TY - JOUR
T1 - Alteration of intestinal intraepithelial lymphocytes after massive small bowel resection
AU - Yang, Hua
AU - Fan, Yongyi
AU - Finaly, Robert
AU - Teitelbaum, Daniel H.
N1 - Funding Information:
This study was supported by NIH grant AI44076-01 and Abbott Laboratories, Hospital Division. The work was also supported in part by the UM-Comprehensive Cancer Center NIH CA46592, the UM-Multipurpose Arthritic Center BIH AR20557, and the UM-BRCF Core Flow Cytometry facility.
PY - 2003/1/1
Y1 - 2003/1/1
N2 - Background. Intraepithelial lymphocytes (IEL) comprise the inner most layer of the gut immune system, and play a critical role in protecting the host from enteric organisms. Massive small bowel resection (MSBR) is one such clinical condition where patients are at particularly high risk for the development of such enteric infectious complications. Because of this, we hypothesized that the IEL may change significantly after the formation of a MSBR. To address this, a mouse model of MSBR was created and the acute phenotypic and functional characteristics of the IEL were studied. Materials and methods. Mice underwent a 70% mid-small bowel resection. After 7 days, IEL were isolated and analyzed for phenotypic changes by flow cytometry. IEL cytokine expression was performed with semiquantitative polymerase chain reaction techniques. To assess the functional significance of these changes, IEL proliferative response was assessed in vitro. Results. MSBR led to significant decreases in specific IEL subpopulations: CD 44+ (used as a marker of cell maturity); CD 8αβ+ (marker of thymic derivation), and CD 69+ (marker of T cell activation). Compared with controls, IEL TNF-α mRNA expression increased 84%, while IL-2 and IL-10 mRNA expression decreased by 69 and 72%, respectively. Spontaneous proliferation of IEL in the MSBR group was significantly higher than controls, however, proliferation failed to increase with T cell stimulation. Conclusion. These changes suggest a shift to a more immature and possibly less activated cell population. It is possible that such alterations may play an important role in the increase in enterically derived infections in patients with MSBR.
AB - Background. Intraepithelial lymphocytes (IEL) comprise the inner most layer of the gut immune system, and play a critical role in protecting the host from enteric organisms. Massive small bowel resection (MSBR) is one such clinical condition where patients are at particularly high risk for the development of such enteric infectious complications. Because of this, we hypothesized that the IEL may change significantly after the formation of a MSBR. To address this, a mouse model of MSBR was created and the acute phenotypic and functional characteristics of the IEL were studied. Materials and methods. Mice underwent a 70% mid-small bowel resection. After 7 days, IEL were isolated and analyzed for phenotypic changes by flow cytometry. IEL cytokine expression was performed with semiquantitative polymerase chain reaction techniques. To assess the functional significance of these changes, IEL proliferative response was assessed in vitro. Results. MSBR led to significant decreases in specific IEL subpopulations: CD 44+ (used as a marker of cell maturity); CD 8αβ+ (marker of thymic derivation), and CD 69+ (marker of T cell activation). Compared with controls, IEL TNF-α mRNA expression increased 84%, while IL-2 and IL-10 mRNA expression decreased by 69 and 72%, respectively. Spontaneous proliferation of IEL in the MSBR group was significantly higher than controls, however, proliferation failed to increase with T cell stimulation. Conclusion. These changes suggest a shift to a more immature and possibly less activated cell population. It is possible that such alterations may play an important role in the increase in enterically derived infections in patients with MSBR.
KW - Interferon (INF)
KW - Interleukin (IL)-2
KW - Intraepithelial lymphocytes (IEL)
KW - Small bowel resection
KW - Tumor necrosis factor (TNF)
UR - http://www.scopus.com/inward/record.url?scp=0037354852&partnerID=8YFLogxK
U2 - 10.1016/S0022-4804(03)00032-5
DO - 10.1016/S0022-4804(03)00032-5
M3 - Article
AN - SCOPUS:0037354852
SN - 0022-4804
VL - 110
SP - 276
EP - 286
JO - Journal of Surgical Research
JF - Journal of Surgical Research
IS - 1
ER -