TY - JOUR
T1 - Effects of colonization of gnotobiotic swiss webster mice with helicobacter bilis
AU - Whaiy, Mark T.
AU - Wang, Chuanwu
AU - Ruff, Catherine F.
AU - DiVincenzo, Mallory J.
AU - Labriola, Caralyn
AU - Ge, Lillian
AU - Feng, Yan
AU - Ge, Zhongming
AU - Bakthavatchalu, Vasu
AU - Muthupalani, Suresh
AU - Horwitz, Bruce H.
AU - Fox, James G.
N1 - Funding Information:
This research was supported by the following grants to James G Fox: 1R01OD011141, POI CA028842, P30-ES02109, and T32 OD010978. We extend special thanks to Carlos Umana, Allen Discua, Yassin Ibrahim, and Oscar Acevedo for their expert care of the gnotobiotic mice. We are very grateful to Christian Kaufman, Lenzie Cheney, and Dylan Puglisi for valuable assistance in necropsy and to Joanna Richards and Caroline Atkinson for histology preparations.
Publisher Copyright:
© 2020 American Association for Laboratory Animal Science. All right reserved.
PY - 2020/6
Y1 - 2020/6
N2 - Helicobacter bilis (Hb) causes hepatitis in some strains of inbred mice. The current study confirmed that Hb directly causes portal hepatitis in outbred gnotobiotic Swiss Webster (SW) mice, as we previously reported for conventional SW mice. Hbmonoassociated SW mice also developed mild enterocolitis, expanded gut-associated lymphoid tissue (GALT), and tertiary lymphoid tissue in the lower bowel. At 1 and 10 mo after infection, Hb-induced GALT hyperplasia exhibited well-organized, ectopic germinal centers with increased mononuclear cell apoptosis, MHC class II antigen presentation, and pronounced endothelial venule formation, consistent with features of tertiary lymphoid tissue. In the lower bowel, Hb induced mainly B220+ cells as well as CD4+IL17+, CD4+IFNyf, and CD4+FoxP3+ regulatory T cells and significantly increased ILIO mRNA expression. This gnotobiotic model confirmed that Hb causes portal hepatitis in outbred SW mice but stimulated GALT with an antiinflammatory bias. Because Hb had both anti- and proinflammatory effects on GALT, it should be considered a 'pathosymbiont provocateur' and merits further evaluation in mouse models of human disease.
AB - Helicobacter bilis (Hb) causes hepatitis in some strains of inbred mice. The current study confirmed that Hb directly causes portal hepatitis in outbred gnotobiotic Swiss Webster (SW) mice, as we previously reported for conventional SW mice. Hbmonoassociated SW mice also developed mild enterocolitis, expanded gut-associated lymphoid tissue (GALT), and tertiary lymphoid tissue in the lower bowel. At 1 and 10 mo after infection, Hb-induced GALT hyperplasia exhibited well-organized, ectopic germinal centers with increased mononuclear cell apoptosis, MHC class II antigen presentation, and pronounced endothelial venule formation, consistent with features of tertiary lymphoid tissue. In the lower bowel, Hb induced mainly B220+ cells as well as CD4+IL17+, CD4+IFNyf, and CD4+FoxP3+ regulatory T cells and significantly increased ILIO mRNA expression. This gnotobiotic model confirmed that Hb causes portal hepatitis in outbred SW mice but stimulated GALT with an antiinflammatory bias. Because Hb had both anti- and proinflammatory effects on GALT, it should be considered a 'pathosymbiont provocateur' and merits further evaluation in mouse models of human disease.
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U2 - 10.30802/AALAS-CM-19-000087
DO - 10.30802/AALAS-CM-19-000087
M3 - Article
C2 - 32349859
AN - SCOPUS:85086346612
VL - 70
SP - 216
EP - 232
JO - Comparative Medicine
JF - Comparative Medicine
SN - 1532-0820
IS - 3
ER -