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Article ; Online: Glutamatergic Transmission to Hypothalamic Kisspeptin Neurons Is Differentially Regulated by Estradiol through Estrogen Receptor α in Adult Female Mice.

Wang, Luhong / Burger, Laura L / Greenwald-Yarnell, Megan L / Myers, Martin G / Moenter, Suzanne M

The Journal of neuroscience : the official journal of the Society for Neuroscience

2017 Volume 38, Issue 5, Page(s) 1061–1072

Abstract: Estradiol feedback regulates gonadotropin-releasing hormone (GnRH) neurons and subsequent luteinizing hormone (LH) release. Estradiol acts via estrogen receptor α (ERα)-expressing afferents of GnRH neurons, including kisspeptin neurons in the ... ...

Abstract	Estradiol feedback regulates gonadotropin-releasing hormone (GnRH) neurons and subsequent luteinizing hormone (LH) release. Estradiol acts via estrogen receptor α (ERα)-expressing afferents of GnRH neurons, including kisspeptin neurons in the anteroventral periventricular (AVPV) and arcuate nuclei, providing homeostatic feedback on episodic GnRH/LH release as well as positive feedback to control ovulation. Ionotropic glutamate receptors are important for estradiol feedback, but it is not known where they fit in the circuitry. Estradiol-negative feedback decreased glutamatergic transmission to AVPV and increased it to arcuate kisspeptin neurons; positive feedback had the opposite effect. Deletion of ERα in kisspeptin cells decreased glutamate transmission to AVPV neurons and markedly increased it to arcuate kisspeptin neurons, which also exhibited increased spontaneous firing rate. KERKO mice had increased LH pulse frequency, indicating loss of negative feedback. These observations indicate that ERα in kisspeptin cells is required for appropriate differential regulation of these neurons and neuroendocrine output by estradiol.
MeSH term(s)	Animals ; Arcuate Nucleus of Hypothalamus/physiology ; Dynorphins/pharmacology ; Estradiol/pharmacology ; Female ; Gene Expression Regulation/genetics ; Gene Expression Regulation/physiology ; Glutamates/physiology ; Hypothalamus/cytology ; Hypothalamus/drug effects ; Hypothalamus/physiology ; Kisspeptins/physiology ; Luteinizing Hormone/physiology ; Mice ; Midline Thalamic Nuclei/physiology ; Neurons/drug effects ; Neurons/physiology ; Pituitary Gland/drug effects ; Pituitary Gland/physiology ; Proestrus/physiology ; Receptors, Estrogen/drug effects ; Receptors, Ionotropic Glutamate/drug effects ; Receptors, Ionotropic Glutamate/physiology ; Synaptic Transmission/drug effects ; Synaptic Transmission/physiology ; ERRalpha Estrogen-Related Receptor
Chemical Substances	Glutamates ; Kisspeptins ; Receptors, Estrogen ; Receptors, Ionotropic Glutamate ; Estradiol (4TI98Z838E) ; Dynorphins (74913-18-1) ; Luteinizing Hormone (9002-67-9)
Language	English
Publishing date	2017-11-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	604637-x
ISSN	1529-2401 ; 0270-6474
ISSN (online)	1529-2401
ISSN	0270-6474
DOI	10.1523/JNEUROSCI.2428-17.2017
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Zs.A 1668: Show issues

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Article ; Online: Leptin action through hypothalamic nitric oxide synthase-1-expressing neurons controls energy balance.

Leshan, Rebecca L / Greenwald-Yarnell, Megan / Patterson, Christa M / Gonzalez, Ian E / Myers, Martin G

Nature medicine

2012 Volume 18, Issue 5, Page(s) 820–823

Abstract: Few effective measures exist to combat the worldwide obesity epidemic(1), and the identification of potential therapeutic targets requires a deeper understanding of the mechanisms that control energy balance. Leptin, an adipocyte-derived hormone that ... ...

