Increased presence of effector lymphocytes during Helicobacter hepaticus-induced colitis

AIM： To identify and characterize drosophila mothers against decapentaplegic （SMAD）3-dependent changes in immune cell populations following infection with He- Iicobacter hepaticus （H. hepaticus）. METHODS： SMAD3/ （n = L9） and colitis-resistant SMAD3＋/ （n = 24） mice （8-10 wk of age） were in- fected wi...

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Published in:World journal of gastroenterology : WJG 2012-04, Vol.18 (13), p.1459-1469
Main Authors: McCaskey, Sarah J, Rondini, Elizabeth A, Clinthorne, Jonathan F, Langohr, Ingeborg M, Gardner, Elizabeth M, Fenton, Jenifer I
Format: Article
Language:English
Subjects:
Animals
Colitis - immunology
Colitis - microbiology
Colon - cytology
Colon - immunology
Colon - pathology
Female
Granzymes - metabolism
Helicobacter hepaticus - immunology
Helicobacter hepaticus - pathogenicity
Killer Cells, Natural - cytology
Killer Cells, Natural - immunology
Lymphocytes - cytology
Lymphocytes - immunology
Male
Mice
Mice, Knockout
Original
Signal Transduction - immunology
SMAD3
Smad3 Protein - genetics
Smad3 Protein - immunology
SMAD蛋白
T-Lymphocyte Subsets - cytology
T-Lymphocyte Subsets - immunology
T-Lymphocytes - cytology
T-Lymphocytes - immunology
T淋巴细胞
感染过程
结肠炎
肝
螺杆菌
诱导
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Summary:AIM： To identify and characterize drosophila mothers against decapentaplegic （SMAD）3-dependent changes in immune cell populations following infection with He- Iicobacter hepaticus （H. hepaticus）. METHODS： SMAD3/ （n = L9） and colitis-resistant SMAD3＋/ （n = 24） mice （8-10 wk of age） were in- fected with/-/, hepaticus and changes in immune cell populations [T lymphocytes, natural killer （NK） cells, T regulatory cells] were measured in the spleen and mesenteric lymph nodes （MsLNs） at 0 d, 3 d, 7 d and 28 d post-infection using flow cytometry. Genotype-dependent changes in T lymphocytes and granzyme B＋ cells were also assessed after 28 d in proximal colon tissue using immunohistochemistry. RESULTS： As previously observed, SMAD3＋, but not SMAD3＋/- mice, developed colitis, peaking at 4 wk post-infection. No significant changes in T cell subsets were observed in the spleen or in the MsLNs between genotypes at any time point. However, CD4＋ and CD8＋/ CD62L＋＋ cells, an effector T lymphocyte population, as well as NK cells （NKp46/DX5＋） were significantly higher in the MsLNs of SMAD3/ mice at 7 d and 28 d post-in- fection. In the colon, a higher number of CD3＋ cells were present in SMAD3＋ compared to SMAD3＋/- mice at base- line, which did not significantly change during infection. However, the number of granzyme B＋ cells, a marker of cytolytic lymphoo/tes, significantly increased in SMAD3＋ mice 28 d post-infection compared to both SMAD3＋/- mice and to baseline values. This was consistent with more severe colitis development in these animals. CONCLUSION： Data suggest that defects in SMAD3 signaling increase susceptibility to H. hepaticus-induced colitis through aberrant activation and/or dysregulation of effector lymphoo/tes.
ISSN:1007-9327
2219-2840
DOI:10.3748/wjg.v18.i13.1459