Journal Club – 2021.03.26

The influence of adolescent nicotine exposure on ethanol intake and brain gene expression

PLoS One . 2018 Jun 18;13(6):e0198935. doi: 10.1371/journal.pone.0198935. eCollection 2018.

Constanza P Silva 1, William J Horton 2, Michael J Caruso 1, Aswathy Sebastian 3, Laura C Klein 1, Istvan Albert 3, Helen M Kamens 1

Abstract

Nicotine and alcohol are often co-abused. Adolescence is a vulnerable period for the initiation of both nicotine and alcohol use, which can lead to subsequent neurodevelopmental and behavioral alterations. It is possible that during this vulnerable period, use of one drug leads to neurobiological alterations that affect subsequent consumption of the other drug. The aim of the present study was to determine the effect of nicotine exposure during adolescence on ethanol intake, and the effect of these substances on brain gene expression. Forty-three adolescent female C57BL/6J mice were assigned to four groups. In the first phase of the experiment, adolescent mice (PND 36-41 days) were exposed to three bottles filled with water or nicotine (200 μg/ml) for 22 h a day and a single bottle of water 2 h a day for six days. In the second phase (PND 42-45 days), the 4-day Drinking-in-the-Dark paradigm consisting of access to 20% v/v ethanol or water for 2h or 4h (the last day) was overlaid during the time when the mice did not have nicotine available. Ethanol consumption (g/kg) and blood ethanol concentrations (BEC, mg %) were measured on the final day and whole brains including the cerebellum, were dissected for RNA sequencing. Differentially expressed genes (DEG) were detected with CuffDiff and gene networks were built using WGCNA. Prior nicotine exposure increased ethanol consumption and resulting BEC. Significant DEG and biological pathways found in the group exposed to both nicotine and ethanol included genes important in stress-related neuropeptide signaling, hypothalamic-pituitary-adrenal (HPA) axis activity, glutamate release, GABA signaling, and dopamine release. These results replicate our earlier findings that nicotine exposure during adolescence increases ethanol consumption and extends this work by examining gene expression differences which could mediate these behavioral effects.

pone.0198935Download

Journal Club – 2021.03.26 Read More »

Crotamiton, an Anti-Scabies Agent, Suppresses Histamine- and Chloroquine-Induced Itch Pathways in Sensory Neurons and Alleviates Scratching in Mice

Da-Som Choi, Yeounjung Ji, Yongwoo Jang, Wook-Joo Lee, Won-Sik Shim: Crotamiton, an Anti-Scabies Agent, Suppresses Histamine- and Chloroquine-Induced Itch Pathways in Sensory Neurons and Alleviates Scratching in Mice. In: Biomolecules & Therapeutics, vol. 28, no. 6, pp. 569–575, 2020, ISSN: 2005-4483.
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Crotamiton, an Anti-Scabies Agent, Suppresses Histamine- and Chloroquine-Induced Itch Pathways in Sensory Neurons and Alleviates Scratching in MiceRead More »

Crotamiton, an Anti-Scabies Agent, Suppresses Histamine- and Chloroquine-Induced Itch Pathways in Sensory Neurons and Alleviates Scratching in Mice Read More »

2019-05-24 Journal Club

2019 May 14. doi: 10.1111/all.13870. [Epub ahead of print]

Pruritus in ordinary scabies: IL-31 from macrophages induced by overexpression of TSLP and periostin.

Hashimoto T1,2, Satoh T2, Yokozeki H1.

Abstract

BACKGROUND:

Scabies is a common contagious skin disease caused by an infestation of the skin by Sarcoptes scabiei var. hominis. A hallmark symptom of scabies is severe itch.

METHODS:

We sought to determine the generation of a pruritogenic cytokine, interleukin (IL)-31, together with immune profiles in skin lesions of ordinary scabies through immunohistochemical and immunofluorescent studies. To elucidate the pathological mechanisms of IL-31 generation, murine peritoneal macrophages were stimulated with various T helper 2 (Th2) cytokines and proteins ex vivo.

RESULTS:

A large number of CCR4(+) Th2 cells, eosinophils, and basophils infiltrated in scabies lesions. Increased generation of IL-31, TSLP, and periostin was also observed. A major population of IL-31(+) cells were Arginase-1(+)/CD163(+) M2 macrophages. Murine peritoneal macrophages showed an M2 phenotype and generated IL-31 when stimulated with TSLP and periostin.

