Tissue-specific expression of the NOD-like receptor protein 3 in BALB/c mice

被引:21
作者
Huang, Zhiqiang [1 ,2 ]
Yu, Meng [1 ,2 ]
Tong, Shuang [1 ,2 ]
Jia, Kun [1 ,2 ]
Liu, Rongchang [1 ,2 ]
Wang, Heng [1 ,2 ]
Li, Shoujun [1 ,2 ]
Ning, Zhangyong [1 ,2 ]
机构
[1] South China Agr Univ, Coll Vet Med, Guangzhou 510642, Guangdong, Peoples R China
[2] Key Lab Comprehens Prevent & Control Severe Clin, Guangzhou 510642, Guangdong, Peoples R China
关键词
BALB/c mice; gene expression profile; NLRP3; tissue distribution; INTERLEUKIN-1-BETA SECRETION; AUTOINFLAMMATORY DISEASES; NALP3; INFLAMMASOME; IMMUNITY; PATHOGENESIS; AUTOIMMUNE; INFECTION; ACTIVATE; CELLS; NLRS;
D O I
10.4142/jvs.2014.15.2.173
中图分类号
S85 [动物医学(兽医学)];
学科分类号
0906 ;
摘要
Activation of the innate immune system requires recognition of pathogen-associated molecular patterns, such as NOD-like receptors. The NOD-like receptor protein 3 (NLRP3) inflammasome is involved in induction of the pro-inflammatory cytokine, IL-113, and subsequent inflammatory responses NLRP3 inflammasome plays important roles in the inflammatory and innate immune responses associated with autohrunune/inflammatory syndrome. However, analysis of the tissue distribution and expression profiles in BALB/c mice is still incomplete. In this study, we investigated the tissue distribution and expression pattern of NLRP3 in BALB/c mice to further elucidate its function in innate immunity in this commonly used laboratory animal model. NLRP3 mRNA expression levels and tissue distribution of the protein were investigated by real-time quantitative PCR and immnunohistochemical analyses, respectively. NLRP3 mRNA expression was higher in the kidney and inguinal lymph nodes than in other tissues. Cytoplasmic expression of NLRP3 was detected in the epithelial reticular cells of the spleen and thymus, lymphocytes in the inguinal lymph nodes, cardiac muscle cells, cerebral cortex neurons, alveolar macrophages, renal tubule cells and liver sinusoidal endothelial cells. The results of this study will assist investigators in interpreting site-specific functions and roles of NLRP3 in inflammatory responses.
引用
收藏
页码:173 / 177
页数:5
相关论文
共 31 条
[1]   NALP3 forms an IL-lβ-Processing inflammasome with increased activity in Muckle-Wells autoinflammatory disorder [J].
Agostini, L ;
Martinon, F ;
Burns, K ;
McDermott, MF ;
Hawkins, PN ;
Tschopp, J .
IMMUNITY, 2004, 20 (03) :319-325
[2]   Structural, expression, and evolutionary analysis of mouse CIASI [J].
Anderson, JP ;
Mueller, JL ;
Rosengren, S ;
Boyle, DL ;
Schaner, P ;
Cannon, SB ;
Goodyear, CS ;
Hoffman, HM .
GENE, 2004, 338 (01) :25-34
[3]   RETRACTED: Hepatitis C virus activates interleukin-1β via caspase-1-inflammasome complex (Publication with Expression of Concern. See vol. 100, pg. 1342, 2019) (Retracted article. See vol. 100, pg. 1714, 2019) [J].
Burdette, Dylan ;
Haskett, Adam ;
Presser, Lance ;
McRae, Steven ;
Iqbal, Jawed ;
Waris, Gulam .
JOURNAL OF GENERAL VIROLOGY, 2012, 93 :235-246
[4]   The pathogenesis of neonatal autoimmune and autoinflammatory diseases: A comprehensive review [J].
Chang, Christopher .
JOURNAL OF AUTOIMMUNITY, 2013, 41 :100-110
[5]   Innate instruction of adaptive immunity revisited: the inflammasome [J].
Eisenbarth, Stephanie C. ;
Flavell, Richard A. .
EMBO MOLECULAR MEDICINE, 2009, 1 (02) :92-98
[6]   Chronic infantile neurological cutaneous and articular syndrome is caused by mutations in CIAS1, a gene highly expressed in polymorphonuclear cells and chondrocytes [J].
Feldmann, J ;
Prieur, AM ;
Quartier, P ;
Berquin, P ;
Certain, S ;
Cortis, E ;
Teillac-Hamel, D ;
Fischer, A ;
de Saint Basile, G .
AMERICAN JOURNAL OF HUMAN GENETICS, 2002, 71 (01) :198-203
[7]   Chronic inflammation:: importance of NOD2 and NALP3 in interleukin-1β generation [J].
Ferrero-Miliani, L. ;
Nielsen, O. H. ;
Andersen, P. S. ;
Girardin, S. E. .
CLINICAL AND EXPERIMENTAL IMMUNOLOGY, 2007, 147 (02) :227-235
[8]   Experimental autoimmune gastritis: Mouse models of human organ-specific autoimmune disease [J].
Field, J ;
Biondo, MA ;
Murphy, K ;
Alderuccio, F ;
Toh, BH .
INTERNATIONAL REVIEWS OF IMMUNOLOGY, 2005, 24 (1-2) :93-110
[9]   How Toll-like receptors and Nod-like receptors contribute to innate immunity in mammals [J].
Fritz, JH ;
Girardin, SE .
JOURNAL OF ENDOTOXIN RESEARCH, 2005, 11 (06) :390-394
[10]   Influenza virus activates inflammasomes via its intracellular M2 ion channel [J].
Ichinohe, Takeshi ;
Pang, Iris K. ;
Iwasaki, Akiko .
NATURE IMMUNOLOGY, 2010, 11 (05) :404-U61