A novel mouse model of atopic dermatitis with epicutaneous allergen sensitization and the effect of Lactobacillus rhamnosus

Atopic dermatitis (AD) is a chronic and relapsing inflammatory skin disease, and the pathogenesis is not completely understood. Although there are some mouse models of AD, it is not easy to establish model to represent the natural AD development in human. In this study, we developed an AD model base...

Full description

Saved in:
Bibliographic Details
Published inExperimental dermatology Vol. 21; no. 9; pp. 672 - 675
Main Authors Kim, Ha-Jung, Kim, Young-Joon, Kang, Mi-Jin, Seo, Ju-Hee, Kim, Hyung-Young, Jeong, Se Kyoo, Lee, Seung-Hun, Kim, Ji-Min, Hong, Soo-Jong
Format Journal Article
LanguageEnglish
Published Oxford Blackwell Publishing Ltd 01.09.2012
Blackwell
Subjects
Online AccessGet full text
ISSN0906-6705
1600-0625
1600-0625
DOI10.1111/j.1600-0625.2012.01539.x

Cover

Abstract Atopic dermatitis (AD) is a chronic and relapsing inflammatory skin disease, and the pathogenesis is not completely understood. Although there are some mouse models of AD, it is not easy to establish model to represent the natural AD development in human. In this study, we developed an AD model based on outside–inside theory and investigated the effect of Lactobacillus rhamnosus (Lcr35), which have known as an immune modulator in allergic diseases. SKH‐1 hairless mice underwent three 1‐week exposures (separated by 2‐week intervals) to an ovalbumin (OVA) or saline (control) patch at the same site to develop the mouse model of AD. Lcr35 (1 × 109 CFU) was administered orally every day from 1 week before the first sensitization until the end of the study. The AD model induced erythematous and itchy skin, increasing TEWL and increasing skin inflammation as assessed by histology in the mice. Oral Lcr35 attenuated all disease parameters previously mentioned. OVA‐specific IgE and skin expression of interleukin‐4 (IL‐4) and thymic stromal lymphopoietin (TSLP) increased in AD mice, but were reduced in AD mice treated with Lcr35. Moreover, Lcr35 treatment led to an increase in CD4+CD25+ Foxp3+ Treg cells in the mesenteric lymph nodes of AD mice. In conclusions, based on the ‘outside–inside’ theory, topical allergen may induce AD without skin injury. Oral application of Lcr35 prevented the development of AD in this model by suppressing production of the inflammatory cytokines, IL‐4 and TSLP in the skin via a mechanism that may involve CD4+CD25+Foxp3+Treg cells.
AbstractList Atopic dermatitis (AD) is a chronic and relapsing inflammatory skin disease, and the pathogenesis is not completely understood. Although there are some mouse models of AD, it is not easy to establish model to represent the natural AD development in human. In this study, we developed an AD model based on outside-inside theory and investigated the effect of Lactobacillus rhamnosus (Lcr35), which have known as an immune modulator in allergic diseases. SKH-1 hairless mice underwent three 1-week exposures (separated by 2-week intervals) to an ovalbumin (OVA) or saline (control) patch at the same site to develop the mouse model of AD. Lcr35 (1 × 10(9)  CFU) was administered orally every day from 1 week before the first sensitization until the end of the study. The AD model induced erythematous and itchy skin, increasing TEWL and increasing skin inflammation as assessed by histology in the mice. Oral Lcr35 attenuated all disease parameters previously mentioned. OVA-specific IgE and skin expression of interleukin-4 (IL-4) and thymic stromal lymphopoietin (TSLP) increased in AD mice, but were reduced in AD mice treated with Lcr35. Moreover, Lcr35 treatment led to an increase in CD4(+) CD25(+) Foxp3(+) Treg cells in the mesenteric lymph nodes of AD mice. In conclusions, based on the 'outside-inside' theory, topical allergen may induce AD without skin injury. Oral application of Lcr35 prevented the development of AD in this model by suppressing production of the inflammatory cytokines, IL-4 and TSLP in the skin via a mechanism that may involve CD4(+) CD25(+) Foxp3(+) Treg cells.
Atopic dermatitis (AD) is a chronic and relapsing inflammatory skin disease, and the pathogenesis is not completely understood. Although there are some mouse models of AD, it is not easy to establish model to represent the natural AD development in human. In this study, we developed an AD model based on outside-inside theory and investigated the effect of Lactobacillus rhamnosus (Lcr35), which have known as an immune modulator in allergic diseases. SKH-1 hairless mice underwent three 1-week exposures (separated by 2-week intervals) to an ovalbumin (OVA) or saline (control) patch at the same site to develop the mouse model of AD. Lcr35 (1 109CFU) was administered orally every day from 1 week before the first sensitization until the end of the study. The AD model induced erythematous and itchy skin, increasing TEWL and increasing skin inflammation as assessed by histology in the mice. Oral Lcr35 attenuated all disease parameters previously mentioned. OVA-specific IgE and skin expression of interleukin-4 (IL-4) and thymic stromal lymphopoietin (TSLP) increased in AD mice, but were reduced in AD mice treated with Lcr35. Moreover, Lcr35 treatment led to an increase in CD4+CD25+Foxp3+Treg cells in the mesenteric lymph nodes of AD mice. In conclusions, based on the 'outside-inside' theory, topical allergen may induce AD without skin injury. Oral application of Lcr35 prevented the development of AD in this model by suppressing production of the inflammatory cytokines, IL-4 and TSLP in the skin via a mechanism that may involve CD4+CD25+Foxp3+Treg cells.