Abstract	Few effective measures exist to combat the worldwide obesity epidemic(1), and the identification of potential therapeutic targets requires a deeper understanding of the mechanisms that control energy balance. Leptin, an adipocyte-derived hormone that signals the long-term status of bodily energy stores, acts through multiple types of leptin receptor long isoform (LepRb)-expressing neurons (called here LepRb neurons) in the brain to control feeding, energy expenditure and endocrine function(2-4). The modest contributions to energy balance that are attributable to leptin action in many LepRb populations(5-9) suggest that other previously unidentified hypothalamic LepRb neurons have key roles in energy balance. Here we examine the role of LepRb in neuronal nitric oxide synthase (NOS1)-expressing LebRb (LepRb(NOS1)) neurons that comprise approximately 20% of the total hypothalamic LepRb neurons. Nos1(cre)-mediated genetic ablation of LepRb (Lepr(Nos1KO)) in mice produces hyperphagic obesity, decreased energy expenditure and hyperglycemia approaching that seen in whole-body LepRb-null mice. In contrast, the endocrine functions in Lepr(Nos1KO) mice are only modestly affected by the genetic ablation of LepRb in these neurons. Thus, hypothalamic LepRb(NOS1) neurons are a key site of action of the leptin-mediated control of systemic energy balance.
MeSH term(s)	Animals ; Energy Metabolism ; Hypothalamus/physiology ; Leptin/physiology ; Mice ; Neurons/physiology ; Nitric Oxide Synthase Type I/physiology ; Receptors, Leptin/physiology
Chemical Substances	Leptin ; Receptors, Leptin ; Nitric Oxide Synthase Type I (EC 1.14.13.39) ; Nos1 protein, mouse (EC 1.14.13.39)
Language	English
Publishing date	2012-04-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1220066-9
ISSN	1546-170X ; 1078-8956
ISSN (online)	1546-170X
ISSN	1078-8956
DOI	10.1038/nm.2724
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Zs.A 4212: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Activation of Ventral Tegmental Area 5-HT

Valencia-Torres, Lourdes / Olarte-Sánchez, Cristian M / Lyons, David J / Georgescu, Teodora / Greenwald-Yarnell, Megan / Myers, Martin G / Bradshaw, Christopher M / Heisler, Lora K

Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology

2017 Volume 42, Issue 7, Page(s) 1511–1521

Abstract: Obesity is primarily due to food intake in excess of the body's energetic requirements, intake that is not only associated with hunger but also the incentive value of food. The 5-hydroxytryptamine 2C receptor (5- ... ...

Abstract	Obesity is primarily due to food intake in excess of the body's energetic requirements, intake that is not only associated with hunger but also the incentive value of food. The 5-hydroxytryptamine 2C receptor (5-HT
MeSH term(s)	Animals ; Benzazepines/pharmacology ; Conditioning, Operant/drug effects ; Conditioning, Operant/physiology ; Eating/drug effects ; Eating/physiology ; Eating/psychology ; Female ; Male ; Mice ; Mice, Transgenic ; Motivation/drug effects ; Motivation/physiology ; Receptor, Serotonin, 5-HT2C/metabolism ; Serotonin 5-HT2 Receptor Agonists/pharmacology ; Ventral Tegmental Area/drug effects ; Ventral Tegmental Area/metabolism
Chemical Substances	Benzazepines ; Receptor, Serotonin, 5-HT2C ; Serotonin 5-HT2 Receptor Agonists ; lorcaserin (637E494O0Z)
Language	English
Publishing date	2017-06
Publishing country	England
Document type	Journal Article
ZDB-ID	639471-1
ISSN	1740-634X ; 0893-133X
ISSN (online)	1740-634X
ISSN	0893-133X
DOI	10.1038/npp.2016.264
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Zs.A 2379: Show issues

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Article ; Online: Nucleus of the Solitary Tract Serotonin 5-HT

D'Agostino, Giuseppe / Lyons, David / Cristiano, Claudia / Lettieri, Miriam / Olarte-Sanchez, Cristian / Burke, Luke K / Greenwald-Yarnell, Megan / Cansell, Celine / Doslikova, Barbora / Georgescu, Teodora / Martinez de Morentin, Pablo Blanco / Myers, Martin G / Rochford, Justin J / Heisler, Lora K

Cell metabolism

2018 Volume 28, Issue 4, Page(s) 619–630.e5

Abstract: To meet the challenge to human health posed by obesity, a better understanding of the regulation of feeding is essential. Medications targeting 5-hydroxytryptamine (5-HT; serotonin) 2C receptors (htr2c; 5- ... ...

