scholarly journals Cellular Distribution of C-C Motif Chemokine Ligand 2 Like Immunoreactivities in Frontal Cortex and Corpus Callosum of Normal and Lipopolysaccharide Treated Animal

2021 ◽  
Author(s):  
Xue Shi ◽  
Xinrui Gong ◽  
Huangui Xiong ◽  
Jingdong Zhang
Keyword(s):  
Corpus Callosum ◽  
Brain Cortex ◽  
Immunofluorescent Staining ◽  
Cellular Distribution ◽  
Lateral Ventricles ◽  
Cellular Expression ◽  
Ependymal Layer ◽  
Ccl2 Level ◽  
Chemokine Ligand ◽  
Chemokine Ligand 2

Abstract Background: C-C motif chemokine ligand 2 (CCL2) is reported to be involved in the pathogenesis of various neurological and/or psychiatric diseases. Tissue or cellular expression of CCL2, in normal or pathological condition, may play an essential role in recruiting of monocytes or macrophages into the targeted organs, and be involved in a certain pathogenic mechanism. However, only a few studies focused on tissue and cellular distribution of the CCL2 peptide in the brain’s grey and white matters (GM, WM), and the changes of the GM and WM cellular CCL2 level in septic or endotoxic encephalopathy was not explored. Hence, the CCL2 cellular distribution in the front brain cortex and the corpus callosum (CC) WM was investigated in the present work by using immunofluorescent staining. Results: 1) Normally, CCL2 like immunoreactivity (CCL2-ir) in the CC is significantly higher than the cortex, especially when the measurement includes ependymal layer attached to the CC. 2) Structures surrounding the vasculatures contribute major CCL2-ir positive profiles in both GM and WM, but significantly more in the CC WM, in which they are bilaterally distributed and predominantly located in the lateral CC between the cingulate cortex and the lateral ventricles. 3) Following systemic lipopolysaccharide (LPS), the number of neuron-like CCL2-ir positive cells are increased significantly in the cortex, but not in the CC. 4) More CCL2-ir positive elements are accumulated inside microvasculature like structures in the CC WM, compared to those found in the cortex following systemic LPS. 5) Few macrophage/microglia marker-Iba-1 labeled structures exhibit CCL2-ir in normal cortex and CC, but the co-localization is significantly increased following systemic LPS. 6) Following saline or LPS injection, CCL2-ir and GFAP or Iba-1 double labeled structures are observed within the ependymal layer between the lateral ventricles and the CC. No accumulation of neutrophils was detected.Conclusion: there exist differences in the cellular distribution of the CCL2 peptide in the front brain cortex GM and the subcortical WM - the CC, in both the physiological condition and experimental endotoxemia. Which might cause different pathological change in the GM and WM.

scholarly journals Study on plasma CC chemokine ligand 2 level and its promoter region 2518A/G polymorphism in MS patients

2020 ◽  
Vol 18 ◽  
pp. 205873922095991 ◽  
Author(s):  
Zenghui Fu ◽  
Yan Jiang ◽  
Jing Liu ◽  
Zaihong Lin ◽  
Yan Jin
Keyword(s):  
Promoter Region ◽  
Gene Promoter ◽  
Cc Chemokine ◽  
Ccl2 Level ◽  
Relapsing Remitting ◽  
Chemokine Ligand ◽  
Cc Chemokine Ligand 2 ◽  
The Relationship ◽  
Chemokine Ligand 2 ◽  
Gene Promoter Region

The increase of CC chemokine ligand 2 (CCL2) is associated with multiple sclerosis (MS), but the relationship between gene promoter region 2518A/G and the pathogenesis of MS is still not obvious. Collected 54 cases of relapsing-remitting MS patients and 54 healthy controls. By detecting the CCL2-2518A/G polymorphism of MS patients and analyzing the plasma CCL2 level. High levels of A/A genotype and A allele frequency in serum CCL2 and PBMC were found in MS patients. The serum CCL2 of MS patients with A/A genotype is higher than other genotypes. Lipopolysaccharide stimulated PBMC, CCL2 levels in the supernatant of all genotypes were higher, and the A/A genotype levels of MS patients were the highest. Finally, CCL2-2518A/G polymorphism is related to the pathogenesis of MS.

scholarly journals Exploring the Role of C-C Motif Chemokine Ligand-2 Single Nucleotide Polymorphism in Pulmonary Tuberculosis: A Genetic Association Study from North India