Atopic dermatitis (AD) is a chronic and relapsing inflammatory skin disease, and the pathogenesis is not completely understood. Although there are some mouse models of AD, it is not easy to establish model to represent the natural AD development in human. In this study, we developed an AD model based on outside-inside theory and investigated the effect of Lactobacillus rhamnosus (Lcr35), which have known as an immune modulator in allergic diseases. SKH-1 hairless mice underwent three 1-week exposures (separated by 2-week intervals) to an ovalbumin (OVA) or saline (control) patch at the same site to develop the mouse model of AD. Lcr35 (1 × 10(9) CFU) was administered orally every day from 1 week before the first sensitization until the end of the study. The AD model induced erythematous and itchy skin, increasing TEWL and increasing skin inflammation as assessed by histology in the mice. Oral Lcr35 attenuated all disease parameters previously mentioned. OVA-specific IgE and skin expression of interleukin-4 (IL-4) and thymic stromal lymphopoietin (TSLP) increased in AD mice, but were reduced in AD mice treated with Lcr35. Moreover, Lcr35 treatment led to an increase in CD4(+) CD25(+) Foxp3(+) Treg cells in the mesenteric lymph nodes of AD mice. In conclusions, based on the 'outside-inside' theory, topical allergen may induce AD without skin injury. Oral application of Lcr35 prevented the development of AD in this model by suppressing production of the inflammatory cytokines, IL-4 and TSLP in the skin via a mechanism that may involve CD4(+) CD25(+) Foxp3(+) Treg cells.Atopic dermatitis (AD) is a chronic and relapsing inflammatory skin disease, and the pathogenesis is not completely understood. Although there are some mouse models of AD, it is not easy to establish model to represent the natural AD development in human. In this study, we developed an AD model based on outside-inside theory and investigated the effect of Lactobacillus rhamnosus (Lcr35), which have known as an immune modulator in allergic diseases. SKH-1 hairless mice underwent three 1-week exposures (separated by 2-week intervals) to an ovalbumin (OVA) or saline (control) patch at the same site to develop the mouse model of AD. Lcr35 (1 × 10(9) CFU) was administered orally every day from 1 week before the first sensitization until the end of the study. The AD model induced erythematous and itchy skin, increasing TEWL and increasing skin inflammation as assessed by histology in the mice. Oral Lcr35 attenuated all disease parameters previously mentioned. OVA-specific IgE and skin expression of interleukin-4 (IL-4) and thymic stromal lymphopoietin (TSLP) increased in AD mice, but were reduced in AD mice treated with Lcr35. Moreover, Lcr35 treatment led to an increase in CD4(+) CD25(+) Foxp3(+) Treg cells in the mesenteric lymph nodes of AD mice. In conclusions, based on the 'outside-inside' theory, topical allergen may induce AD without skin injury. Oral application of Lcr35 prevented the development of AD in this model by suppressing production of the inflammatory cytokines, IL-4 and TSLP in the skin via a mechanism that may involve CD4(+) CD25(+) Foxp3(+) Treg cells.
Atopic dermatitis (AD) is a chronic and relapsing inflammatory skin disease, and the pathogenesis is not completely understood. Although there are some mouse models of AD, it is not easy to establish model to represent the natural AD development in human. In this study, we developed an AD model based on outside–inside theory and investigated the effect of Lactobacillus rhamnosus (Lcr35), which have known as an immune modulator in allergic diseases. SKH‐1 hairless mice underwent three 1‐week exposures (separated by 2‐week intervals) to an ovalbumin (OVA) or saline (control) patch at the same site to develop the mouse model of AD. Lcr35 (1 × 109 CFU) was administered orally every day from 1 week before the first sensitization until the end of the study. The AD model induced erythematous and itchy skin, increasing TEWL and increasing skin inflammation as assessed by histology in the mice. Oral Lcr35 attenuated all disease parameters previously mentioned. OVA‐specific IgE and skin expression of interleukin‐4 (IL‐4) and thymic stromal lymphopoietin (TSLP) increased in AD mice, but were reduced in AD mice treated with Lcr35. Moreover, Lcr35 treatment led to an increase in CD4+CD25+ Foxp3+ Treg cells in the mesenteric lymph nodes of AD mice. In conclusions, based on the ‘outside–inside’ theory, topical allergen may induce AD without skin injury. Oral application of Lcr35 prevented the development of AD in this model by suppressing production of the inflammatory cytokines, IL‐4 and TSLP in the skin via a mechanism that may involve CD4+CD25+Foxp3+Treg cells.
