Database : MEDLINE
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[PMID]: 26246141
[Au] Autor:Nacionales DC; Szpila B; Ungaro R; Lopez MC; Zhang J; Gentile LF; Cuenca AL; Vanzant E; Mathias B; Jyot J; Westerveld D; Bihorac A; Joseph A; Mohr A; Duckworth LV; Moore FA; Baker HV; Leeuwenburgh C; Moldawer LL; Brakenridge S; Efron PA
[Ad] Address:Department of Surgery, University of Florida College of Medicine, Gainesville, FL 32610;...
[Ti] Title:A Detailed Characterization of the Dysfunctional Immunity and Abnormal Myelopoiesis Induced by Severe Shock and Trauma in the Aged.
[So] Source:J Immunol;195(5):2396-407, 2015 Sep 1.
[Is] ISSN:1550-6606
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The elderly are particularly susceptible to trauma, and their outcomes are frequently dismal. Such patients often have complicated clinical courses and ultimately die of infection and sepsis. Recent research has revealed that although elderly subjects have increased baseline inflammation as compared with their younger counterparts, the elderly do not respond to severe infection or injury with an exaggerated inflammatory response. Initial retrospective analysis of clinical data from the Glue Grant trauma database demonstrated that despite a similar frequency, elderly trauma patients have worse outcomes to pneumonia than younger subjects do. Subsequent analysis with a murine trauma model also demonstrated that elderly mice had increased mortality after posttrauma Pseudomonas pneumonia. Blood, bone marrow, and bronchoalveolar lavage sample analyses from juvenile and 20-24-mo-old mice showed that increased mortality to trauma combined with secondary infection in the aged are not due to an exaggerated inflammatory response. Rather, they are due to a failure of bone marrow progenitors, blood neutrophils, and bronchoalveolar lavage cells to initiate and complete an emergency myelopoietic response, engendering myeloid cells that fail to clear secondary infection. In addition, elderly people appeared unable to resolve their inflammatory response to severe injury effectively.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1508
[Cu] Class update date: 150822
[Lr] Last revision date:150822
[Js] Journal subset:AIM; IM
[St] Status:In-Data-Review
[do] DOI:10.4049/jimmunol.1500984

  2 / 324904 MEDLINE  
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[PMID]: 26232427
[Au] Autor:Mazzi P; Caveggion E; Lapinet-Vera JA; Lowell CA; Berton G
[Ad] Address:Section of General Pathology, Department of Pathology and Diagnostics, University of Verona, Verona, 37134, Italy; and....
[Ti] Title:The Src-Family Kinases Hck and Fgr Regulate Early Lipopolysaccharide-Induced Myeloid Cell Recruitment into the Lung and Their Ability To Secrete Chemokines.
[So] Source:J Immunol;195(5):2383-95, 2015 Sep 1.
[Is] ISSN:1550-6606
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Myeloid leukocyte recruitment into the lung in response to environmental cues represents a key factor for the induction of lung damage. We report that Hck- and Fgr-deficient mice show a profound impairment in early recruitment of neutrophils and monocytes in response to bacterial LPS. The reduction in interstitial and airway neutrophil recruitment was not due to a cell-intrinsic migratory defect, because Hck- and Fgr-deficient neutrophils were attracted to the airways by the chemokine CXCL2 as wild type cells. However, early accumulation of chemokines and TNF-α in the airways was reduced in hck(-/-)fgr(-/-) mice. Considering that chemokine and TNF-α release into the airways was neutrophil independent, as suggested by a comparison between control and neutrophil-depleted mice, we examined LPS-induced chemokine secretion by neutrophils and macrophages in wild type and mutant cells. Notably, mutant neutrophils displayed a marked deficit in their capability to release the chemokines CXCL1, CXCL2, CCL3, and CCL4 and TNF-α in response to LPS. However, intracellular accumulation of these chemokines and TNF-α, as well as secretion of a wide array of cytokines, including IL-1α, IL-1, IL-6, and IL-10, by hck(-/-)fgr(-/-) neutrophils was normal. Intriguingly, secretion of CXCL1, CXCL2, CCL2, CCL3, CCL4, RANTES, and TNF-α, but not IL-1α, IL-1, IL-6, IL-10, and GM-CSF, was also markedly reduced in bone marrow-derived macrophages. Consistently, the Src kinase inhibitors PP2 and dasatinib reduced chemokine secretion by neutrophils and bone marrow-derived macrophages. These findings identify Src kinases as a critical regulator of chemokine secretion in myeloid leukocytes during lung inflammation.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1508
[Cu] Class update date: 150822
[Lr] Last revision date:150822
[Js] Journal subset:AIM; IM
[St] Status:In-Data-Review
[do] DOI:10.4049/jimmunol.1402011