Abstract	To meet the challenge to human health posed by obesity, a better understanding of the regulation of feeding is essential. Medications targeting 5-hydroxytryptamine (5-HT; serotonin) 2C receptors (htr2c; 5-HT
MeSH term(s)	Analysis of Variance ; Animals ; Appetite Depressants/metabolism ; Appetite Depressants/therapeutic use ; Appetite Regulation/drug effects ; Arcuate Nucleus of Hypothalamus/cytology ; Benzazepines/metabolism ; Benzazepines/therapeutic use ; Cell Line, Tumor ; Eating/physiology ; Feeding Behavior/physiology ; Male ; Mice ; Mice, Knockout ; Neurons/metabolism ; Obesity/drug therapy ; Receptor, Serotonin, 5-HT2C/metabolism ; Serotonin 5-HT2 Receptor Agonists/metabolism ; Serotonin 5-HT2 Receptor Agonists/therapeutic use ; Solitary Nucleus/metabolism ; Statistics, Nonparametric ; Transfection
Chemical Substances	Appetite Depressants ; Benzazepines ; Receptor, Serotonin, 5-HT2C ; Serotonin 5-HT2 Receptor Agonists ; lorcaserin (637E494O0Z)
Language	English
Publishing date	2018-08-23
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2176834-1
ISSN	1932-7420 ; 1550-4131
ISSN (online)	1932-7420
ISSN	1550-4131
DOI	10.1016/j.cmet.2018.07.017
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Zs.A 6169: Show issues

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Article ; Online: ERα in Tac2 Neurons Regulates Puberty Onset in Female Mice.

Greenwald-Yarnell, Megan L / Marsh, Courtney / Allison, Margaret B / Patterson, Christa M / Kasper, Chelsea / MacKenzie, Alexander / Cravo, Roberta / Elias, Carol F / Moenter, Suzanne M / Myers, Martin G

Endocrinology

2016 Volume 157, Issue 4, Page(s) 1555–1565

Abstract: A variety of data suggest that estrogen action on kisspeptin (Kiss1)-containing arcuate nucleus neurons (which coexpress Kiss1, neurokinin B (the product of Tac2) and dynorphin (KNDy) neurons restrains reproductive onset and function, but roles for ... ...

Abstract	A variety of data suggest that estrogen action on kisspeptin (Kiss1)-containing arcuate nucleus neurons (which coexpress Kiss1, neurokinin B (the product of Tac2) and dynorphin (KNDy) neurons restrains reproductive onset and function, but roles for estrogen action in these Kiss1 neurons relative to a distinct population of rostral hypothalamic Kiss1 neurons (which does not express Tac2 or dynorphin) have not been directly tested. To test the role for estrogen receptor (ER)α in KNDy cells, we thus generated Tac2(Cre) and Kiss1(Cre) knock-in mice and bred them onto the Esr1(flox) background to ablate ERα specifically in Tac2-expressing cells (ERα(Tac2)KO mice) or all Kiss1 cells (ERα(Kiss1)KO mice), respectively. Most ERα-expressing Tac2 neurons represent KNDy cells. Arcuate nucleus Kiss1 expression was elevated in ERα(Tac2)KO and ERα(Kiss1)KO females independent of gonadal hormones, whereas rostral hypothalamic Kiss1 expression was normal in ERα(Tac2)KO but decreased in ERα(Kiss1)KO females; this suggests that ERα in rostral Kiss1 cells is crucial for control of Kiss1 expression in these cells. Both ERα(Kiss1)KO and ERα(Tac2)KO females displayed early vaginal opening, early and persistent vaginal cornification, increased gonadotropins, uterine hypertrophy, and other evidence of estrogen excess. Thus, deletion of ERα in Tac2 neurons suffices to drive precocious gonadal hyperstimulation, demonstrating that ERα in Tac2 neurons typically restrains pubertal onset and hypothalamic reproductive drive.
MeSH term(s)	Animals ; Body Composition/genetics ; Body Composition/physiology ; Dynorphins/genetics ; Dynorphins/metabolism ; Estradiol/metabolism ; Estrogen Receptor alpha/genetics ; Estrogen Receptor alpha/metabolism ; Female ; Gonadotropins/metabolism ; Hypothalamus/cytology ; Hypothalamus/metabolism ; Kisspeptins/genetics ; Kisspeptins/metabolism ; Mice, Knockout ; Mice, Transgenic ; Microscopy, Fluorescence ; Neurons/metabolism ; Ovariectomy ; Ovary/metabolism ; Protein Precursors/genetics ; Protein Precursors/metabolism ; Reproduction/genetics ; Reproduction/physiology ; Reverse Transcriptase Polymerase Chain Reaction ; Sexual Maturation/genetics ; Sexual Maturation/physiology ; Tachykinins/genetics ; Tachykinins/metabolism ; Time Factors ; Uterus/metabolism
Chemical Substances	Estrogen Receptor alpha ; Gonadotropins ; Kiss1 protein, mouse ; Kisspeptins ; Protein Precursors ; Tachykinins ; preprotachykinin ; Estradiol (4TI98Z838E) ; Dynorphins (74913-18-1)
Language	English
Publishing date	2016-02-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/en.2015-1928
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Article: Leptin action via LepR-b Tyr1077 contributes to the control of energy balance and female reproduction.