Author Lee, Seung-Hun
Seo, Ju-Hee
Kim, Ji-Min
Kang, Mi-Jin
Kim, Young-Joon
Kim, Ha-Jung
Kim, Hyung-Young
Jeong, Se Kyoo
Hong, Soo-Jong
Author_xml – sequence: 1
  givenname: Ha-Jung
  surname: Kim
  fullname: Kim, Ha-Jung
  organization: Asan Institute for Life Sciences, University of Ulsan College of Medicine, Seoul, Korea
– sequence: 2
  givenname: Young-Joon
  surname: Kim
  fullname: Kim, Young-Joon
  organization: Asan Institute for Life Sciences, University of Ulsan College of Medicine, Seoul, Korea
– sequence: 3
  givenname: Mi-Jin
  surname: Kang
  fullname: Kang, Mi-Jin
  organization: Asan Institute for Life Sciences, University of Ulsan College of Medicine, Seoul, Korea
– sequence: 4
  givenname: Ju-Hee
  surname: Seo
  fullname: Seo, Ju-Hee
  organization: Department of Pediatrics, Childhood Asthma Atopy Center, Research Center for Standardization of Allergic Diseases, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea
– sequence: 5
  givenname: Hyung-Young
  surname: Kim
  fullname: Kim, Hyung-Young
  organization: Department of Pediatrics, Childhood Asthma Atopy Center, Research Center for Standardization of Allergic Diseases, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea
– sequence: 6
  givenname: Se Kyoo
  surname: Jeong
  fullname: Jeong, Se Kyoo
  organization: Applied Research Division, NeoPharm Co., Ltd., Daejeon, Korea
– sequence: 7
  givenname: Seung-Hun
  surname: Lee
  fullname: Lee, Seung-Hun
  organization: Department of Dermatology, Human Barrier Research Institute, Brain Korea 21 Project for Medical Science, Yonsei University College of Medicine, Seoul, Korea
– sequence: 8
  givenname: Ji-Min
  surname: Kim
  fullname: Kim, Ji-Min
  organization: Department of Dermatology, Human Barrier Research Institute, Brain Korea 21 Project for Medical Science, Yonsei University College of Medicine, Seoul, Korea
– sequence: 9
  givenname: Soo-Jong
  surname: Hong
  fullname: Hong, Soo-Jong
  email: sjhong@amc.seoul.kr
  organization: Department of Pediatrics, Childhood Asthma Atopy Center, Research Center for Standardization of Allergic Diseases, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea
BackLink http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=26290505$$DView record in Pascal Francis
https://www.ncbi.nlm.nih.gov/pubmed/22742655$$D View this record in MEDLINE/PubMed
BookMark eNqNkU1v1DAQhi3Uim4LfwH5gsQlYewkdnLgUJV2ga74kEBwsxxnwnpJnCV26Bb-PA67LFd8sEee5x3Jfs7JiRscEkIZpCyu55uUCYAEBC9SDoynwIqsSncPyOLYOCELqEAkQkJxRs693wAwmcniITnjXOZcFMWC_LqkbviBHe2HyWPcm1gPLdVh2FpDGxx7HWywnt7ZsKYYL6egHUaa6q7D8Ss66tH5yPyM5OCodg0Na6TYtmjCPGylTRhqbWzXxdi41r0b_OQfkdNWdx4fH84L8unm-uPVq2T1bvn66nKV2EyIKmmZyctaNFii0aiL0siKtQ1gbTTPm9rIHLOyRjSlhrZp6rzMdYayhrzKjSyyC_JsP3c7Dt8n9EH11hvsuv07FIOsFIxLWf0PmnOAjM_okwM61T02ajvaXo_36u_fRuDpAdDe6K4dtTPW_-MEr6CAmXux5-5sh_fHPgM1u1YbNStVs1I1u1Z_XKuduv7ycq5iPtnnrQ-4O-b1-E2J2bf6_Hapbpf8Pbv58EYts9_g8rBC
ContentType Journal Article
Copyright 2012 John Wiley & Sons A/S
2015 INIST-CNRS
2012 John Wiley & Sons A/S.
Copyright_xml – notice: 2012 John Wiley & Sons A/S
– notice: 2015 INIST-CNRS
– notice: 2012 John Wiley & Sons A/S.
