Altered phenotype of NK cells from obese rats can be normalized by transfer into lean animals.

Anne Lautenbach; Christiane D Wrann; Roland Jacobs; Guenter Müller; Georg Brabant; Heike Nave

Altered phenotype of NK cells from obese rats can be normalized by transfer into lean animals.

Standard

Altered phenotype of NK cells from obese rats can be normalized by transfer into lean animals. / Lautenbach, Anne; Wrann, Christiane D; Jacobs, Roland; Müller, Guenter; Brabant, Georg; Nave, Heike.

in: OBESITY, Jahrgang 17, Nr. 10, 10, 2009, S. 1848-1855.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Lautenbach, A, Wrann, CD, Jacobs, R, Müller, G, Brabant, G & Nave, H 2009, 'Altered phenotype of NK cells from obese rats can be normalized by transfer into lean animals.', OBESITY, Jg. 17, Nr. 10, 10, S. 1848-1855. <http://www.ncbi.nlm.nih.gov/pubmed/19444229?dopt=Citation>

APA

Lautenbach, A., Wrann, C. D., Jacobs, R., Müller, G., Brabant, G., & Nave, H. (2009). Altered phenotype of NK cells from obese rats can be normalized by transfer into lean animals. OBESITY, 17(10), 1848-1855. [10]. http://www.ncbi.nlm.nih.gov/pubmed/19444229?dopt=Citation

Vancouver

Lautenbach A, Wrann CD, Jacobs R, Müller G, Brabant G, Nave H. Altered phenotype of NK cells from obese rats can be normalized by transfer into lean animals. OBESITY. 2009;17(10):1848-1855. 10.

Bibtex

@article{970c235d834c48f69dc23f3e0f39f59c,

title = "Altered phenotype of NK cells from obese rats can be normalized by transfer into lean animals.",

abstract = "In diet-induced obese rats, leptin-mediated natural killer (NK) cell activation has been demonstrated to be impaired by abrogated intracellular JAK2-STAT3 signaling. The contribution of the obese microenvironment to this NK cell dysfunction and its reversibility remains elusive. In this study, the functions of NK cells from diet-induced obese rats after adoptive transfer into lean littermates were investigated using in vivo and in vitro approaches. Endogenous NK cells of normal-weight and diet-induced obese F344 rats were depleted in vivo. Then, NK cells from either normal-weight or obese donors were transferred. The numbers of peripheral blood NK cells were analyzed by fluorescence-activated cell sorting (FACS) and the distribution pattern of NK cells in lung and spleen by immunohistochemistry. Ob-R expression was evaluated by immunohistology and activation of intracellular target proteins of Ob-R by immunoblotting. The numbers of NK cells in blood and lung were significantly higher in obese animals compared to lean ones after transfer of NK cells from obese F344 rats. This was correlated with increased postreceptor signaling (JAK-2p, PKBpT308, ERK-2p) without altered Ob-R expression in those NK cells transferred to lean (ob-->nw) vs. obese (ob-->ob) animals. These results show for the first time that the altered phenotype of NK cells from obese rats can be normalized by generation of a physiological (metabolic) environment of lean rats.",

keywords = "Animals, Male, Immunohistochemistry, Rats, Phenotype, Immunoblotting, Signal Transduction, Flow Cytometry, Specific Pathogen-Free Organisms, Random Allocation, Adoptive Transfer, Janus Kinase 2/blood, Killer Cells, Natural/*immunology/pathology, Liver/immunology/pathology, Lung/immunology/pathology, Obesity/blood/*immunology/pathology, Rats, Inbred F344, Receptors, Leptin/immunology, STAT3 Transcription Factor/blood, Spleen/immunology/pathology, Animals, Male, Immunohistochemistry, Rats, Phenotype, Immunoblotting, Signal Transduction, Flow Cytometry, Specific Pathogen-Free Organisms, Random Allocation, Adoptive Transfer, Janus Kinase 2/blood, Killer Cells, Natural/*immunology/pathology, Liver/immunology/pathology, Lung/immunology/pathology, Obesity/blood/*immunology/pathology, Rats, Inbred F344, Receptors, Leptin/immunology, STAT3 Transcription Factor/blood, Spleen/immunology/pathology",

author = "Anne Lautenbach and Wrann, {Christiane D} and Roland Jacobs and Guenter M{\"u}ller and Georg Brabant and Heike Nave",

year = "2009",

language = "English",

volume = "17",

pages = "1848--1855",

number = "10",

}

RIS

TY - JOUR

T1 - Altered phenotype of NK cells from obese rats can be normalized by transfer into lean animals.