Patterson, Christa M / Villanueva, Eneida C / Greenwald-Yarnell, Megan / Rajala, Michael / Gonzalez, Ian E / Saini, Natinder / Jones, Justin / Myers, Martin G

Molecular metabolism

2012 Volume 1, Issue 1-2, Page(s) 61–69

Abstract: Leptin action in the brain signals the repletion of adipose energy stores, suppressing feeding and permitting energy expenditure on a variety of processes, including reproduction. Leptin binding to its receptor (LepR-b) promotes the tyrosine ... ...

Abstract	Leptin action in the brain signals the repletion of adipose energy stores, suppressing feeding and permitting energy expenditure on a variety of processes, including reproduction. Leptin binding to its receptor (LepR-b) promotes the tyrosine phosphorylation of three sites on LepR-b, each of which mediates distinct downstream signals. While the signals mediated by LepR-b Tyr1138 and Tyr985 control important aspects of energy homeostasis and LepR-b signal attenuation, respectively, the role of the remaining LepR-b phosphorylation site (Tyr1077) in leptin action has not been studied. To examine the function of Tyr1077, we generated a "knock-in" mouse model expressing LepR-b (F1077), which is mutant for LepR-b Tyr1077. Mice expressing LepR-b (F1077) demonstrate modestly increased body weight and adiposity. Furthermore, females display impairments in estrous cycling. Our results suggest that signaling by LepR-b Tyr1077 plays a modest role in the control of metabolism by leptin, and is an important link between body adiposity and the reproductive axis.
Language	English
Publishing date	2012-07-26
Publishing country	Germany
Document type	Journal Article
ZDB-ID	2708735-9
ISSN	2212-8778
ISSN	2212-8778
DOI	10.1016/j.molmet.2012.05.001
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Article ; Online: Testosterone interacts with the feedback mechanisms engaged by Tyr985 of the leptin receptor and diet-induced obesity.

Johnson, Joshua A / Calo, Sal / Nair, Lekshmi / IglayReger, Heidi B / Greenwald-Yarnell, Megan / Skorupski, Josh / Myers, Martin G / Bodary, Peter F

The Journal of steroid biochemistry and molecular biology

2012 Volume 132, Issue 3-5, Page(s) 212–219

Abstract: Inhibitory signaling through Tyr985 of the leptin receptor contributes to the attenuation of anorectic leptin action in obese animals. Leptin receptor (LEPR-B) Tyr985Leu homozygote mutant mice (termed l/l) were previously generated to study Tyr985's ... ...

Abstract	Inhibitory signaling through Tyr985 of the leptin receptor contributes to the attenuation of anorectic leptin action in obese animals. Leptin receptor (LEPR-B) Tyr985Leu homozygote mutant mice (termed l/l) were previously generated to study Tyr985's contributions to inhibition of LEPR-B signaling; young female l/l mice display a lean, leptin-sensitive phenotype, while young male l/l are not significantly different from wild-type. We report here that testosterone (but not estrogen) determines the sex-specificity of the l/l phenotype. This provides additional insight into the cellular mechanism by which gonadal hormones determine central sensitivity to leptin, and may help elucidate the long-noted sex differences in leptin sensitivity. Additionally, we observed that Tyr985 signaling protects against a diet-dependent switch that exacerbates obesity with high fat feeding, such that the enhanced leptin sensitivity of l/l mice on a normal diet leads to increased adiposity in the face of chronic high-fat diet.
MeSH term(s)	Animals ; Diet, High-Fat/adverse effects ; Estradiol/metabolism ; Estradiol/pharmacology ; Feedback, Physiological ; Female ; Hypothalamus/metabolism ; Longitudinal Studies ; Male ; Mice ; Mice, Knockout ; Obesity/etiology ; Obesity/metabolism ; Orchiectomy ; Ovariectomy ; Receptors, Androgen/metabolism ; Receptors, Leptin/genetics ; Receptors, Leptin/metabolism ; Testosterone/metabolism ; Testosterone/pharmacology ; Tyrosine/metabolism
Chemical Substances	Receptors, Androgen ; Receptors, Leptin ; leptin receptor, mouse ; Testosterone (3XMK78S47O) ; Tyrosine (42HK56048U) ; Estradiol (4TI98Z838E)
Language	English
Publishing date	2012-11
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1049188-0
ISSN	1879-1220 ; 0960-0760
ISSN (online)	1879-1220
ISSN	0960-0760
DOI	10.1016/j.jsbmb.2012.06.002
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Article: Testosterone interacts with the feedback mechanisms engaged by Tyr985 of the leptin receptor and diet-induced obesity