DBID BSCLL
IQODW
CGR
CUY
CVF
ECM
EIF
NPM
7X8
7QL
7T5
C1K
H94
DOI 10.1111/j.1600-0625.2012.01539.x
DatabaseName Istex
Pascal-Francis
Medline
MEDLINE
MEDLINE (Ovid)
MEDLINE
MEDLINE
PubMed
MEDLINE - Academic
Bacteriology Abstracts (Microbiology B)
Immunology Abstracts
Environmental Sciences and Pollution Management
AIDS and Cancer Research Abstracts
DatabaseTitle MEDLINE
Medline Complete
MEDLINE with Full Text
PubMed
MEDLINE (Ovid)
MEDLINE - Academic
AIDS and Cancer Research Abstracts
Immunology Abstracts
Bacteriology Abstracts (Microbiology B)
Environmental Sciences and Pollution Management
DatabaseTitleList MEDLINE
AIDS and Cancer Research Abstracts
MEDLINE - Academic

Database_xml – sequence: 1
  dbid: NPM
  name: PubMed
  url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed
  sourceTypes: Index Database
– sequence: 2
  dbid: EIF
  name: MEDLINE
  url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search
  sourceTypes: Index Database
DeliveryMethod fulltext_linktorsrc
Discipline Medicine
EISSN 1600-0625
EndPage 675
ExternalDocumentID 22742655
26290505
EXD1539
ark_67375_WNG_KG2P1FQJ_G
Genre article
Research Support, U.S. Gov't, Non-P.H.S
Journal Article
GrantInformation_xml – fundername: Korea government (MEST)
  funderid: 2010‐0022233
– fundername: National Research Foundation of Korea
GroupedDBID ---
.3N
.GA
.Y3
05W
0R~
10A
1OB
1OC
29G
31~
33P
36B
3SF
4.4
50Y
50Z
51W
51X
52M
52N
52O
52P
52R
52S
52T
52U
52V
52W
52X
53G
5GY
5HH
5LA
5VS
66C
702
7PT
8-0
8-1
8-3
8-4
8-5
8UM
930
A01
A03
AAESR
AAEVG
AAHQN
AAIPD
AAKAS
AAMMB
AAMNL
AANHP
AANLZ
AAONW
AASGY
AAXRX
AAYCA
AAZKR
ABCQN
ABCUV
ABDBF
ABEML
ABJNI
ABPVW
ABQWH
ABXGK
ACAHQ
ACBWZ
ACCZN
ACGFO
ACGFS
ACGOF
ACMXC
ACPOU
ACPRK
ACRPL
ACSCC
ACUHS
ACXBN
ACXQS
ACYXJ
ADBBV
ADBTR
ADEOM
ADIZJ
ADKYN
ADMGS
ADNMO
ADOZA
ADXAS
ADZCM
ADZMN
AEFGJ
AEGXH
AEIGN
AEIMD
AENEX
AEUYR
AEYWJ
AFBPY
AFEBI
AFFPM
AFGKR
AFWVQ
AFZJQ
AGHNM
AGQPQ
AGXDD
AGYGG
AHBTC
AHEFC
AIACR
AIAGR
AIDQK
AIDYY
AIQQE
AITYG
AIURR
ALAGY
ALMA_UNASSIGNED_HOLDINGS
ALUQN
ALVPJ
AMBMR
AMYDB
ASPBG
ATUGU
AVWKF
AZBYB
AZFZN
AZVAB
BAFTC
BDRZF
BFHJK
BHBCM
BMXJE
BROTX
BRXPI
BSCLL
BY8
C45
CAG
COF
CS3
CYRXZ
D-6
D-7
D-E
D-F
DC6
DCZOG
DPXWK
DR2
DRFUL
DRMAN
DRSTM
DU5
EAD
EAP
EBC
EBD
EBS
EJD
EMB
EMK
EMOBN
ESX
EX3
F00
F01
F04
F5P
FEDTE
FUBAC
FZ0
G-S
G.N
GODZA
H.X
HF~
HGLYW
HVGLF
HZI
HZ~
IHE
IX1
J0M
K48
KBYEO
LATKE
LC2
LC3
LEEKS
LH4
LITHE
LOXES
LP6
LP7
LUTES
LW6
LYRES
MEWTI
MK4
MRFUL
MRMAN
MRSTM
MSFUL
MSMAN
MSSTM
MXFUL
MXMAN
MXSTM
N04
N05
N9A
NF~
O66
O9-
OIG
OVD
P2P
P2W
P2X
P2Z
P4B
P4D
PALCI
Q.N
Q11
QB0
R.K
RIWAO
RJQFR
ROL
RX1
SAMSI
SUPJJ
SV3
TEORI
TUS
UB1
V8K
W8V
W99
WBKPD
WHWMO
WIH
WIJ
WIK
WOHZO
WOW
WQJ
WVDHM
WXI
WXSBR
XG1
YFH
YUY
ZZTAW
~IA
~WT
AAHHS
ACCFJ
ADZOD
AEEZP
AEQDE
AEUQT
AFPWT
AIWBW
AJBDE
WRC
WUP
IQODW
CGR
CUY
CVF
ECM
EIF
NPM
7X8
7QL
7T5
C1K
H94
ID FETCH-LOGICAL-i3669-f1c48b6de8ecaea58c791fd0ebca24dbc74e38beec8a0fddb484a3e7b0494c753