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Sanjay K. Biswas ◽  
Mayank Mittal ◽  
Ekata Sinha ◽  
Vandana Singh ◽  
Nidhi Arela ◽  
...  
Keyword(s):  
Risk Factor ◽  
Pulmonary Tuberculosis ◽  
North India ◽  
Pulmonary Tb ◽  
Tnf Α ◽  
Ccl2 Level ◽  
Chemokine Ligand ◽  
Ifn Γ ◽  
Chemokine Ligand 2

The C-C motif chemokine ligand-2 (CCL2) was evidenced to be associated with tuberculosis susceptibility in some ethnic groups. In the present study, effort was made to find out the association of CCL2-2518 A>G and -362 G>C variants with susceptibility to TB in a population from North India. The genotyping was carried out in 373 participants with pulmonary TB (PTB) and 248 healthy controls (HCs) for CCL2-2518 A>G and -362 G>C polymorphisms by PCR-RFLP and by melting curve analysis using fluorescence-labeled hybridization fluorescent resonance energy transfer (FRET) probes, respectively, followed by DNA sequencing in a few representative samples. Genotype and allele frequencies were compared by the chi-squared test and crude and Mantel-Haenszel (M-H) odds ratio (OR). OR was calculated using STATA/MP16.1 software. Further, CCL2, IL-12p70, IFN-γ, TNF-α, and TGF-β levels were measured in serum samples of these participants using commercially available kits. Our analysis indicated that the homozygous mutant in both -2518 GG ( OR = 2.07 , p = 0.02 ) and -362 CC ( OR = 1.92 , p = 0.03 ) genotypes was associated with susceptibility to pulmonary TB. Further, heterozygous genotypes -2518AG ( OR = 0.60 , p = 0.003 ) and -362GC ( OR = 0.64 , p = 0.013 ) provide resistance from PTB disease. Haplotype analysis revealed AC haplotype ( p = 0.006 ) to be a risk factor associated with PTB susceptibility. The serum CCL2 level was significantly elevated among participants with -2518 AA genotype compared to -2518 GG genotype. CCL2 level was observed to be positively correlated with IL12p70, IFN-γ and TNF-α, thus suggesting the immunological regulatory role of CCL2 against pulmonary tuberculosis. CCL2-2518 GG and -362 CC genotypes were found to be associated with susceptibility to pulmonary tuberculosis and CCL2-2518AG and CCL2-362GC with resistance from PTB. AC haplotype was found to be a risk factor for PTB in the present study. It may be hypothesized from the findings that -2518G allele could be responsible for lower production of CCL2 which leads to defective Th1 response and makes a host susceptible for pulmonary tuberculosis.

scholarly journals Macrophage Migration Inhibitory Factor Induces Macrophage Recruitment via CC Chemokine Ligand 2

2006 ◽  
Vol 177 (11) ◽  
pp. 8072-8079 ◽  
Author(s):  
Julia L. Gregory ◽  
Eric F. Morand ◽  
Sonja J. McKeown ◽  
Jennifer A. Ralph ◽  
Pamela Hall ◽  
...  
Keyword(s):  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Inhibitory Factor ◽  
Macrophage Migration ◽  
Cc Chemokine ◽  
Macrophage Recruitment ◽  
Chemokine Ligand ◽  
Cc Chemokine Ligand 2 ◽  
Chemokine Ligand 2

scholarly journals MiR-144-3p is associated with pathological inflammation in patients infected with Mycobacteroides abscessus

2021 ◽  
Vol 53 (1) ◽  
pp. 136-149
Author(s):  
Hyeon Ji Kim ◽  
In Soo Kim ◽  
Sung-Gwon Lee ◽  
Young Jae Kim ◽  
Prashanta Silwal ◽  
...  
Keyword(s):  
Proinflammatory Cytokines ◽  
Mononuclear Cells ◽  
Nontuberculous Mycobacteria ◽  
Expression Profiles ◽  
Host Factors ◽  
Integrated Analysis ◽  
Peripheral Blood Mononuclear ◽  
Global Health Issue ◽  
Chemokine Ligand ◽  
Chemokine Ligand 2

