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Lack of Receptor for Advanced Glycation End products leads to less severe staphylococcal skin infection but more skin abscesses and prolonged wound healing.

Artikel i vetenskaplig tidskrift
Författare Manli Na
Majd Mohammad
Ying Fei
Wanzhong Wang
André Holdfeldt
Huamei Forsman
Abukar Ali
Rille Pullerits
Tao Jin
Publicerad i The Journal of infectious diseases
Volym 218
Nummer/häfte 5
Sidor 791-800
ISSN 1537-6613
Publiceringsår 2018
Publicerad vid Institutionen för medicin, avdelningen för reumatologi och inflammationsforskning
Sidor 791-800
Språk en
Länkar dx.doi.org/10.1093/infdis/jiy007
www.ncbi.nlm.nih.gov/entrez/query.f...
Ämnesord Receptor for advanced glycation end products; Staphylococcus aureus; mouse; skin infection
Ämneskategorier Bakteriologi, Immunbiologi, Reumatologi och inflammation

Sammanfattning

Lack of Receptor for Advanced Glycation End products (RAGE) ameliorates several infections including Staphylococcus aureus (S. aureus) pneumonia. We sought to investigate the role of RAGE in staphylococcal skin infection in mice.Wild-type (WT) and RAGE deficient (RAGE-/-) mice were subcutaneously inoculated with S. aureus SH1000 strain in abscess forming dose or necrotic dose. Clinical signs of dermatitis, along with histopathological changes, were compared between the groups.The skin lesion size was smaller in RAGE-/- mice. Infected RAGE-/- mice expressed lower pro-inflammatory cytokines in local skins compared to control mice. Low dose of bacteria caused more abscess formation in RAGE-/- mice compared to skin necrosis that was more often observed in WT mice. As a result of more abscess formation, the wound healing was prolonged in RAGE-/- mice. Importantly, RAGE-/- mice had lower bacterial loads in the skin than controls, which is correlated with higher local levels of myeloperoxidase before skin infection. In vitro, enhanced phagocytic capacity of neutrophils and macrophages obtained from RAGE-/- mice compared to control mice was observed.RAGE deficiency up-regulates phagocytic capacity of phagocytes, resulting in lower bacterial burden in local skin and milder skin lesions in mice with staphylococcal skin infection.

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