IEDL.DBID DR2
ISSN 0906-6705
1600-0625
IngestDate Fri Jul 11 05:26:27 EDT 2025
Fri Jul 11 07:22:02 EDT 2025
Mon Jul 21 05:53:30 EDT 2025
Mon Jul 21 09:15:01 EDT 2025
Wed Jan 22 16:42:29 EST 2025
Sun Sep 21 06:18:28 EDT 2025
IsPeerReviewed true
IsScholarly true
Issue 9
Keywords Probiotic
Immunopathology
Allergy
Skin disease
Thymus gland
Dermatology
Rodentia
regulatory
mice
Atopy
Vertebrata
T-lymphocytes
thymic stromal lymphopoietin
Mammalia
Mouse
Atopic dermatitis
Animal
T-Lymphocyte
Bacteria
Lactobacillaceae
Models
Sensitization
Lactobacillus rhamnosus
probiotics
Language English
License CC BY 4.0
2012 John Wiley & Sons A/S.
LinkModel DirectLink
MergedId FETCHMERGED-LOGICAL-i3669-f1c48b6de8ecaea58c791fd0ebca24dbc74e38beec8a0fddb484a3e7b0494c753
Notes ArticleID:EXD1539
Korea government (MEST) - No. 2010-0022233
National Research Foundation of Korea
istex:D193D364CF66AEBB149FE36E27978A4B32FDF287
ark:/67375/WNG-KG2P1FQJ-G
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ObjectType-Article-2
ObjectType-Feature-1
PMID 22742655
PQID 1034200329
PQPubID 23479
PageCount 4
ParticipantIDs proquest_miscellaneous_1038612779
proquest_miscellaneous_1034200329
pubmed_primary_22742655
pascalfrancis_primary_26290505
wiley_primary_10_1111_j_1600_0625_2012_01539_x_EXD1539
istex_primary_ark_67375_WNG_KG2P1FQJ_G
PublicationCentury 2000
PublicationDate September 2012
PublicationDateYYYYMMDD 2012-09-01
PublicationDate_xml – month: 09
  year: 2012
  text: September 2012
PublicationDecade 2010
PublicationPlace Oxford
PublicationPlace_xml – name: Oxford
– name: Denmark
PublicationTitle Experimental dermatology
PublicationTitleAlternate Exp Dermatol
PublicationYear 2012
Publisher Blackwell Publishing Ltd
Blackwell
Publisher_xml – name: Blackwell Publishing Ltd
– name: Blackwell
References Oshio T, Sasaki Y, Funakoshi-Tago M et al. Int Immunopharmacol 2009: 9: 403-411.
Kang J S, Yoon W K, Youm J K et al. Exp Dermatol 2008: 17: 958-964.
Lee E B, Kim K W, Hong J Y et al. Pediatr Allergy Immunol 2010: 21: e457-e460.
Yoo J, Omori M, Gyarmati D et al. J Exp Med 2005: 202: 541-549.
Vercelli D. Nat Genet 2009: 41: 512-513.
Sunada Y, Nakamura S, Kamei C. Int Immunopharmacol 2008: 8: 1761-1766.
Hatano Y, Elias P M, Crumrine D et al. J Invest Dermatol 2011: 131: 1845-1852.
Spergel J M, Mizoguchi E, Brewer J P et al. J Clin Invest 1998: 101: 1614-1622.
Tanaka A, Fukushima Y, Benyacoub J et al. Eur J Dermatol 2008: 18: 136-140.
Cooper K D. J Invest Dermatol 1994: 102: 128-137.
Chan L S. Curr Dir Autoimmun 2008: 10: 76-118.
Hong S W, Kim M R, Lee E Y et al. Allergy 2011: 66: 351-359.
Kwon H K, Lee C G, So J S et al. Proc Natl Acad Sci U S A 2010: 107: 2159-2164.
Feleszko W, Jaworska J, Rha R D et al. Clin Exp Allergy 2007: 37: 498-505.
Broide D H, Finkelman F, Bochner B S et al. J Allergy Clin Immunol 2011: 127: 689-695.
Segawa S, Kuroda H, Kaneko T et al. Biosci Biotechnol Biochem 2008: 72: 974-981.
Maintz L, Novak N. Eur J Dermatol 2007: 17: 267-283.
Kalliomaki M, Salminen S, Poussa T et al. Lancet 2003: 361: 169-171.
Liu Y J, Soumelis V, Watanabe N et al. Annu Rev Immunol 2006: 25: 193-219.
Campbell D J, Koch M A. Nat Rev Immunol 2011: 11: 119-130.
Proksch E, Fölster-Holst R, Jensen J M. J Dermatol Sci 2006: 43: 159-169.
Sawada J, Morita H, Tanaka A et al. Clin Exp Allergy 2007: 37: 296-303.
Marteau P. Gut 2006: 55: 1692-1693.
Kitagawa H, Yamanaka K, Kakeda M et al. Exp Dermatol 2011: 20: 157-158.
Soumelis V, Reche P A, Kanzler H et al. Nat Immunol 2002: 3: 673-680.