AbstractInfection with rapidly growing nontuberculous mycobacteria is emerging as a global health issue; however, key host factors remain elusive. Here, we investigated the characteristic immune profiles of peripheral blood mononuclear cells (PBMCs) from patients infected with Mycobacteroides abscessus subsp. abscessus (Mabc) and M. abscessus subsp. massiliense (Mmass). Using an integrated analysis of global mRNA and microRNA expression profiles, we found that several inflammatory cytokines/chemokines [interleukin (IL)-1β, IL-6, C-X-C motif chemokine ligand 2, and C-C motif chemokine ligand 2] and miR-144-3p were significantly upregulated in PBMCs from patients compared with those from healthy controls (HCs). Notably, there was a strong correlation between the expression levels of miR-144-3p and proinflammatory cytokines/chemokines. Similarly, upregulated expression of miR-144-3p and proinflammatory cytokines/chemokines was found in macrophages and lungs from mice after infection with Mabc and Mmass. We showed that the expression of negative regulators of inflammation (SARM1 and TNIP3) was significantly downregulated in PBMCs from the patients, although they were not putative targets of miR-144-3p. Furthermore, overexpression of miR-144-3p led to a marked increase in proinflammatory cytokines/chemokines and promoted bacterial growth in macrophages. Together, our results highlight the importance of miR-144-3p linking to pathological inflammation during M. abscessus infection.

scholarly journals NLRP7 deubiquitination by USP10 promotes tumor progression and tumor-associated macrophage polarization in colorectal cancer

2021 ◽  
Vol 40 (1) ◽  
Author(s):  
Bing Li ◽  
Zhi-Peng Qi ◽  
Dong-Li He ◽  
Zhang-Han Chen ◽  
Jing-Yi Liu ◽  
...  
Keyword(s):  
Tumor Progression ◽  
Acceptor Site ◽  
Protein Levels ◽  
Qrt Pcr ◽  
Chemokine Ligand ◽  
Specific Protease ◽  
Ubiquitin Specific Protease ◽  
Chemokine Ligand 2

Abstract Background NOD-like receptors affect multiple stages of cancer progression in many malignancies. NACHT, LRR, and PYD domain-containing protein 7 (NLRP7) is a member of the NOD-like receptor family, although its role in tumorigenesis remains unclear. By analyzing clinical samples, we found that NLRP7 protein levels were upregulated in colorectal cancer (CRC). We proposed the hypothesis that a high level of NLRP7 in CRC may promote tumor progression. Here, we further investigated the role of NLRP7 in CRC and the underlying mechanism. Methods NLRP7 expression in human CRC and adjacent non-tumorous tissues was examined by quantitative real-time polymerase chain reaction (qRT-PCR), western blotting, and immunohistochemistry. The effect of NLRP7 in CRC progression was investigated in vitro and in vivo. Proteins interacting with NLRP7 were identified by immunoprecipitation and mass spectrometry analysis while immunofluorescence staining revealed the cellular location of the proteins. Cellular ubiquitination and protein stability assays were applied to demonstrate the ubiquitination effect on NLRP7. Cloning and mutagenesis were used to identify a lysine acceptor site that mediates NLRP7 ubiquitination. Cytokines/chemokines affected by NLRP7 were identified by RNA sequencing, qRT-PCR, and enzyme-linked immunosorbent assay. Macrophage phenotypes were determined using qRT-PCR, flow cytometry, and immunohistochemistry. Results NLRP7 protein levels, but not mRNA levels, were upregulated in CRC, and increased NLRP7 protein expression was associated with poor survival. NLRP7 promoted tumor cell proliferation and metastasis in vivo and in vitro and interacted with ubiquitin-specific protease 10, which catalyzed its deubiquitination in CRC cells. NLRP7 stability and protein levels in CRC cells were modulated by ubiquitination and deubiquitination, and NLRP7 was involved in the ubiquitin-specific protease 10 promotion of tumor progression and metastasis in CRC. K379 was an important lysine acceptor site that mediates NLRP7 ubiquitination in CRC cells. In CRC, NLRP7 promoted the polarization of pro-tumor M2-like macrophages by inducing the secretion of C-C motif chemokine ligand 2. Furthermore, NLRP7 promoted NF-κB nuclear translocation and activation of C-C motif chemokine ligand 2 transcription. Conclusions We showed that NLRP7 promotes CRC progression and revealed an as-yet-unidentified mechanism by which NLRP7 induces the polarization of pro-tumor M2-like macrophages. These results suggest that NLRP7 could serve as a biomarker and novel therapeutic target for the treatment of CRC.

Sign in / Sign up

Export Citation Format

Share Document