of liver histology. It is speculated that these clinicopathological features may be due to the activation of cytodestructive mechanisms by αHBe antibodies. The aim of the present study was to investigate the pathogenic potential of αHBe antibodies in a transgenic mouse model. Therefore, αHBe autoantibodies were elicited in double-transgenic mice expressing high amounts of HBeAg and interferon-γ in the liver. Interferon-γ has previously been shown to play an important role in the development of hepatic necroinflammation associated with hepadnaviral infection, probably via tumor-necrosis-factor-α secreted by activated macrophages. We found no evidence that αHBe antibodies have the potential to destroy HBeAg-secreting hepatocytes even if the cells were predisposed to injury due to high-level interferon-γ expression. We conclude that seroconversion from HBeAg to αHBe of persons chronically infected with HBV seems to be an immunological epiphenomenon without pathogenic significance.
    Type of Medium: Electronic Resource
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