Kalliomaki M, Salminen S, Arvilommi H et al. Lancet 2001: 357: 1076-1079.
2007; 17
2009; 41
2010; 107
2006; 55
2008; 18
2008; 17
2002; 3
2011; 11
2008; 8
2008; 10
2008; 72
2007; 37
2011; 131
2011; 127
1994; 102
2010; 21
2006; 43
2005; 202
2006; 25
2011; 20
2009; 9
2011; 66
1998; 101
2001; 357
2003; 361
References_xml – reference: Sawada J, Morita H, Tanaka A et al. Clin Exp Allergy 2007: 37: 296-303.
– reference: Segawa S, Kuroda H, Kaneko T et al. Biosci Biotechnol Biochem 2008: 72: 974-981.
– reference: Soumelis V, Reche P A, Kanzler H et al. Nat Immunol 2002: 3: 673-680.
– reference: Spergel J M, Mizoguchi E, Brewer J P et al. J Clin Invest 1998: 101: 1614-1622.
– reference: Lee E B, Kim K W, Hong J Y et al. Pediatr Allergy Immunol 2010: 21: e457-e460.
– reference: Vercelli D. Nat Genet 2009: 41: 512-513.
– reference: Liu Y J, Soumelis V, Watanabe N et al. Annu Rev Immunol 2006: 25: 193-219.
– reference: Marteau P. Gut 2006: 55: 1692-1693.
– reference: Chan L S. Curr Dir Autoimmun 2008: 10: 76-118.
– reference: Sunada Y, Nakamura S, Kamei C. Int Immunopharmacol 2008: 8: 1761-1766.
– reference: Kwon H K, Lee C G, So J S et al. Proc Natl Acad Sci U S A 2010: 107: 2159-2164.
– reference: Kalliomaki M, Salminen S, Poussa T et al. Lancet 2003: 361: 169-171.
– reference: Campbell D J, Koch M A. Nat Rev Immunol 2011: 11: 119-130.
– reference: Kitagawa H, Yamanaka K, Kakeda M et al. Exp Dermatol 2011: 20: 157-158.
– reference: Oshio T, Sasaki Y, Funakoshi-Tago M et al. Int Immunopharmacol 2009: 9: 403-411.
– reference: Tanaka A, Fukushima Y, Benyacoub J et al. Eur J Dermatol 2008: 18: 136-140.
– reference: Hatano Y, Elias P M, Crumrine D et al. J Invest Dermatol 2011: 131: 1845-1852.
– reference: Cooper K D. J Invest Dermatol 1994: 102: 128-137.
– reference: Proksch E, Fölster-Holst R, Jensen J M. J Dermatol Sci 2006: 43: 159-169.
– reference: Kalliomaki M, Salminen S, Arvilommi H et al. Lancet 2001: 357: 1076-1079.
– reference: Hong S W, Kim M R, Lee E Y et al. Allergy 2011: 66: 351-359.
– reference: Yoo J, Omori M, Gyarmati D et al. J Exp Med 2005: 202: 541-549.
– reference: Feleszko W, Jaworska J, Rha R D et al. Clin Exp Allergy 2007: 37: 498-505.
– reference: Kang J S, Yoon W K, Youm J K et al. Exp Dermatol 2008: 17: 958-964.
– reference: Maintz L, Novak N. Eur J Dermatol 2007: 17: 267-283.
– reference: Broide D H, Finkelman F, Bochner B S et al. J Allergy Clin Immunol 2011: 127: 689-695.
– volume: 107
  start-page: 2159
  year: 2010
  end-page: 2164
  publication-title: Proc Natl Acad Sci U S A
– volume: 11
  start-page: 119
  year: 2011
  end-page: 130
  publication-title: Nat Rev Immunol
– volume: 361
  start-page: 169
  year: 2003
  end-page: 171
  publication-title: Lancet
– volume: 55
  start-page: 1692
  year: 2006
  end-page: 1693
  publication-title: Gut
– volume: 37
  start-page: 498
  year: 2007
  end-page: 505
  publication-title: Clin Exp Allergy
– volume: 17
  start-page: 267
  year: 2007
  end-page: 283
  publication-title: Eur J Dermatol
– volume: 131
  start-page: 1845
  year: 2011
  end-page: 1852
  publication-title: J Invest Dermatol
– volume: 10
  start-page: 76
  year: 2008
  end-page: 118
  publication-title: Curr Dir Autoimmun
– volume: 41
  start-page: 512
  year: 2009
  end-page: 513
  publication-title: Nat Genet
– volume: 9
  start-page: 403
  year: 2009
  end-page: 411
