PMID- 30078223
OWN - NLM
STAT- MEDLINE
DCOM- 20191004
LR  - 20191007
IS  - 1097-4652 (Electronic)
IS  - 0021-9541 (Linking)
VI  - 234
IP  - 1
DP  - 2018 Jan
TI  - In vivo study: Th1-Th17 reduction in pristane-induced systemic lupus 
      erythematosus mice after treatment with tolerogenic Lactobacillus probiotics.
PG  - 642-649
LID - 10.1002/jcp.26819 [doi]
AB  - Uncontrolled inflammation in systemic lupus erythematosus (SLE) could cause 
      dysfunction in multiple organs. T helper 17 (Th17) cells are a main branch of 
      inflammatory responses in the pathogenesis of SLE, and by producing interleukin 
      17 (IL-17), represent a major functional tool in the progression of inflammation. 
      Animal models provide a special field for better studies of the pathogenesis of 
      diseases. Tolergenic probiotics could decrease inflammation in autoimmune 
      diseases by modulating the immune system and maintaining homeostasis. The aim of 
      this project was to evaluate the effects of Lactobacillus rhamnosus and 
      Lactobacillus delbrueckii on Th17 cells and their related mediators in a 
      pristane-induced BALB/c mice model of SLE. The mice were divided into 
      pretreatment groups, which received probiotics or prednisolone at Day 0, and 
      treatment groups, which received probiotics and prednisolone 2 months after 
      injection. The presence of antinuclear antibody (ANA), anti-double-stranded DNA 
      (anti-dsDNA), and anti-ribonucleoprotein (anti-RNP) and lipogranuloma was 
      evaluated; also, the population of Th1-Th17 cells as well as interferon gamma 
      (IFN-gamma), IL-17, and IL-10 levels, and the expression of RAR-related orphan 
      related receptor gamma (RORgammat) and IL-17 were determined. We observed that 
      probiotics and prednisolone could delay SLE in pretreatment and treatment mice 
      groups, with a reduction in ANA, anti-dsDNA, anti-RNP, and mass of lipogranuloma. 
      Probiotics and prednisolone decreased the population of Th1-Th17 cells and 
      reduced IFN-gamma and IL-17 as inflammatory cytokines in the pretreatment and 
      treatment groups in comparison with SLE-induced mice. Our results indicated that, 
      due to their anti-inflammatory properties and reduction of Th17, Th1, and 
      cytotoxic T lymphocyte (CTL) cells, the use of these probiotics could probably 
      represent a new tool for the better management of SLE.
CI  - (c) 2018 Wiley Periodicals, Inc.
FAU - Mardani, Fatemeh
AU  - Mardani F
AUID- ORCID: 0000-0002-2185-7105
AD  - Immunology Research Center, Mashhad University of Medical Sciences, Mashhad, 
      Iran.
AD  - Immunology Department, Faculty of Medicine, Mashhad University of Medical 
      Sciences, Mashhad, Iran.
AD  - Student Research Committeen, Mashhad University of Medical Sciences, Mashhad, 
      Iran.
FAU - Mahmoudi, Mahmoud
AU  - Mahmoudi M
AUID- ORCID: 0000-0002-3193-5242
AD  - Immunology Research Center, Mashhad University of Medical Sciences, Mashhad, 
      Iran.
AD  - Immunology Department, Faculty of Medicine, Mashhad University of Medical 
      Sciences, Mashhad, Iran.
FAU - Esmaeili, Seyed-Alireza
AU  - Esmaeili SA
AD  - Immunology Research Center, Mashhad University of Medical Sciences, Mashhad, 
      Iran.
AD  - Immunology Department, Faculty of Medicine, Mashhad University of Medical 
      Sciences, Mashhad, Iran.
AD  - Student Research Committeen, Mashhad University of Medical Sciences, Mashhad, 
      Iran.
FAU - Khorasani, Sahar
AU  - Khorasani S
AD  - Immunology Research Center, Mashhad University of Medical Sciences, Mashhad, 
      Iran.
AD  - Immunology Department, Faculty of Medicine, Mashhad University of Medical 
      Sciences, Mashhad, Iran.
AD  - Student Research Committeen, Mashhad University of Medical Sciences, Mashhad, 
      Iran.
FAU - Tabasi, Nafiseh
AU  - Tabasi N
AD  - Immunology Research Center, Mashhad University of Medical Sciences, Mashhad, 
      Iran.
FAU - Rastin, Maryam
AU  - Rastin M
AUID- ORCID: 0000-0001-6675-2430
AD  - Immunology Research Center, Mashhad University of Medical Sciences, Mashhad, 
      Iran.
AD  - Immunology Department, Faculty of Medicine, Mashhad University of Medical 
      Sciences, Mashhad, Iran.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20180804
PL  - United States
TA  - J Cell Physiol
JT  - Journal of cellular physiology
JID - 0050222
RN  - 0 (Interleukin-17)
RN  - 0 (Terpenes)
RN  - 130068-27-8 (Interleukin-10)
RN  - 26HZV48DT1 (pristane)
SB  - IM
MH  - Animals
MH  - Disease Models, Animal
MH  - Humans
MH  - Immunity, Cellular/drug effects/*genetics
MH  - Inflammation/*drug therapy/genetics/immunology
MH  - Interleukin-10/genetics
MH  - Interleukin-17/genetics
MH  - Lactobacillus/chemistry
MH  - Lupus Erythematosus, Systemic/chemically induced/*drug 
      therapy/immunology/pathology
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Probiotics/*administration & dosage/chemistry
MH  - T-Lymphocytes, Regulatory/immunology
MH  - Terpenes/toxicity
MH  - Th1 Cells/drug effects/immunology/pathology
MH  - Th17 Cells/drug effects/immunology/pathology
OTO - NOTNLM
OT  - Lactobacillus
OT  - SLE
OT  - Th1-Th17
OT  - pristine-induced mice model of SLE
OT  - tolerogenic probiotics
EDAT- 2018/08/06 06:00
MHDA- 2019/10/08 06:00
CRDT- 2018/08/06 06:00
PHST- 2018/01/13 00:00 [received]
PHST- 2018/04/30 00:00 [accepted]
PHST- 2018/08/06 06:00 [pubmed]
PHST- 2019/10/08 06:00 [medline]
PHST- 2018/08/06 06:00 [entrez]
AID - 10.1002/jcp.26819 [doi]
PST - ppublish
SO  - J Cell Physiol. 2018 Jan;234(1):642-649. doi: 10.1002/jcp.26819. Epub 2018 Aug 4.