CONCLUSION:

IL-31 appeared to be largely generated by M2 macrophages in ordinary scabies lesions. This IL-31 induction was mediated by TSLP and periostin. This article is protected by copyright. All rights reserved.

This article is protected by copyright. All rights reserved.

KEYWORDS:

TSLP ; IL-31; macrophage; periostin; scabies

2019-05-24 Journal Club Read More »

2019.05.03

https://doi.org/10.1016/j.jdermsci.2018.11.009
Filename : zhou2018.pdf (507 KB)
Caption : https://doi.org/10.1016/j.jdermsci.2018.11.009

2018 Dec;92(3):264-271. doi: 10.1016/j.jdermsci.2018.11.009. Epub 2018 Nov 26.

TRPV1 mediates inflammation and hyperplasia in imiquimod (IMQ)-induced psoriasiform dermatitis (PsD) in mice.

Zhou Y1, Follansbee T2, Wu X3, Han D1, Yu S3, Domocos DT2, Shi Z3, Carstens M2, Carstens E2, Hwang ST4.

Abstract

BACKGROUND:

Transient Receptor Potential Vanilloid 1 (TRPV1) is known to mediate itch and neurogenic inflammation, but the role of TRPV1 in psoriasiform dermal inflammation is poorly understood.

OBJECTIVE:

To investigate the function of TRPV1 in imiquimod (IMQ)-induced psoriasiform dermatitis (PsD) in mice.

METHODS:

Following daily treatment of topical IMQ cream for consecutive 5 days in C57BL/6 wide-type (WT) and TRPV1 gene knockout (KO) mice, we assessed the psoriasis severity index (PSI) scores, transepidermal water loss (TEWL), dermal inflammatory infiltrates, as well as gene expression levels for psoriasis related genes in mouse skin lesions.

RESULTS:

Compared with WT mice, the clinical and TEWL scores, the extent of skin hyperplasia, the area of Munro microabscesses (MM) and angiogenesis of psoriasis were all significantly decreased in TRPV1 KO mice triggered with IMQ, suggesting a reduction in skin inflammation and barrier defects. In addition, the infiltration of CD45+ leukocytes, mast cells as well as CD3+ T cells was all reduced in the IMQ-treated skin of TRPV1 KO mice. Quantitative Real-time PCR (RT-qPCR) revealed that expression levels of IL-1β, IL-6, IL-23, S100A8 were decreased while IL-10 was increased in TRPV1 KO mice.

CONCLUSIONS:

In summary, key markers of psoriatic inflammation and epidermal hyperplasia are reduced in TRPV1 KO mice, indicating the involvement of TRPV1 in the psoriasiform inflammation and suggesting its potential as a therapeutic target.

Copyright © 2018 Japanese Society for Investigative Dermatology. Published by Elsevier B.V. All rights reserved.

KEYWORDS:

Itch; Pain neuroinflammation; Psoriasis

PMID:
30527377
DOI:
10.1016/j.jdermsci.2018.11.009

2019.05.03 Read More »

Journal Club 2015.11.19

J Allergy Clin Immunol. 2012 Sep;130(3):671-682.e4. doi: 10.1016/j.jaci.2012.05.027. Epub 2012 Jul 4.

Artemin causes hypersensitivity to warm sensation, mimicking warmth-provoked pruritus in atopic dermatitis.

Murota H1, Izumi M, Abd El-Latif MI, Nishioka M, Terao M, Tani M, Matsui S, Sano S, Katayama I.

1-s2.0-S0091674912008664-main
Filename : 1-s2-0-s0091674912008664-main.pdf (3 MB)
Caption :

Abstract

BACKGROUND:

Itch impairs the quality of life for many patients with dermatoses, especially atopic dermatitis (AD), and is frequently induced by a warm environment.

OBJECTIVE:

To determine the mechanism underlying itch induction by warmth, we focused on artemin, a member of glial cell line-derived neurotrophic factors (GDNFs).