  publication-title: Int Immunopharmacol
– volume: 37
  start-page: 296
  year: 2007
  end-page: 303
  publication-title: Clin Exp Allergy
– volume: 202
  start-page: 541
  year: 2005
  end-page: 549
  publication-title: J Exp Med
– volume: 21
  start-page: e457
  year: 2010
  end-page: e460
  publication-title: Pediatr Allergy Immunol
– volume: 101
  start-page: 1614
  year: 1998
  end-page: 1622
  publication-title: J Clin Invest
– volume: 18
  start-page: 136
  year: 2008
  end-page: 140
  publication-title: Eur J Dermatol
– volume: 25
  start-page: 193
  year: 2006
  end-page: 219
  publication-title: Annu Rev Immunol
– volume: 17
  start-page: 958
  year: 2008
  end-page: 964
  publication-title: Exp Dermatol
– volume: 127
  start-page: 689
  year: 2011
  end-page: 695
  publication-title: J Allergy Clin Immunol
– volume: 102
  start-page: 128
  year: 1994
  end-page: 137
  publication-title: J Invest Dermatol
– volume: 3
  start-page: 673
  year: 2002
  end-page: 680
  publication-title: Nat Immunol
– volume: 72
  start-page: 974
  year: 2008
  end-page: 981
  publication-title: Biosci Biotechnol Biochem
– volume: 20
  start-page: 157
  year: 2011
  end-page: 158
  publication-title: Exp Dermatol
– volume: 8
  start-page: 1761
  year: 2008
  end-page: 1766
  publication-title: Int Immunopharmacol
– volume: 66
  start-page: 351
  year: 2011
  end-page: 359
  publication-title: Allergy
– volume: 43
  start-page: 159
  year: 2006
  end-page: 169
  publication-title: J Dermatol Sci
– volume: 357
  start-page: 1076
  year: 2001
  end-page: 1079
  publication-title: Lancet
SSID ssj0017375
Score 2.2422142
Snippet Atopic dermatitis (AD) is a chronic and relapsing inflammatory skin disease, and the pathogenesis is not completely understood. Although there are some mouse...
SourceID proquest
pubmed
pascalfrancis
wiley
istex
SourceType Aggregation Database
Index Database
Publisher
StartPage 672
SubjectTerms Allergens
Allergic diseases
Analysis of Variance
Animal models
Animals
Atopic dermatitis
Biological and medical sciences
CD4 Antigens - metabolism
Cytokines - metabolism
Dermatitis, Atopic - immunology
Dermatitis, Atopic - metabolism
Dermatitis, Atopic - physiopathology
Dermatology
Disease Models, Animal
Female
Forkhead Transcription Factors - metabolism
Hairless
Immunoglobulin E
Immunoglobulin E - blood
Immunomodulation
Immunopathology
Inflammation
Inflammatory diseases
Injuries
Interleukin 4
Interleukin-2 Receptor alpha Subunit - metabolism
Interleukin-4 - metabolism
Lactobacillus rhamnosus
Lactobacillus rhamnosus - immunology
Lymph nodes
Lymph Nodes - immunology
Lymphocyte Count
Medical sciences
Mesentery
Mice
Mice, Hairless
Ovalbumin
Ovalbumin - immunology
Permeability - drug effects
probiotics
Probiotics - pharmacology
regulatory
Skin - metabolism
Skin allergic diseases. Stinging insect allergies
Skin diseases
T-lymphocytes
T-Lymphocytes, Regulatory - immunology
T-Lymphocytes, Regulatory - metabolism
Thymic stromal lymphopoietin
Water - metabolism
Title A novel mouse model of atopic dermatitis with epicutaneous allergen sensitization and the effect of Lactobacillus rhamnosus
URI https://api.istex.fr/ark:/67375/WNG-KG2P1FQJ-G/fulltext.pdf
https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fj.1600-0625.2012.01539.x
https://www.ncbi.nlm.nih.gov/pubmed/22742655
https://www.proquest.com/docview/1034200329
