Lipopolysaccharide stimulation upregulated Toll-like receptor 4 expression in chicken cerebellum

Ansari, Abdur Rahman; Wen, Le; Huang, Haibo; Wang, Ji‐Xiang; Huang, Xiang; Peng, Kaiman; Liu, Huazhen

doi:10.1016/j.vetimm.2015.05.004

Cited by 10 publications

(8 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…PCs are the sole output neurons of the cerebellar cortex and are critical for cerebellar information processing (De Schutter and Steuber, 2009 ; Popa et al, 2012 ) and execution of motor functions (Fu et al, 1997 ; Ebner et al, 2011 ); their dysfunction can result in loss of motor coordination (Donald et al, 2008 ; He et al, 2014 ; Bosch et al, 2015 ) and cerebellar ataxia (Walter et al, 2006 ; Wang et al, 2015 ). We found that TLR4 was highly expressed in PCs but not in BG and GCs consistent with the reported expression patterns of TLR4 in other species (Ansari et al, 2015 ). We also found that loss of TLR4 was associated with a reduction in PC number and ML thickness.…”

Section: Discussionsupporting

confidence: 92%

Toll-Like Receptor 4 Deficiency Impairs Motor Coordination

Zhu

Wang

et al. 2016

Front. Neurosci.

View full text Add to dashboard Cite

The cerebellum plays an essential role in balance and motor coordination. Purkinje cells (PCs) are the sole output neurons of the cerebellar cortex and are critical for the execution of its functions, including motor coordination. Toll-like receptor (TLR) 4 is involved in the innate immune response and is abundantly expressed in the central nervous system; however, little is known about its role in cerebellum-related motor functions. To address this question, we evaluated motor behavior in TLR4 deficient mice. We found that TLR4−∕− mice showed impaired motor coordination. Morphological analyses revealed that TLR4 deficiency was associated with a reduction in the thickness of the molecular layer of the cerebellum. TLR4 was highly expressed in PCs but not in Bergmann glia or cerebellar granule cells; however, loss of TLR4 decreased the number of PCs. These findings suggest a novel role for TLR4 in cerebellum-related motor coordination through maintenance of the PC population.

show abstract

Section: Discussionsupporting

confidence: 92%

Toll-Like Receptor 4 Deficiency Impairs Motor Coordination

Zhu

Wang

et al. 2016

Front. Neurosci.

View full text Add to dashboard Cite

show abstract

“…Immunohistochemical staining of BF sections was carried out using antibodies against proliferative cell nuclear antigen (PCNA) (1:200), TLR4 (1:100) and NF-κB-p50 (1:250) (Santa Cruz Biotechnology, Inc., Santa Cruz, CA, USA) following previously described methods [ 49 ]. Formamide-monoclonal antibody (MAb) assay was performed with the anti-ssDNA monoclonal antibody (1:20; EMD Millipore, Billerica, USA) as previously described [ 14 , 15 ].…”

Section: Methodsmentioning

confidence: 99%

Lipopolysaccharide induces acute bursal atrophy in broiler chicks by activating TLR4-MAPK-NF-κB/AP-1 signaling

Ansari

Sun

et al. 2017

Oncotarget

Self Cite

View full text Add to dashboard Cite

We investigated the mechanisms that induce atrophy of the chicken bursa of Fabricius (BF) upon lipopolysaccharide (LPS) treatment in young chicks. LPS treatment resulted in ∼36% decrease in bursal weight within 36 h (P < 0.01). Histological analysis showed infiltration of eosinophilic heterophils and nucleated oval shaped RBCs in or near blood vessels of the BF from LPS-treated chicks. Scanning electron micrographs showed severe erosion and breaks in the mucosal membrane at 12 h and complete exuviation of bursal mucosal epithelial cells at 36 h. We observed decreased cell proliferation (low PCNA positivity) and increased apoptosis (high TUNEL and ssDNA positivity) in the BF 12-72 h after LPS treatment. RNA-seq analysis of the BF transcriptome showed 736 differentially expressed genes with most expression changes (637/736) 12 h after LPS treatment. KEGG pathway analysis identified TLR4-MAPK-NF-κB/AP-1 as the key signaling pathway affected in response to LPS stimulation. These findings indicate LPS activates the TLR4-MAPK-NF-κB/AP-1 signaling pathway that mediates acute atrophy of the chicken bursa of Fabricius by inducing inflammation and apoptosis.

