A novel human CC chemokine PARC that is most homologous to macrophage-inflammatory protein-1 alpha/LD78 alpha and chemotactic for T lymphocytes, but not for monocytes.

Hieshima, Kunio; Imai, Toshio; Baba, Masataka; Shoudai, Kiyomitsu; Ishizuka, Koko; Nakagawa, Takayuki; Tsuruta, Junji; Takeya, Mieko; Sakaki, Yoshiyuki; Takatsuki, Kiyoshi; Miura, Retsu; Opdenakker, Ghislain; Damme, Jo Van; Yoshie, Osamu; Nomiyama, Hisayuki

doi:10.4049/jimmunol.159.3.1140

Cited by 230 publications

(18 citation statements)

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“…CCL18 is constitutively expressed at high levels in the lungs and is selectively chemotactic to T cells [ 194 , 195 , 196 , 197 ]. The synergistic effects of CCL18 overexpression and BLM injury increased the inflammation in the lungs, especially T-cell infiltration, TNF-α, IFN-γ, MMP-2, and MMP-9 [ 50 ].…”

Section: Mechanisms Of Wound Healing and Fibrosismentioning

confidence: 99%

Immune Mechanisms of Pulmonary Fibrosis with Bleomycin

Ishida

Kuninaka

Mukaida

et al. 2023

IJMS

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Fibrosis and structural remodeling of the lung tissue can significantly impair lung function, often with fatal consequences. The etiology of pulmonary fibrosis (PF) is diverse and includes different triggers such as allergens, chemicals, radiation, and environmental particles. However, the cause of idiopathic PF (IPF), one of the most common forms of PF, remains unknown. Experimental models have been developed to study the mechanisms of PF, and the murine bleomycin (BLM) model has received the most attention. Epithelial injury, inflammation, epithelial–mesenchymal transition (EMT), myofibroblast activation, and repeated tissue injury are important initiators of fibrosis. In this review, we examined the common mechanisms of lung wound-healing responses after BLM-induced lung injury as well as the pathogenesis of the most common PF. A three-stage model of wound repair involving injury, inflammation, and repair is outlined. Dysregulation of one or more of these three phases has been reported in many cases of PF. We reviewed the literature investigating PF pathogenesis, and the role of cytokines, chemokines, growth factors, and matrix feeding in an animal model of BLM-induced PF.

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Section: Mechanisms Of Wound Healing and Fibrosismentioning

confidence: 99%

Immune Mechanisms of Pulmonary Fibrosis with Bleomycin

Ishida

Kuninaka

Mukaida

et al. 2023

IJMS

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“…CCL18, or CC motif chemokine ligand 18, is a human specific chemokine produced by macrophage and microglia. CCL18 is most closely related to CCL3 [ 80 ], another chemokine that has been shown to be elevated in NPC1 CSF ([ 57 , 81 ] and this study). CCL18 has previously been shown to be elevated in serum/plasma from individuals with lysosomal diseases, specifically Gaucher disease [ 82 ], Niemann-Pick disease type B or acid sphingomyelinase deficiency [ 83 ], GM1 gangliosidosis [ 84 ], NPC [ 40 ] and possibly lysosomal acid lipase deficiency [ 85 ].…”

Section: Discussionmentioning

confidence: 67%

Identification of cerebral spinal fluid protein biomarkers in Niemann-Pick disease, type C1