METHODS:

A gene array assay revealed that artemin was expressed in substance P-treated dermal fibroblasts. The expression of artemin in healthy and AD-lesional skin was evaluated with immunohistochemistry and in situ hybridization. The impact of fibroblast-derived artemin on the proliferation and morphology of neural cell was investigated in vitro. To confirm the involvement of artemin in skin sensibility, wild-type and GDNF family receptor α3 knockout mice were employed for sensory examination.

RESULTS:

Artemin-expressing fibroblasts accumulated in skin lesions of patients with AD. Artemin induced cell proliferation of a neuroblastoma cell line in vitro, and intradermal injection of artemin in mice resulted in peripheral nerve sprouting and thermal hyperalgesia. Artemin-treated mice demonstrated scratching behavior in a warm environment, but mice deficient for GDNF family receptor α3, a potent artemin receptor, did not show this behavior. Furthermore, the escaping response to heat stimulus was attenuated in GDNF family receptor α3 knockout mice, suggesting that artemin may contribute to sensitivity to heat.

CONCLUSION:

These data suggest that dermal fibroblasts secrete artemin in response to substance P, leading to abnormal peripheral innvervation and thermal hyperalgesia. We hypothesize that artemin lowers the threshold of temperature-dependent itch sensation and might therefore be a novel therapeutic target for treating pruritic skin disorders, including AD.

Copyright © 2012 American Academy of Allergy, Asthma & Immunology. Published by Mosby, Inc. All rights reserved.

Journal Club 2015.11.19 Read More »

Journal Club 2015.10.16

Cell Rep. 2015 Oct 13;13(2):387-98. doi: 10.1016/j.celrep.2015.09.002. Epub 2015 Oct 1.

ASIC3 Mediates Itch Sensation in Response to Coincident Stimulation by Acid and Nonproton Ligand.

Peng Z, Li WG, Huang C, Jiang YM, Wang X, Zhu MX, Cheng X, Xu TL.

Abstract

The regulation and mechanisms underlying itch sensation are complex. Here, we report a role for acid-sensing ion channel 3 (ASIC3) in mediating itch evoked by certain pruritogens during tissue acidosis. Co-administration of acid with Ser-Leu-Ile-Gly-Arg-Leu-NH2 (SL-NH2) increased scratching behavior in wild-type, but not ASIC3-null, mice, implicating the channel in coincident detection of acidosis and pruritogens. Mechanistically, SL-NH2 slowed desensitization of proton-evoked currents by targeting the previously identified nonproton ligand-sensing domain located in the extracellular region of ASIC3 channels in primary sensory neurons. Ablation of the ASIC3 gene reduced dry-skin-induced scratching behavior and pathological changes under conditions with concomitant inflammation. Taken together, our data suggest that ASIC3 mediates itch sensation via coincident detection of acidosis and nonproton ligands that act at the nonproton ligand-sensing domain of the channel.

ASIC3 Mediates Itch Sensation in Response to Coincident Stimulation by Acid and Nonproton Ligand
Filename : asic3-mediates-itch-sensation-in-response-to-coincident-stimulation-by-acid-and-nonproton-ligand.pdf (3 MB)
Caption :

Journal Club 2015.10.16 Read More »

Journal Club 2014-10-06

1-s2.0-S156757691300297X-main
Filename : 1-s2-0-s156757691300297x-main.pdf (953 KB)
Caption :

Int Immunopharmacol. 2013 Nov;17(3):502-7. doi: 10.1016/j.intimp.2013.07.012. Epub 2013 Aug 9.

Nobiletin and tangeretin ameliorate scratching behavior in mice by inhibiting the action of histamine and the activation of NF-κB, AP-1 and p38.

Jang SE1, Ryu KR, Park SH, Chung S, Teruya Y, Han MJ, Woo JT, Kim DH.