show abstract

“…In swine, TLR4 expression in seen in cortex, cerebellum, hippocampus and hypothalamus, and TLR4 expression has also been demonstrated in rat neurons and mouse primary neuronal cultures, glial cells, human and rodent brain endothelial cells and cell lines, human and rodent microglia, and in immature and mature choroid plexus under physiologic conditions and associated with systemic inflammation (Leow‐Dyke et al, 2012; Nagyoszi et al, 2010; Stridh et al, 2013a; Vaure and Liu, 2014; Skipor et al, 2015; Chakravarty and Herkenham, 2005). In immature chickens, TLR4 expression was observed in the Purkinje cell layer, pia mater, neurons in the medulla and blood vessels in the cerebellum (Ansari et al, 2015). In inflammatory and ischemic CNS disease, TLR4 and TLR3 expression is upregulated in the brain and microglia predominantly express TLR4 (Vontell et al, 2013, 2015; Vaure and Liu, 2014; Ansari et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

“…In immature chickens, TLR4 expression was observed in the Purkinje cell layer, pia mater, neurons in the medulla and blood vessels in the cerebellum (Ansari et al, 2015). In inflammatory and ischemic CNS disease, TLR4 and TLR3 expression is upregulated in the brain and microglia predominantly express TLR4 (Vontell et al, 2013, 2015; Vaure and Liu, 2014; Ansari et al, 2015). In the present study, TLR4 gene expression increased significantly in the ferret brain from P1 and P10 to the later neonatal and adult ages.…”

Section: Discussionmentioning

confidence: 99%

Ontogeny of white matter, toll‐like receptor expression, and motor skills in the neonatal ferret

Snyder

Wood

Corry

et al. 2018

Intl J of Devlp Neuroscience

View full text Add to dashboard Cite

Inflammation caused by perinatal infection, superimposed with hypoxia and/or hyperoxia, appears to be important in the pathogenesis of preterm neonatal encephalopathy, with white matter particularly vulnerable during the third trimester. The associated inflammatory response is at least partly mediated through Toll-like receptor (TLR)-dependent mechanisms. Immunohistochemistry, gene expression, and behavioral studies were used to characterize white matter development and determine TLR3 and TLR4 expression and accumulation in the neonatal ferret brain. Expression of markers of white matter development increased significantly between postnatal day (P)1 and P10 (NG2, PDGFRα) or P15 (Olig2), and either remained elevated (NG2), or decreased again at P40 (PDGFRα, Olig2). Olig2 immunostaining within the internal capsule was also greatest at P15. Myelin basic protein (MBP) immunostaining and mRNA expression increased markedly from P15 to P40 and into adulthood, which correlated with increasing performance on behavioral tests (negative geotaxis, cliff aversion, righting reflex, and catwalk gait analysis). TLR4 and TLR3 positive staining was low at all ages, but TLR3 and TLR4 mRNA expression both increased significantly from P1 to P40. Following lipopolysaccharide (LPS) and hypoxia/hyperoxia exposure at P10, meningeal and parenchymal inflammation was seen, including an increase in TLR4 positive cells. These data suggest that the neuroinflammation associated with prematurity could be modeled in the newborn ferret.

show abstract

Lipopolysaccharide stimulation upregulated Toll-like receptor 4 expression in chicken cerebellum

Cited by 10 publications

References 26 publications

Toll-Like Receptor 4 Deficiency Impairs Motor Coordination

Toll-Like Receptor 4 Deficiency Impairs Motor Coordination

Lipopolysaccharide induces acute bursal atrophy in broiler chicks by activating TLR4-MAPK-NF-κB/AP-1 signaling

Ontogeny of white matter, toll‐like receptor expression, and motor skills in the neonatal ferret

Contact Info

Product

Resources

About