  3 / 324904 MEDLINE  
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[PMID]: 26188063
[Au] Autor:Wu H; Xu LL; Teuscher P; Liu H; Kaplan MH; Dent AL
[Ad] Address:Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN 46202; and....
[Ti] Title:An Inhibitory Role for the Transcription Factor Stat3 in Controlling IL-4 and Bcl6 Expression in Follicular Helper T Cells.
[So] Source:J Immunol;195(5):2080-9, 2015 Sep 1.
[Is] ISSN:1550-6606
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The transcription factor Bcl6 is required for development of follicular helper T (TFH) cells. Cytokines that activate Stat3 promote Bcl6 expression and TFH cell differentiation. Previous studies with an acute virus infection model showed that TFH cell differentiation was decreased but not blocked in the absence of Stat3. In this study, we further analyzed the role of Stat3 in TFH cells. In Peyer's patches, we found that compared with wild-type, Stat3-deficient TFH cells developed at a 25% lower rate and expressed increased IFN-γ and IL-4. Whereas Peyer's patch germinal center B cells developed at normal numbers with Stat3-deficient TFH cells, IgG1 class switching was greatly increased. Following immunization with sheep RBCs, splenic Stat3-deficient TFH cells developed at a slower rate than in control mice, and splenic germinal center B cells were markedly decreased. Stat3-deficient TFH cells developed poorly in a competitive bone marrow chimera environment. Under all conditions tested, Stat3-deficient TFH cells overexpressed both IL-4 and Bcl6, a pattern specific for the TFH cell population. Finally, we found in vitro that repression of IL-4 expression in CD4 T cells by Bcl6 required Stat3 function. Our data indicate that Stat3 can repress the expression of Bcl6 and IL-4 in TFH cells, and that Stat3 regulates the ability of Bcl6 to repress target genes. Overall, we conclude that Stat3 is required to fine-tune the expression of multiple key genes in TFH cells, and that the specific immune environment determines the function of Stat3 in TFH cells.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1508
[Cu] Class update date: 150822
[Lr] Last revision date:150822
[Js] Journal subset:AIM; IM
[St] Status:In-Data-Review
[do] DOI:10.4049/jimmunol.1500335

  4 / 324904 MEDLINE  
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[PMID]: 26288818
[Au] Autor:Ferrajoli A; Ivan C; Ciccone M; Shimizu M; Kita Y; Ohtsuka M; D'Abundo L; Qiang J; Lerner S; Nouraee N; Rabe KG; Rassenti LZ; Van Roosbroeck K; Manning JT; Yuan Y; Zhang X; Shanafelt TD; Wierda WG; Sabbioni S; Tarrand JJ; Estrov Z; Radovich M; Liang H; Negrini M; Kipps TJ; Kay NE; Keating M; Calin GA
[Ad] Address:Department of Leukemia, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd, Houston, TX 77030-1402, USA....
[Ti] Title:Epstein-Barr Virus MicroRNAs are Expressed in Patients with Chronic Lymphocytic Leukemia and Correlate with Overall Survival.
[So] Source:EBioMedicine;2(6):572-82, 2015 Jun.
[Is] ISSN:2352-3964
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Although numerous studies highlighted the role of Epstein-Barr Virus (EBV) in B-cell transformation, the involvement of EBV proteins or genome in the development of the most frequent adult leukemia, chronic lymphocytic leukemia (CLL), has not yet been defined. We hypothesized that EBV microRNAs contribute to progression of CLL and demonstrated the presence of EBV miRNAs in B-cells, in paraffin-embedded bone marrow biopsies and in the plasma of patients with CLL by using three different methods (small RNA-sequencing, quantitative reverse transcription PCR [q-RT-PCR] and miRNAs in situ hybridization [miRNA-ISH]). We found that EBV miRNA BHRF1-1 expression levels were significantly higher in the plasma of patients with CLL compared with healthy individuals (p<00001). Notably, BHRF1-1 as well as BART4 expression were detected in the plasma of either seronegative or seropositive (anti-EBNA-1 IgG and EBV DNA tested) patients; similarly, miRNA-ISH stained positive in bone marrow specimens while LMP1 and EBER immunohistochemistry failed to detect viral proteins and RNA. We also found that BHRF1-1 plasma expression levels were positively associated with elevated beta-2-microglobulin levels and advanced Rai stages and observed a correlation between higher BHRF1-1 expression levels and shorter survival in two independent patients' cohorts. Furthermore, in the majority of CLL cases where BHRF1-1 was exogenously induced in primary malignant B cells the levels of TP53 were reduced. Our findings suggest that EBV may have a role in the process of disease progression in CLL and that miRNA RT-PCR and miRNAs ISH could represent additional methods to detect EBV miRNAs in patients with CLL.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1508
[Cu] Class update date: 150822
[Lr] Last revision date:150822
[Da] Date of entry for processing:150820
[St] Status:PubMed-not-MEDLINE
[do] DOI:10.1016/j.ebiom.2015.04.018