https://www.proquest.com/docview/1038612779
Volume 21
hasFullText 1
inHoldings 1
isFullTextHit
isPrint
link http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV1La9wwEBYlh9BL34_tI6hQevNiW7JkH0OS3ZC2oS0N3ZvQkyy79Yb1bgnNn8-M5Gy7JfRQejOyJCPNjPyN9GmGkLelFqAptQYnpzEZ96XJ6iZnGS9cKIIWUvhIkD0Vx2f8ZFJNev4T3oVJ8SE2G25oGXG9RgPXpts2coG3ogHAI0OrHMKPDQSPeLJgAsPoH37ZRJIqJIsxd_MGHGgh82qb1HNrRwBXcaYvkS6pO5ixkFJd3IZFt6Ft_DeN7pPZzagSJWU2XK_M0P78I-Dj_xn2A3Kvh7B0P-ncQ3LHt4_I7sf-kP4xudqn7eKHn1PcVfA05tqhi0DBvb-YWup8QsnTjuImMPVQuAaI6qE2xcwueB2UdkisX_WXRKluHQWkShP7BDv7gHmCjLbT-RyaLc_193bRrbsn5Gx09PXgOOtzPGRTJkSThcLy2gjna2-111VtZVMElyNHq-TOWMk9q433ttZ5cM7wmmvmpcG4NhZ8radkp120_jnIs7LGchMA0mnuWDAu5NYwF2AdZRULA_IuylNdpDgeSi9nSGuTlfp2Olbvx-WnYvT5RI0HZG9L4JsGpSgbzPw3IG9uNECBNeIRS5olVWBERVgoy-avdWrAlVJCnWdJfX59AU_ORQVfEFEJNi9-89VA_ArFr1D8KopfXaqjySE-vfjXhi_JXSxO9LlXZGe1XPvXgLdWZi9a0jXD6SBQ
linkProvider Wiley-Blackwell
linkToHtml http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV1LbxMxELZQkYALb0p4FCMhbhvtw2vvHivaJLRpBKgVuVl-iqhhU2UTVMGfZ8beBoIqDojbatf2yp4Z-xv78wwhb3LFQVMqBU5OrRPmcp1UdVokLLM-84oL7gJBdsJHZ-xoWk67dEB4FybGh9hsuKFlhPkaDRw3pLetnOO1aEDwSNHK-7CygeQBUN7E4zq00oNPm1hSmShC1N20Bheai7TcpvVc2xIAVhzrSyRMqhbGzMdkF9eh0W1wG1anwT0yv-pXJKWc99cr3Tff_wj5-J86fp_c7VAs3Y9q94DccM1DcuukO6d_RH7s02bxzc0pbiw4GtLt0IWn4OFfzAy1LgLlWUtxH5g6eLkGlOqgNMXkLngjlLbIrV9190SpaiwFsEojAQUbG2OqIK3MbD6Hassv6muzaNftY3I2ODx9N0q6NA_JrOC8TnxmWKW5dZUzyqmyMqLOvE2RppUzq41grqi0c6ZSqbdWs4qpwgmNoW0MuFtPyE6zaNxTEGhptGHaA6pTzBZeW58aXVgPU2lRFr5H3gaByosYykOq5Tky20QpP0-G8niYf8gGH4_ksEf2tiS-qZDzvMbkfz3y-koFJBgknrLEUZIZBlWEuTKv_1qmAmgpBJTZjfrz6w94eM5L-AMPWrD58Ju7BuKXKH6J4pdB_PJSHk4P8OnZv1Z8RW6PTk_Gcvx-cvyc3MEikU33guyslmv3EuDXSu8Fs_oJvuEkbQ
linkToPdf http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV3db9MwELfQkCZegPFZYMNIiLdUSew4zuPE1o5tVAMx0TfLn6JqSaumRRP889zFWaFo4gHxFiW2I_vu7N_ZP98R8jrXAjRFanByKpNwn5tEVilLeOZCFrQohW8JsiNxcslPx8W44z_hXZgYH2Kz4YaW0c7XaOALF7aNXOCtaADwyNDK-7CwgeABT97mApwtBEgfN6GkspK1QXfTCjxoUabFNqvnxpYAr-JQXyFfUjcwZCHmurgJjG5j23ZxGtwj0-tuRU7KtL9emb79_kfEx__T7_vkbodh6WFUuj1yy9cPyO777pT-IflxSOv5Nz-juK3gaZtsh84DBf9-MbHU-QiTJw3FXWDq4eUaMKqH0hRTu-B9UNogs37V3RKlunYUoCqN9BNs7BwTBRltJ7MZVFt-0V_rebNuHpHLwfGntydJl-QhmTAhqiRklksjnJfeaq8LacsqCy5FklbOnbEl90wa763UaXDOcMk186XBwDYWnK3HZKee1_4pyLOwxnITANNp7lgwLqTWMBdgImUFCz3yppWnWsRAHkovp8hrKwv1eTRUZ8P8Iht8OFXDHjnYEvimQi7yClP_9ciraw1QYI54xhJHSWUYUhFmyrz6axkJwLIsocyTqD6__oBH56KAP4hWCTYffnPWQPwKxa9Q_KoVv7pSx-MjfHr2rxVfkt2Lo4E6fzc6e07uYIlIpXtBdlbLtd8H7LUyB61R_QQyQCMc
openUrl ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=A+novel+mouse+model+of+atopic+dermatitis+with+epicutaneous+allergen+sensitization+and+the+effect+of+Lactobacillus+rhamnosus&rft.jtitle=Experimental+dermatology&rft.au=Kim%2C+Ha-Jung&rft.au=Kim%2C+Young-Joon&rft.au=Kang%2C+Mi-Jin&rft.au=Seo%2C+Ju-Hee&rft.date=2012-09-01&rft.pub=Blackwell+Publishing+Ltd&rft.issn=0906-6705&rft.eissn=1600-0625&rft.volume=21&rft.issue=9&rft.spage=672&rft.epage=675&rft_id=info:doi/10.1111%2Fj.1600-0625.2012.01539.x&rft.externalDBID=n%2Fa&rft.externalDocID=ark_67375_WNG_KG2P1FQJ_G
thumbnail_l http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=0906-6705&client=summon
thumbnail_m http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=0906-6705&client=summon
thumbnail_s http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=0906-6705&client=summon