CXCL5

Chemokine (C-X-C motif) ligand 5

Solution structure of chemokine CXCL5. PDB entry 2mgs​[1]
Available structures
PDB Ortholog search: PDBe, RCSB
Identifiers
Symbols CXCL5 ; ENA-78; SCYB5
External IDs OMIM: 600324 HomoloGene: 88672 GeneCards: CXCL5 Gene
RNA expression pattern
More reference expression data
Orthologs
Species Human Mouse
Entrez 6374 n/a
Ensembl ENSG00000163735 n/a
UniProt P42830 n/a
RefSeq (mRNA) NM_002994 n/a
RefSeq (protein) NP_002985 n/a
Location (UCSC) Chr 4:
74 – 74 Mb		 n/a
PubMed search n/a

C-X-C motif chemokine 5 (CXCL5 or ENA78) is a protein that in humans is encoded by the CXCL5 gene.[2][3]

Function

The protein encoded by this gene, CXCL5 is a small cytokine belonging to the CXC chemokine family that is also known as epithelial-derived neutrophil-activating peptide 78 (ENA-78). It is produced following stimulation of cells with the inflammatory cytokines interleukin-1 or tumor necrosis factor-alpha.[4] Expression of CXCL5 has also been observed in eosinophils, and can be inhibited with the type II interferon IFN-γ.[5] This chemokine stimulates the chemotaxis of neutrophils possessing angiogenic properties. It elicits these effects by interacting with the cell surface chemokine receptor CXCR2.[5] The gene for CXCL5 is encoded on four exons and is located on human chromosome 4 amongst several other CXC chemokine genes.[4][6] CXCL5 has been implicated in connective tissue remodelling.[5] CXCL5 has been also described to regulate neutrophil homeostasis.[7]

Clinical significance

CXCL5 plays a role in reducing sensitivity to sunburn pain in some subjects, and is a "potential target which can be utilized to understand more about pain in other inflammatory conditions like arthritis and cystitis.".[8] CXCL5 is well known to have chemotactic and activating functions on neutrophil, mainly during acute inflammatory responses. However CXCL5 expression is also higher in atherosclerosis (a chronic inflammatory condition) but is not associated with neutrophil infiltration. Instead CXCL5 has a protective role in atherosclerosis by directly controlling macrophage foam cell formation.[9]

References

  1. ↑ Sepuru, K. M.; Poluri, K. M.; Rajarathnam, K. (2014). "Solution Structure of CXCL5 — A Novel Chemokine and Adipokine Implicated in Inflammation and Obesity". PLoS ONE 9 (4): e93228. doi:10.1371/journal.pone.0093228. PMC 3973705. PMID 24695525.
  2. ↑ Chang MS, McNinch J, Basu R, Simonet S (Nov 1994). "Cloning and characterization of the human neutrophil-activating peptide (ENA-78) gene". J Biol Chem 269 (41): 25277–82. PMID 7929219.
  3. ↑ "Entrez Gene: CXCL5 chemokine (C-X-C motif) ligand 5".
  4. 1 2 Chang MS, McNinch J, Basu R, Simonet S (1994). "Cloning and characterization of the human neutrophil-activating peptide (ENA-78) gene". J. Biol. Chem. 269 (41): 25277–82. PMID 7929219.
  5. 1 2 3 Persson T, Monsef N, Andersson P, Bjartell A, Malm J, Calafat J, Egesten A (2003). "Expression of the neutrophil-activating CXC chemokine ENA-78/CXCL5 by human eosinophils". Clin. Exp. Allergy 33 (4): 531–7. doi:10.1046/j.1365-2222.2003.01609.x. PMID 12680872.
  6. ↑ O'Donovan N, Galvin M, Morgan JG (1999). "Physical mapping of the CXC chemokine locus on human chromosome 4". Cytogenet. Cell Genet. 84 (1–2): 39–42. doi:10.1159/000015209. PMID 10343098.
  7. ↑ Mei J, Liu Y, Dai N, Hoffmann C, Hudock KM, Zhang P, Guttentag SH, Kolls JK, Oliver PM, Bushman FD, Worthen GS. (2012). "Cxcr2 and Cxcl5 regulate the IL-17/G-CSF axis and neutrophil homeostasis in mice". Journal of Clinical Investigation. 122 (3): 974–986. doi:10.1172/JCI60588. PMID 22326959.
  8. ↑ Dawes JM, Calvo M, Perkins JR, Paterson KJ, Kiesewetter H, Hobbs C, Kaan TK, Orengo C, Bennett DL, McMahon SB (July 2011). "CXCL5 Mediates UVB Irradiation-Induced Pain". Sci Transl Med 3 (90): 90ra60. doi:10.1126/scitranslmed.3002193. PMC 3232447. PMID 21734176. Lay summary – FierceBiotech.
  9. ↑ Rousselle A, Qadri F, Leukel L, Yilmaz R, Fontaine JF, Sihn G, Bader M, Ahluwalia A, Duchene J. (2013). "CXCL5 limits macrophage foam cell formation in atherosclerosis.". Journal of Clinical Investigation. 123 (3): 1343–7. doi:10.1172/JCI66580. PMID 23376791.

Further reading

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