AU - Lautenbach, Anne

AU - Wrann, Christiane D

AU - Jacobs, Roland

AU - Müller, Guenter

AU - Brabant, Georg

AU - Nave, Heike

PY - 2009

Y1 - 2009

N2 - In diet-induced obese rats, leptin-mediated natural killer (NK) cell activation has been demonstrated to be impaired by abrogated intracellular JAK2-STAT3 signaling. The contribution of the obese microenvironment to this NK cell dysfunction and its reversibility remains elusive. In this study, the functions of NK cells from diet-induced obese rats after adoptive transfer into lean littermates were investigated using in vivo and in vitro approaches. Endogenous NK cells of normal-weight and diet-induced obese F344 rats were depleted in vivo. Then, NK cells from either normal-weight or obese donors were transferred. The numbers of peripheral blood NK cells were analyzed by fluorescence-activated cell sorting (FACS) and the distribution pattern of NK cells in lung and spleen by immunohistochemistry. Ob-R expression was evaluated by immunohistology and activation of intracellular target proteins of Ob-R by immunoblotting. The numbers of NK cells in blood and lung were significantly higher in obese animals compared to lean ones after transfer of NK cells from obese F344 rats. This was correlated with increased postreceptor signaling (JAK-2p, PKBpT308, ERK-2p) without altered Ob-R expression in those NK cells transferred to lean (ob-->nw) vs. obese (ob-->ob) animals. These results show for the first time that the altered phenotype of NK cells from obese rats can be normalized by generation of a physiological (metabolic) environment of lean rats.

AB - In diet-induced obese rats, leptin-mediated natural killer (NK) cell activation has been demonstrated to be impaired by abrogated intracellular JAK2-STAT3 signaling. The contribution of the obese microenvironment to this NK cell dysfunction and its reversibility remains elusive. In this study, the functions of NK cells from diet-induced obese rats after adoptive transfer into lean littermates were investigated using in vivo and in vitro approaches. Endogenous NK cells of normal-weight and diet-induced obese F344 rats were depleted in vivo. Then, NK cells from either normal-weight or obese donors were transferred. The numbers of peripheral blood NK cells were analyzed by fluorescence-activated cell sorting (FACS) and the distribution pattern of NK cells in lung and spleen by immunohistochemistry. Ob-R expression was evaluated by immunohistology and activation of intracellular target proteins of Ob-R by immunoblotting. The numbers of NK cells in blood and lung were significantly higher in obese animals compared to lean ones after transfer of NK cells from obese F344 rats. This was correlated with increased postreceptor signaling (JAK-2p, PKBpT308, ERK-2p) without altered Ob-R expression in those NK cells transferred to lean (ob-->nw) vs. obese (ob-->ob) animals. These results show for the first time that the altered phenotype of NK cells from obese rats can be normalized by generation of a physiological (metabolic) environment of lean rats.

KW - Animals

KW - Male

KW - Immunohistochemistry

KW - Rats

KW - Phenotype

KW - Immunoblotting

KW - Signal Transduction

KW - Flow Cytometry

KW - Specific Pathogen-Free Organisms

KW - Random Allocation

KW - Adoptive Transfer

KW - Janus Kinase 2/blood

KW - Killer Cells, Natural/immunology/pathology

KW - Liver/immunology/pathology

KW - Lung/immunology/pathology

KW - Obesity/blood/immunology/pathology

KW - Rats, Inbred F344

KW - Receptors, Leptin/immunology

KW - STAT3 Transcription Factor/blood

KW - Spleen/immunology/pathology