PMID- 15257086 OWN - NLM STAT- MEDLINE DCOM- 20050131 LR - 20190917 IS - 1073-2322 (Print) IS - 1073-2322 (Linking) VI - 22 IP - 2 DP - 2004 Aug TI - Polymicrobial sepsis induces divergent effects on splenic and peritoneal dendritic cell function in mice. PG - 137-44 AB - Dendritic cells (DCs) are professional antigen-presenting cells that act as sentinels in the cell-mediated response against invading pathogens associated with septic challenge. The purpose of the present study was to determine whether there is a loss of dendritic cells and/or changes in function of these cells in septic mice. Here we report that the number of DCs, in both spleen and peritoneum, decreased over 24 h postsepsis [cecal ligation and puncture (CLP)] when compared with sham. The most dramatic change was seen in the peritoneal cavity. This decrease appeared to be caused mainly by the depletion of immature DCs rather than mature DCs. This change was LPS independent and minimally affected by FasL; however, overexpression of human Bcl-2 gene provides protection of the septic peritoneal DCs. Moreover, although the level of IL-12 release decreased significantly in splenic DCs obtained from CLP mice, IL-12 secretion was markedly elevated by peritoneal DCs as well as in both plasma and peritoneal fluid at 24 h post-CLP. In peritoneal cells, the expression of CD40, CD80, and CD86 was unchanged, but their respective ligands CD40L, CD28, and CD152 all increased in mice 24 h after CLP, although no such change was observed in splenocytes. Regardless of the presence or absence of antigen, peritoneal DCs from CLP mice showed higher capacity to stimulate T-cell proliferation than those cells from the sham control. However, splenic DCs from CLP mice only showed augmented capacity to induce antigen-dependent stimulation of T-cell proliferation. Together, these data indicate that sepsis produces divergent functional changes in splenic and peritoneal DC populations. FAU - Ding, Yanli AU - Ding Y AD - Division of Surgical Research, Department of Surgery, Rhode Island Hospital, Brown University School of Medicine, Providence, Rhode Island 02903, USA. FAU - Chung, Chun-Shiang AU - Chung CS FAU - Newton, Sarah AU - Newton S FAU - Chen, Yaping AU - Chen Y FAU - Carlton, Stacey AU - Carlton S FAU - Albina, Jorge E AU - Albina JE FAU - Ayala, Alfred AU - Ayala A LA - eng GR - R01 GM046354/GM/NIGMS NIH HHS/United States GR - R01 GM046354-12/GM/NIGMS NIH HHS/United States GR - R01 HL073525/HL/NHLBI NIH HHS/United States GR - R01-GM46354/GM/NIGMS NIH HHS/United States PT - Journal Article PT - Research Support, U.S. Gov't, P.H.S. PL - United States TA - Shock JT - Shock (Augusta, Ga.) JID - 9421564 RN - 0 (Antigens, CD) RN - 0 (Antigens, Differentiation) RN - 0 (B7-1 Antigen) RN - 0 (B7-2 Antigen) RN - 0 (CD11c Antigen) RN - 0 (CD40 Antigens) RN - 0 (CTLA-4 Antigen) RN - 0 (CTLA4 protein, human) RN - 0 (Cd86 protein, mouse) RN - 0 (Ctla4 protein, mouse) RN - 0 (Culture Media, Conditioned) RN - 0 (FASLG protein, human) RN - 0 (Fas Ligand Protein) RN - 0 (Fasl protein, mouse) RN - 0 (Ligands) RN - 0 (Lipopolysaccharides) RN - 0 (Membrane Glycoproteins) RN - 0 (Proto-Oncogene Proteins c-bcl-2) RN - 0 (Receptors, Cell Surface) RN - 0 (Tlr4 protein, mouse) RN - 0 (Toll-Like Receptor 4) RN - 187348-17-0 (Interleukin-12) SB - IM MH - Animals MH - Antigen Presentation MH - Antigens, CD/biosynthesis MH - Antigens, Differentiation/biosynthesis MH - B7-1 Antigen/biosynthesis MH - B7-2 Antigen MH - CD11c Antigen/biosynthesis MH - CD40 Antigens/biosynthesis MH - CTLA-4 Antigen MH - Culture Media, Conditioned/pharmacology MH - Dendritic Cells/*cytology/metabolism/microbiology MH - Fas Ligand Protein MH - Flow Cytometry MH - Interleukin-12/blood/metabolism MH - Ligands MH - Lipopolysaccharides/metabolism MH - Male MH - Membrane Glycoproteins/biosynthesis/metabolism MH - Mice MH - Mice, Inbred C3H MH - Peritoneal Lavage MH - Peritoneum/metabolism MH - Phenotype MH - Proto-Oncogene Proteins c-bcl-2/metabolism MH - Receptors, Cell Surface/metabolism MH - Sepsis/*microbiology MH - Spleen/*cytology/microbiology MH - Time Factors MH - Toll-Like Receptor 4 PMC - PMC2253681 MID - NIHMS40047 EDAT- 2004/07/17 05:00 MHDA- 2005/02/03 09:00 PMCR- 2008/02/24 CRDT- 2004/07/17 05:00 PHST- 2004/07/17 05:00 [pubmed] PHST- 2005/02/03 09:00 [medline] PHST- 2004/07/17 05:00 [entrez] PHST- 2008/02/24 00:00 [pmc-release] AID - 00024382-200408000-00007 [pii] AID - 10.1097/01.shk.0000131194.80038.3f [doi] PST - ppublish SO - Shock. 2004 Aug;22(2):137-44. doi: 10.1097/01.shk.0000131194.80038.3f.