  5 / 324904 MEDLINE  
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[PMID]: 26268450
[Au] Autor:Gao F; Zhang C; Zhou C; Sun W; Liu X; Zhang P; Han J; Xian L; Bai D; Liu H; Cheng Y; Li B; Cui J; Cai J; Liu C
[Ad] Address:Department of Radiation Medicine, Faculty of Naval Medicine, Second Military Medical University, Shanghai 200433, PR China....
[Ti] Title:A critical role of toll-like receptor 2 (TLR2) and its' in vivo ligands in radio-resistance.
[So] Source:Sci Rep;5:13004, 2015.
[Is] ISSN:2045-2322
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:The role of Toll-like receptor-2 (TLR2) in radio-resistance remained largely unknown. TLR2 knockout (TLR2(-/-)) mice received radiation of 6.5 Gy, and then were studied. We found that radiation resulted in more severe mortality and morbidity rates in TLR2(-/-) mice. The cause of death in TLR2(-/-) mice may be severe and persistent bone marrow cell loss. Injection of the TLR2 agonist Pam3CSK4 into wild type (WT) mice induced radio-resistance. Myd88(-/-) mice were more susceptible to radiation. In conclusion, our data indicate that, similar to TLR4, TLR2 plays a critical role in radio-resistance.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1508
[Cu] Class update date: 150822
[Lr] Last revision date:150822
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1038/srep13004

  6 / 324904 MEDLINE  
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[PMID]: 25807105
[Au] Autor:Moccetti T; Leri A; Goichberg P; Rota M; Anversa P
[Ad] Address:From the *Foundation Cardiocentro Ticino, University of Zurich, Lugano, Switzerland; and Division of Cardiovascular Medicine, Departments of Anesthesia and Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.
[Ti] Title:A Novel Class of Human Cardiac Stem Cells.
[So] Source:Cardiol Rev;23(4):189-200, 2015 Jul-Aug.
[Is] ISSN:1538-4683
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Following the recognition that hematopoietic stem cells improve the outcome of myocardial infarction in animal models, bone marrow mononuclear cells, CD34-positive cells, and mesenchymal stromal cells have been introduced clinically. The intracoronary or intramyocardial injection of these cell classes has been shown to be safe and to produce a modest but significant enhancement in systolic function. However, the identification of resident cardiac stem cells in the human heart (hCSCs) has created great expectation concerning the potential implementation of this category of autologous cells for the management of the human disease. Although phase 1 clinical trials have been conducted with encouraging results, the search for the most powerful hCSC for myocardial regeneration is in its infancy. This manuscript discusses the efforts performed in our laboratory to characterize the critical biological variables that define the growth reserve of hCSCs. Based on the theory of the immortal DNA template, we propose that stem cells retaining the old DNA represent 1 of the most powerful cells for myocardial regeneration. Similarly, the expression of insulin-like growth factor-1 receptors in hCSCs recognizes a cell phenotype with superior replicating reserve. However, the impressive recovery in ventricular hemodynamics and anatomy mediated by clonal hCSCs carrying the "mother" DNA underscores the clinical relevance of this hCSC class for the treatment of human heart failure.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1506
[Cu] Class update date: 150822
[Lr] Last revision date:150822
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1097/CRD.0000000000000064