et al. 2023

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Background Niemann-Pick disease, type C1 (NPC1) is an ultrarare, recessive, lethal, lysosomal disease characterized by progressive cerebellar ataxia and cognitive impairment. Although the NPC1 phenotype is heterogeneous with variable age of onset, classical NPC1 is a pediatric disorder. Currently there are no therapies approved by the FDA and therapeutics trials for NPC1 are complicated by disease rarity, heterogeneity, and the relatively slow rate of neurological decline. Thus, identification of disease relevant biomarkers is necessary to provide tools that can support drug development efforts for this devastating neurological disease. Methods Proximal extension assays (O-link® Explore 1536) were used to compare cerebrospinal fluid (CSF) samples from individuals with NPC1 enrolled in a natural history study and non-NPC1 comparison samples. Relative expression levels of 1467 proteins were determined, and candidate protein biomarkers were identified by evaluating fold-change and adjusted Kruskal–Wallis test p-values. Selected proteins were orthogonally confirmed using ELISA. To gain insight into disease progression and severity we evaluated the altered protein expression with respect to clinically relevant phenotypic aspects: NPC Neurological Severity Score (NPC1 NSS), Annual Severity Increment Score (ASIS) and age of neurological onset. Results This study identified multiple proteins with altered levels in CSF from individuals with NPC1 compared to non-NPC1 samples. These included proteins previously shown to be elevated in NPC1 (NEFL, MAPT, CHIT1, CALB1) and additional proteins confirmed by orthogonal assays (PARK7, CALB2/calretinin, CHI3L1/YKL-40, MIF, CCL18 and ENO2). Correlations with clinically relevant phenotypic parameters demonstrated moderate negative (p = 0.0210, r = -0.41) and possible moderate positive (p = 0.0631, r = 0.33) correlation of CSF CALB2 levels with age of neurological onset and ASIS, respectively. CSF CHI3L1 levels showed a moderate positive (p = 0.0183, r = 0.40) correlation with the concurrent NPC1 NSS. A strong negative correlation (p = 0.0016, r = -0.648) was observed between CSF CCL18 and age of neurological onset for childhood/adolescent cases. CSF CCL18 levels also showed a strong positive correlation (p = 0.0017, r = 0.61) with ASIS. Conclusion Our study identified and validated multiple proteins in CSF from individuals with NPC1 that are candidates for further investigation in a larger cohort. These analytes may prove to be useful as supportive data in therapeutic trials. Trial registrations NCT00344331, NCT00001721, NCT02931682.

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“…In angiogenesis and hematopoiesis, chemokines act as mediators [25][26][27] . A circulating chemokine called CCL18/PARC promotes in inflammation, the recovery from damage, and the normal homing of mononuclear blood cells [28][29][30] . In atherosclerotic plaques, CCL18/PARC is expressed, especially in regions with decreased stability 29,31,32 .…”

Section: Discussionmentioning

confidence: 99%

Serum microRNA-499-5p Expression and Its Correlation with Chemokine (C-C motif) Ligand 18 in Acute Myocardial Infarction

Abdel-Hamed¹,

Nasser²,

Abo-Elmatty³

et al. 2023

The Egyptian Journal of Hospital Medicine

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Background: The major cause of illness and death is acute myocardial infarction (AMI). Therefore, to reduce death rates, effective and precise diagnostic biomarkers are needed. Objective:The aim of the current study was to evaluate the association between the expression of miRNA-499-5p and the chemokine (C-C motif) ligand 18 (CCL18) in AMI and its related characteristics in Egyptian populations. Patients and methods: A total of 150 participants were separated into 2 groups for a cross-sectional analytical study; AMI group was composed of 75 patients with AMI, whereas the control subjects' group was made up of 75 people who seemed to be healthy. Over a six-month period from March to September 2018, patients were chosen from the Cardiac Care Units at Suez Canal University Hospital and General Hospital. Using 6-Quantitative Real-Time Polymerase Chain Reaction, the expression of miRNA-499-5p in serum was measured. Using an enzyme-linked immunosorbent test, plasma CCL18 is determined. Results: Patients with AMI had considerably higher plasma levels of CCL18 than the control group (236.6 vs. 56.05 ng/mL; P<0.001). Significant P-value indicates a positive correlation between plasma CCL18 and male sex, smoking, heart rate, fasting blood sugar, and cardiac markers. In 89.3% of AMI patients, serum miRNA-499-5p expression was significantly increased by 6.36-fold (P<0.001). Creatine kinase MB and cardiac troponin I both exhibited a positive connection with serum miRNA-499-5p expression (P=0.003 and P=0.002, respectively). Additionally, serum miRNA-499-5p expression and plasma CCL18 showed a positive connection (P=0.004). Conclusion: CCL18 and miRNA 499-5p are potential biomarkers for AMI and possible predictors for the risk of myocardial damage in Egyptians.

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A novel human CC chemokine PARC that is most homologous to macrophage-inflammatory protein-1 alpha/LD78 alpha and chemotactic for T lymphocytes, but not for monocytes.

Cited by 230 publications

References 0 publications

Immune Mechanisms of Pulmonary Fibrosis with Bleomycin

Immune Mechanisms of Pulmonary Fibrosis with Bleomycin

Identification of cerebral spinal fluid protein biomarkers in Niemann-Pick disease, type C1

Serum microRNA-499-5p Expression and Its Correlation with Chemokine (C-C motif) Ligand 18 in Acute Myocardial Infarction

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