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Gastric de novo Muc13 expression and spasmolytic polypeptide-expressing metaplasia during Helicobacter heilmannii infection.

Artikel i vetenskaplig tidskrift
Författare Cheng Liu
Annemieke Smet
Caroline Blaecher
Bram Flahou
Richard Ducatelle
Sara K. Lindén
Freddy Haesebrouck
Publicerad i Infection and immunity
Volym 82
Nummer/häfte 8
Sidor 3227-39
ISSN 1098-5522
Publiceringsår 2014
Publicerad vid Institutionen för biomedicin, avdelningen för medicinsk kemi och cellbiologi
Sidor 3227-39
Språk en
Länkar dx.doi.org/10.1128/IAI.01867-14
Ämnesord Animals, Antigens, Surface, biosynthesis, genetics, Disease Models, Animal, Epidermal Growth Factor, biosynthesis, genetics, Female, Gastric Mucosa, microbiology, pathology, Gene Expression Profiling, Helicobacter Infections, complications, microbiology, pathology, Helicobacter heilmannii, growth & development, Metaplasia, microbiology, pathology, Mice, Mice, Inbred BALB C, Peptides, genetics, metabolism
Ämneskategorier Medicinsk biovetenskap, Patobiologi

Sammanfattning

Helicobacter heilmannii is a zoonotic bacterium that has been associated with gastric disease in humans. In this study, the mRNA expression of mucins in the stomach of BALB/c mice was analyzed at several time points during a 1-year infection with this bacterium, during which gastric disease progressed in severity. Markers for acid production by parietal cells and mucous metaplasia were also examined. In the first 9 weeks postinfection, the mRNA expression of Muc6 was clearly upregulated in both the antrum and fundus of the stomach of H. heilmannii-infected mice. Interestingly, Muc13 was upregulated already at 1 day postinfection in the fundus of the stomach. Its expression level remained high in the stomach over the course of the infection. This mucin is, however, not expressed in a healthy stomach, and high expression of this mucin has so far only been described in gastric cancer. In the later stages of infection, mRNA expression of H(+)/K(+)-ATPase α/β and KCNQ1 decreased, whereas the expression of Muc4, Tff2, Dmbt1, and polymeric immunoglobulin receptor (pIgR) increased starting at 16 weeks postinfection onwards, suggesting the existence of spasmolytic polypeptide-expressing metaplasia in the fundus of the stomach. Mucous metaplasia present in the mucosa surrounding low-grade mucosa-associated lymphoid tissue (MALT) lymphoma-like lesions was also histologically confirmed. Our findings indicate that H. heilmannii infection causes severe gastric pathologies and alterations in the expression pattern of gastric mucins, such as Muc6 and Muc13, as well as disrupting gastric homeostasis by inducing the loss of parietal cells, resulting in the development of mucous metaplasia.

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