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  • 1
    Electronic Resource
    Electronic Resource
    Clostridium perfringens type A cytotoxic-enterotoxin(s) as triggers for death in the sudden infant death syndrome: Development of a toxico-infection hypothesis (1993)
    Springer
    Current microbiology 27 (1993), S. 51-59 
    Details
    ISSN: 1432-0991
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract In our studies with the pathogenic bacteriumClostridium perfringens type A and its cytotoxic-enterotoxins (CTEs), we have obtained results that imply an involvement of this organism in the sudden infant death syndrome (SIDS). In fecal samples obtained from SIDS infants (n=164) and non-SIDS infants (n=57),C. perfringens type A was present in high numbers in 〉80% of SIDS and 〈2% of control non-SIDS cases respectively. Fecal samples from SIDS infants analyzed by ELISA forC. perfringens type A CTEs showed a very strong positive correlation with the presence of the organism. Histopathological examination of ileal tissue from SIDS infants showed remarkable similarity to tissue from animal models affected byC. perfringens type A CTEs, where the patterns of damage were positively correlated with the age of the animal. We propose that systemic distribution of the CTEs acts parasympathomimetically to trigger a biochemical cascade that alters cardiorespiratory control. Death may subsequently ensue in an immunologically vulnerable infant.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01576834
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  • 2
    Electronic Resource
    Electronic Resource
    Activation ofClostridium perfringens cytotoxic enterotoxin(s) in vivo and in vitro: Role in triggers for sudden infant death (1994)
    Springer
    Current microbiology 28 (1994), S. 261-267 
    Details
    ISSN: 1432-0991
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The action ofClostridium perfringens cytotoxic enterotoxins may be activated/exacerbated both in vivo and in vitro by the addition of an activator molecule present in a brush border membrane fraction isolated from young rabbits. Increased concentrations of the activator could be induced by immunologically stimulating rabbits with Ribi adjuvant. Comparative studies suggested that the activator was interferon-gamma (IFN-γ). In vitro IFN-γ sensitized cell lines apparently by enhancement of cell permeability, which allowed a more rapid uptake of the toxins, resulting in cell death at lower toxin concentrations. Viral and/or bacterial infections are inducers of IFNs. We propose that some immunologically immature infants are predisposed to infection. In the weeks prior to death, these infants may suffer from an infection that induces the synthesis of IFNs, sensitizing the infant to a more virulent infection and possible sudden death.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01573203
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Evidence for Clostridium perfringens Enterotoxin (CPE) Inducing a Mitogenic and Cytokine Response In Vitro and a Cytokine Response In Vivo (1999)
    Springer
    Current microbiology 38 (1999), S. 96-100 
    Details
    ISSN: 1432-0991
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract. We investigated some immunogenic properties of Clostridium perfringens enterotoxin (CPE) in vitro using murine J774A macrophages (MΦ) and in vivo using Swiss Webster (SW) mice. CPE was a potent mitogen in vitro, where cell proliferation increased with CPE concentration. CPE was nonmitogenic when MΦ were concurrently incubated with CPE and interferon gamma (IFN-γ). MΦ incubated in the presence of CPE induced the synthesis of interleukin-1 (IL-1), interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α) and interferon-gamma (IFN-γ), but not interleukin-2 (IL-2). In vivo, CPE induced a pro-inflammatory cytokine response with striking production of IFN-γ, IL-1, and IL-6. Regardless of route of CPE entry, serum cytokine levels generally peaked within 1 h of administration and were maintained for 4–8 h. Although CPE engenders an intense immune response during toxicosis, the toxin does not appear to be a superantigen. Death from CPE-induced shock appears to result from various interrelating immunological mechanisms.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002849900410
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    Paper (German National Licenses)
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