Johnson, Joshua A / Calo, Sal / Nair, Lekshmi / IglayReger, Heidi B / Greenwald-Yarnell, Megan / Skorupski, Josh / Myers, Martin G., Jr / Bodary, Peter F

Journal of steroid biochemistry and molecular biology. 2012 Nov., v. 132, no. 3-5

2012

Abstract	Inhibitory signaling through Tyr985 of the leptin receptor contributes to the attenuation of anorectic leptin action in obese animals. Leptin receptor (LEPR-B) Tyr985Leu homozygote mutant mice (termed l/l) were previously generated to study Tyr985's contributions to inhibition of LEPR-B signaling; young female l/l mice display a lean, leptin-sensitive phenotype, while young male l/l are not significantly different from wild-type. We report here that testosterone (but not estrogen) determines the sex-specificity of the l/l phenotype. This provides additional insight into the cellular mechanism by which gonadal hormones determine central sensitivity to leptin, and may help elucidate the long-noted sex differences in leptin sensitivity. Additionally, we observed that Tyr985 signaling protects against a diet-dependent switch that exacerbates obesity with high fat feeding, such that the enhanced leptin sensitivity of l/l mice on a normal diet leads to increased adiposity in the face of chronic high-fat diet.
Keywords	adiposity ; females ; gender differences ; high fat diet ; leptin ; leptin receptors ; males ; mice ; mutants ; obesity ; phenotype ; testosterone
Language	English
Dates of publication	2012-11
Size	p. 212-219.
Publishing place	Elsevier Ltd
Document type	Article
ZDB-ID	1049188-0
ISSN	1879-1220 ; 0960-0760
ISSN (online)	1879-1220
ISSN	0960-0760
DOI	10.1016/j.jsbmb.2012.06.002
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Article ; Online: Molecular mapping of the neural pathways linking leptin to the neuroendocrine reproductive axis.

Louis, Gwendolyn W / Greenwald-Yarnell, Megan / Phillips, Rebecca / Coolen, Lique M / Lehman, Michael N / Myers, Martin G

Endocrinology

2011 Volume 152, Issue 6, Page(s) 2302–2310

Abstract: Negative energy balance and insufficient adipose energy stores decrease the production of leptin, thereby diminishing the leptin-supported secretion of GnRH from the hypothalamus and promoting decreased reproductive function. Leptin acts via its receptor ...

Abstract	Negative energy balance and insufficient adipose energy stores decrease the production of leptin, thereby diminishing the leptin-supported secretion of GnRH from the hypothalamus and promoting decreased reproductive function. Leptin acts via its receptor (LepRb) to support the neuroendocrine reproductive axis, but the nature and location of the relevant LepRb neurons remain poorly understood. Possibilities include the direct or indirect action of leptin on hypothalamic GnRH neurons, or on kisspeptin (Kiss1) neurons that are major regulators of GnRH neurons. To evaluate these potential mechanisms, we employed immunohistochemical analysis of the female brain from various molecular mouse models and sheep. Our analysis revealed no LepRb in GnRH neurons or in anteroventral periventricular Kiss1 neurons, and very limited (0-6%) colocalization with arcuate nucleus Kiss1 cells, suggesting that leptin does not modulate reproduction by direct action on any of these neural populations. LepRb neurons, primarily in the hypothalamic ventral premammillary nucleus and a subregion of the preoptic area, lie in close contact with GnRH neurons, however. Furthermore, an unidentified population or populations of LepRb neurons lie in close contact with arcuate nucleus and anteroventral periventricular Kiss1 neurons. Taken together, these findings suggest that leptin communicates with the neuroendocrine reproductive axis via multiple populations of LepRb neurons that lie afferent to both Kiss1 and GnRH neurons.
MeSH term(s)	Animals ; Brain/cytology ; Brain/metabolism ; Female ; Gonadotropin-Releasing Hormone/metabolism ; Kisspeptins/genetics ; Kisspeptins/metabolism ; Leptin/metabolism ; Male ; Mice ; Mice, Transgenic ; Neural Pathways/metabolism ; Neuroendocrine Cells/metabolism ; Neurons/metabolism ; Receptors, Leptin/genetics ; Receptors, Leptin/metabolism ; Reproduction ; Sheep
Chemical Substances	Kiss1 protein, mouse ; Kisspeptins ; Leptin ; Receptors, Leptin ; Gonadotropin-Releasing Hormone (33515-09-2)
Language	English
Publishing date	2011-03-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/en.2011-0096
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Article ; Online: Disruption of leptin receptor-STAT3 signaling enhances leukotriene production and pulmonary host defense against pneumococcal pneumonia.