  7 / 324904 MEDLINE  
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[PMID]: 25869128
[Au] Autor:Singer K; Maley N; Mergian T; DelProposto J; Cho KW; Zamarron BF; Martinez-Santibanez G; Geletka L; Muir L; Wachowiak P; Demirjian C; Lumeng CN
[Ad] Address:From the Department of Pediatrics and Communicable Disease, ksinger@umich.edu....
[Ti] Title:Differences in Hematopoietic Stem Cells Contribute to Sexually Dimorphic Inflammatory Responses to High Fat Diet-induced Obesity.
[So] Source:J Biol Chem;290(21):13250-62, 2015 May 22.
[Is] ISSN:1083-351X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Women of reproductive age are protected from metabolic disease relative to postmenopausal women and men. Most preclinical rodent studies are skewed toward the use of male mice to study obesity-induced metabolic dysfunction because of a similar protection observed in female mice. How sex differences in obesity-induced inflammatory responses contribute to these observations is unknown. We have compared and contrasted the effects of high fat diet-induced obesity on glucose metabolism and leukocyte activation in multiple depots in male and female C57Bl/6 mice. With both short term and long term high fat diet, male mice demonstrated increased weight gain and CD11c(+) adipose tissue macrophage content compared with female mice despite similar degrees of adipocyte hypertrophy. Competitive bone marrow transplant studies demonstrated that obesity induced a preferential contribution of male hematopoietic cells to circulating leukocytes and adipose tissue macrophages compared with female cells independent of the sex of the recipient. Sex differences in macrophage and hematopoietic cell in vitro activation in response to obesogenic cues were observed to explain these results. In summary, this report demonstrates that male and female leukocytes and hematopoietic stem cells have cell-autonomous differences in their response to obesity that contribute to an amplified response in males compared with females.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1505
[Cu] Class update date: 150822
[Lr] Last revision date:150822
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1074/jbc.M114.634568

  8 / 324904 MEDLINE  
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[PMID]: 25810145
[Au] Autor:Shin JW; Discher DE
[Ad] Address:Biophysical Engineering Laboratory, University of Pennsylvania, Philadelphia, PA, USA.
[Ti] Title:Blood and immune cell engineering: Cytoskeletal contractility and nuclear rheology impact cell lineage and localization: Biophysical regulation of hematopoietic differentiation and trafficking.
[So] Source:Bioessays;37(6):633-42, 2015 Jun.
[Is] ISSN:1521-1878
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Clinical success with human hematopoietic stem cell (HSC) transplantation establishes a paradigm for regenerative therapies with other types of stem cells. However, it remains generally challenging to therapeutically treat tissues after engineering of stem cells in vitro. Recent studies suggest that stem and progenitor cells sense physical features of their niches. Here, we review biophysical contributions to lineage decisions, maturation, and trafficking of blood and immune cells. Polarized cellular contractility and nuclear rheology are separately shown to be functional markers of a hematopoietic hierarchy that predict the ability of a lineage to traffic in and out of the bone marrow niche. These biophysical determinants are regulated by a set of structural molecules, including cytoplasmic myosin-II and nuclear lamins, which themselves are modulated by a diverse range of transcriptional and post-translational mechanisms. Small molecules that target these mechanobiological circuits, along with novel bioengineering methods, could prove broadly useful in programming blood and immune cells for therapies ranging from blood transfusions to immune attack of tumors.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1505
[Cu] Class update date: 150822
[Lr] Last revision date:150822
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1002/bies.201400166