Abstract

Nobiletin and tangeretin are polymethoxy flavonoids that are abundantly present in the pericarp of Citrus unshiu (family Rutaceae) and the fruit of Citrus depressa (family Rutaceae). They exhibit various biological activities, including anti-inflammatory and anti-asthmatic effects. To evaluate the anti-allergic effects of nobiletin and tangeretin, we measured their inhibitory effects in histamine- or compound 48/80-induced scratching behavioral mice. Nobiletin and tangeretin potently inhibited scratching behavior, as well as histamine-induced vascular permeability. Furthermore, they inhibited the expression of the allergic cytokines, IL-4 and TNF-α as well as the activation of their transcription factors NF-κB, AP-1 and p38 in histamine-stimulated skin tissues. They also inhibited the expression of IL-4 and TNF-α and the activation of NF-κB and c-jun in PMA-stimulated RBL-2H3 cells. Furthermore, nobiletin and tangeretin inhibited protein kinase C (PKC) activity and the IgE-induced degranulation of RBL-2H3 cells. These agents showed potent anti-histamine effect through the Magnus test when guinea pig ileum was used. Based on these results, nobiletin and tangeretin may ameliorate scratching behavioral reactions by inhibiting the action of histamine as well as the activation of the transcription factors NF-κB and AP-1 via PKC.

© 2013.

KEYWORDS:

1-s2.0-S156757691300297X-mainPMID:

 

23938254

 

[PubMed – indexed for MEDLINE]

Journal Club 2014-10-06 Read More »

Journal Club 2014-05-24

Acta Derm Venereol. 2014 Mar 7. doi: 10.2340/00015555-1834. [Epub ahead of print]

Surfactant-induced Chronic Pruritus: Role of L-Histidine Decarboxylase Expression and Histamine Production in Epidermis.

4143
Filename : 4143.pdf (408 KB)
Caption :

Abstract

Shampoo and cleansers containing anionic surfactants including sodium dodecyl sulphate (SDS) often causepruritus in humans. Daily application of 1-10% SDS for 4 days induced hind-paw scratching (an itch-related behaviour) in a concentration-dependent manner, and 10% SDS also caused dermatitis, skin dryness, barrier disruption, and an increase in skin surface pH in mice. SDS-induced scratching was inhibited by the opioid receptor antagonist naloxone and the H1 histamine receptor antagonist terfenadine. Mast-cell deficiency did not inhibit SDS-induced scratching, although it almost completely depleted histamine in the dermis. Treatment with SDS increased the histamine content of the epidermis, but not that of the dermis. SDS treatment increased the gene expression and post-translation processing of L-histidine decarboxylase in the epidermis. The present results suggest that repeated application of SDS induces itch through increased production of epidermal histamine, which results from an increase in the gene expression and post-translation processing of L-histidine decarboxylase.

PMID: 24603881

Journal Club 2014-05-24 Read More »

Journal Club 2014-05-09

Mol Brain. 2014 Apr 3;7(1):25. doi: 10.1186/1756-6606-7-25.

Extracellular signal-regulated kinase (ERK) activation is required for itch sensation in the spinal cord.

1756-6606-7-25
Filename : 1756-6606-7-25.pdf (3 MB)
Caption :

Abstract

BACKGROUND:

Itch, chronic itch in particular, can have a significant negative impact on an individual’s quality of life. However, the molecular mechanisms underlying itch processing in the central nervous system remain largely unknown.

RESULTS:

We report here that activation of ERK signaling in the spinal cord is required for itch sensation. ERK activation, as revealed by anti-phosphorylated ERK1/2 immunostaining, is observed in the spinal dorsal horn of mice treated with intradermal injections of histamine and compound 48/80 but not chloroquine or SLIGRL-NH2, indicating that ERK activation only occurs in histamine-dependent acute itch. In addition, ERK activation is also observed in 2, 4-dinitrofluorobenzene (DNFB)-induced itch. Consistently, intrathecal administration of the ERK phosphorylation inhibitor U0126 dramatically reduces the scratching behaviors induced by histamine and DNFB, but not by chloroquine. Furthermore, administration of the histamine receptor H1 antagonist chlorpheniramine decreases the scratching behaviors and ERK activation induced by histamine, but has no effect on DNFB-induced itch responses. Finally, the patch-clamp recording shows that in histamine-, chloroquine- and DNFB-treated mice the spontaneous excitatory postsynaptic current (sEPSC) of dorsal horn neurons is increased, and the decrease of action potential threshold is largely prevented by bathing of U0126 in histamine- and DNFB-treated mice but not those treated with chloroquine.

CONCLUSION:

Our results demonstrate a critical role for ERK activation in itch sensation at the spinal level.

Journal Club 2014-05-09 Read More »

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