Mancuso, Peter / Peters-Golden, Marc / Goel, Deepti / Goldberg, Jared / Brock, Thomas G / Greenwald-Yarnell, Megan / Myers, Martin G

Journal of immunology (Baltimore, Md. : 1950)

2010 Volume 186, Issue 2, Page(s) 1081–1090

Abstract: The adipocyte-derived hormone leptin regulates energy homeostasis and the innate immune response. We previously reported that leptin plays a protective role in bacterial pneumonia, but the mechanisms by which leptin regulates host defense remain poorly ... ...

Abstract	The adipocyte-derived hormone leptin regulates energy homeostasis and the innate immune response. We previously reported that leptin plays a protective role in bacterial pneumonia, but the mechanisms by which leptin regulates host defense remain poorly understood. Leptin binding to its receptor, LepRb, activates multiple intracellular signaling pathways, including ERK1/2, STAT5, and STAT3. In this study, we compared the responses of wild-type and s/s mice, which possess a mutant LepRb that prevents leptin-induced STAT3 activation, to determine the role of this signaling pathway in pneumococcal pneumonia. Compared with wild-type animals, s/s mice exhibited greater survival and enhanced pulmonary bacterial clearance after an intratracheal challenge with Streptococcus pneumoniae. We also observed enhanced phagocytosis and killing of S. pneumoniae in vitro in alveolar macrophages (AMs) obtained from s/s mice. Notably, the improved host defense and AM antibacterial effector functions in s/s mice were associated with increased cysteinyl-leukotriene production in vivo and in AMs in vitro. Augmentation of phagocytosis in AMs from s/s mice could be blocked using a pharmacologic cysteinyl-leukotriene receptor antagonist. Phosphorylation of ERK1/2 and cytosolic phospholipase A(2) α, known to enhance the release of arachidonic acid for subsequent conversion to leukotrienes, was also increased in AMs from s/s mice stimulated with S. pneumoniae in vitro. These data indicate that ablation of LepRb-mediated STAT3 signaling and the associated augmentation of ERK1/2, cytosolic phospholipase A(2) α, and cysteinyl-leukotriene synthesis confers resistance to s/s mice during pneumococcal pneumonia. These data provide novel insights into the intracellular signaling events by which leptin contributes to host defense against bacterial pneumonia.
MeSH term(s)	Animals ; Cells, Cultured ; Disease Models, Animal ; Female ; Gene Knock-In Techniques ; Immunity, Innate/genetics ; Leukotrienes/biosynthesis ; Male ; Mice ; Mice, Obese ; Mice, Transgenic ; Pneumonia, Pneumococcal/immunology ; Pneumonia, Pneumococcal/metabolism ; Pneumonia, Pneumococcal/prevention & control ; Protein Isoforms/antagonists & inhibitors ; Protein Isoforms/genetics ; Protein Isoforms/metabolism ; Receptors, Leptin/antagonists & inhibitors ; Receptors, Leptin/genetics ; Receptors, Leptin/metabolism ; STAT3 Transcription Factor/antagonists & inhibitors ; STAT3 Transcription Factor/genetics ; STAT3 Transcription Factor/metabolism ; Signal Transduction/genetics ; Signal Transduction/immunology ; Streptococcus pneumoniae/immunology ; Up-Regulation/genetics ; Up-Regulation/immunology
Chemical Substances	Leukotrienes ; Protein Isoforms ; Receptors, Leptin ; STAT3 Transcription Factor ; Stat3 protein, mouse ; leptin receptor, mouse
Language	English
Publishing date	2010-12-10
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.1001470
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