title: Post-shock mesenteric lymph drainage ameliorates cellular immune function in rats following hemorrhagic shock.
abstract: Disturbance of immunity is an important factor to modulate inflammatory responses after severe shock. Post-shock mesenteric lymph (PSML) return plays an adverse role in multiple organ injuries induced by the hemorrhagic shock, and the inflammatory factors are involved in this process. However, whether the PSML can exacerbate immune dysfunctions that modulate inflammatory response to the hemorrhagic shock remains unknown. In the present study, the effects of PSML drainage on the distribution of T lymphocyte subgroup, the release of inflammatory factors, and apoptosis of thymocytes were investigated; the effect of PSML on the specific parameters of cellular immune function was also determined. Results showed that PSML drainage reduced the increased levels of CD3+, CD3+CD4+, CD4+CD25+ lymphocytes, IFN-γ, and the ratios of CD3 + CD4+/CD3 + CD4- in blood of the shocked rats at 3 h after resuscitation; PSML drainage also abolished the decreased IL-4 level and restored the higher ratio of IFN-γ/IL-4 to normal levels. Tissue injury, including enlarged intermembrance space and edema with congestion in the medulla, increased apoptotic cells and bax expression, decreased number of cells in the S phase, and bcl-2 expression were observed in the thymus after hemorrhagic shock. PSML drainage reversed these effects. In particular, PSML drainage increased the proliferation index and decreased p53 expression of thymocytes. These results suggest that hyperimmunity occurred at early stages of hemorrhagic shock with resuscitation and that PSML drainage could markedly improve cellular immune function that is responsible for the reduced inflammatory responses.
authors.affiliation: Institute of Microcirculation, Hebei North University, 11 Diamond South Road, Hebei, 075000, Zhangjiakou, People's Republic of China.
authors.forename: Hua
authors.initials: H
authors.lastname: Liu
authors.forename: Zi-Gang
authors.initials: ZG
authors.lastname: Zhao
authors.forename: Li-Qiang
authors.initials: LQ
authors.lastname: Xing
authors.forename: Li-Min
authors.initials: LM
authors.lastname: Zhang
authors.forename: Chun-Yu
authors.initials: CY
authors.lastname: Niu
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000276:immunology; D017252:CD3 Complex / Q000097:blood; D015704:CD4 Antigens / Q000097:blood; D007249:Inflammation / Q000276:immunology*; D007371:Interferon-gamma / Q000097:blood; D053645:Interleukin-2 Receptor alpha Subunit / Q000097:blood; D015847:Interleukin-4 / Q000097:blood; D008198:Lymph Nodes / Q000276:immunology / Q000502:physiology*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000096:biosynthesis; D051381:Rats; D017208:Rats, Wistar; D059807:S Phase Cell Cycle Checkpoints / Q000276:immunology; D012771:Shock, Hemorrhagic / Q000276:immunology / Q000473:pathology*; D016176:T-Lymphocyte Subsets / Q000276:immunology*; D013950:Thymus Gland / Q000276:immunology*; D016159:Tumor Suppressor Protein p53 / Q000096:biosynthesis
chemical_list: D017252:CD3 Complex; D015704:CD4 Antigens; D053645:Interleukin-2 Receptor alpha Subunit; D019253:Proto-Oncogene Proteins c-bcl-2; D016159:Tumor Suppressor Protein p53; D015847:Interleukin-4; D007371:Interferon-gamma