  9 / 324904 MEDLINE  
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[PMID]: 25902481
[Au] Autor:Hoeffel G; Chen J; Lavin Y; Low D; Almeida FF; See P; Beaudin AE; Lum J; Low I; Forsberg EC; Poidinger M; Zolezzi F; Larbi A; Ng LG; Chan JK; Greter M; Becher B; Samokhvalov IM; Merad M; Ginhoux F
[Ad] Address:Singapore Immunology Network (SIgN), Agency for Science, Technology and Research (A(∗)STAR), 8A Biomedical Grove, IMMUNOS Building #3-4, BIOPOLIS, 138648 Singapore....
[Ti] Title:C-Myb(+) erythro-myeloid progenitor-derived fetal monocytes give rise to adult tissue-resident macrophages.
[So] Source:Immunity;42(4):665-78, 2015 Apr 21.
[Is] ISSN:1097-4180
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Although classified as hematopoietic cells, tissue-resident macrophages (MFs) arise from embryonic precursors that seed the tissues prior to birth to generate a self-renewing population, which is maintained independently of adult hematopoiesis. Here we reveal the identity of these embryonic precursors using an in utero MF-depletion strategy and fate-mapping of yolk sac (YS) and fetal liver (FL) hematopoiesis. We show that YS MFs are the main precursors of microglia, while most other MFs derive from fetal monocytes (MOs). Both YS MFs and fetal MOs arise from erythro-myeloid progenitors (EMPs) generated in the YS. In the YS, EMPs gave rise to MFs without monocytic intermediates, while EMP seeding the FL upon the establishment of blood circulation acquired c-Myb expression and gave rise to fetal MOs that then seeded embryonic tissues and differentiated into MFs. Thus, adult tissue-resident MFs established from hematopoietic stem cell-independent embryonic precursors arise from two distinct developmental programs.
[Mh] MeSH terms primary: Aging/immunology
Macrophages/immunology
Monocytes/immunology
Myeloid Progenitor Cells/immunology
Proto-Oncogene Proteins c-myb/immunology
[Mh] MeSH terms secundary: Animals
Biological Markers/metabolism
Cell Differentiation
Cell Lineage/immunology
Cell Tracking
Embryo, Mammalian
Female
Fetus
Hematopoietic Stem Cells/cytology
Hematopoietic Stem Cells/immunology
Kidney/cytology
Kidney/immunology
Liver/cytology
Liver/immunology
Lung/cytology
Lung/immunology
Macrophages/cytology
Mice
Microglia/cytology
Microglia/immunology
Monocytes/cytology
Myeloid Progenitor Cells/cytology
Pregnancy
Primary Cell Culture
Proto-Oncogene Proteins c-myb/metabolism
Skin/cytology
Skin/immunology
Yolk Sac/cytology
Yolk Sac/immunology
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Biological Markers); 0 (Proto-Oncogene Proteins c-myb)
[Em] Entry month:1506
[Cu] Class update date: 150822
[Lr] Last revision date:150822
[Js] Journal subset:IM
[Da] Date of entry for processing:150423
[St] Status:MEDLINE

  10 / 324904 MEDLINE  
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[PMID]: 25772073
[Au] Autor:Menon T; Firth AL; Scripture-Adams DD; Galic Z; Qualls SJ; Gilmore WB; Ke E; Singer O; Anderson LS; Bornzin AR; Alexander IE; Zack JA; Verma IM
[Ad] Address:The Salk Institute of Biological Studies, Laboratory of Genetics, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA....
[Ti] Title:Lymphoid regeneration from gene-corrected SCID-X1 subject-derived iPSCs.
[So] Source:Cell Stem Cell;16(4):367-72, 2015 Apr 2.
[Is] ISSN:1875-9777
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:X-linked Severe Combined Immunodeficiency (SCID-X1) is a genetic disease that leaves newborns at high risk of serious infection and a predicted life span of less than 1 year in the absence of a matched bone marrow donor. The disease pathogenesis is due to mutations in the gene encoding the Interleukin-2 receptor gamma chain (IL-2Rγ), leading to a lack of functional lymphocytes. With the leukemogenic concerns of viral gene therapy there is a need to explore alternative therapeutic options. We have utilized induced pluripotent stem cell (iPSC) technology and genome editing mediated by TALENs to generate isogenic subject-specific mutant and gene-corrected iPSC lines. While the subject-derived mutant iPSCs have the capacity to generate hematopoietic precursors and myeloid cells, only wild-type and gene-corrected iPSCs can additionally generate mature NK cells and T cell precursors expressing the correctly spliced IL-2Rγ. This study highlights the potential for the development of autologous cell therapy for SCID-X1 subjects.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1504
[Cu] Class update date: 150822
[Lr] Last revision date:150822
[Js] Journal subset:IM
[St] Status:In-Process


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