Detailed Information on Publication Record
2021
Pro-Inflammatory and Neurotrophic Factor Responses of Cells Derived from Degenerative Human Intervertebral Discs to the Opportunistic Pathogen Cutibacterium acnes
CAPOOR, M. N., Anna KONIECZNA, A. MCDOWELL, Filip RŮŽIČKA, Martin SMRČKA et. al.Basic information
Original name
Pro-Inflammatory and Neurotrophic Factor Responses of Cells Derived from Degenerative Human Intervertebral Discs to the Opportunistic Pathogen Cutibacterium acnes
Authors
CAPOOR, M. N., Anna KONIECZNA (203 Czech Republic, belonging to the institution), A. MCDOWELL, Filip RŮŽIČKA (203 Czech Republic, belonging to the institution), Martin SMRČKA (203 Czech Republic, belonging to the institution), Radim JANČÁLEK (203 Czech Republic, belonging to the institution), Karel MÁCA (203 Czech Republic, belonging to the institution), Michael LUJC (203 Czech Republic, belonging to the institution), Fatima AHMED (586 Pakistan), C. BIRKENMAIER, S. DUDLI and Ondřej SLABÝ (203 Czech Republic, guarantor, belonging to the institution)
Edition
International Journal of Molecular Sciences, Basel, MDPI, 2021, 1422-0067
Other information
Language
English
Type of outcome
Článek v odborném periodiku
Field of Study
10608 Biochemistry and molecular biology
Country of publisher
Switzerland
Confidentiality degree
není předmětem státního či obchodního tajemství
References:
Impact factor
Impact factor: 6.208
RIV identification code
RIV/00216224:14110/21:00121370
Organization unit
Faculty of Medicine
UT WoS
000628279100001
Keywords in English
Cutibacterium acnes; disc cells; co-culture; inflammation; neurotrophic factors; gene expression; intracellular
Tags
International impact, Reviewed
Změněno: 5/4/2022 13:42, Mgr. Tereza Miškechová
Abstract
V originále
Previously, we proposed the hypothesis that similarities in the inflammatory response observed in acne vulgaris and degenerative disc disease (DDD), especially the central role of interleukin (IL)-1 beta, may be further evidence of the role of the anaerobic bacterium Cutibacterium (previously Propionibacterium) acnes in the underlying aetiology of disc degeneration. To investigate this, we examined the upregulation of IL-1 beta, and other known IL-1 beta-induced inflammatory markers and neurotrophic factors, from nucleus-pulposus-derived disc cells infected in vitro with C. acnes for up to 48 h. Upon infection, significant upregulation of IL-1 beta, alongside IL-6, IL-8, chemokine (C-C motif) ligand 3 (CCL3), chemokine (C-C motif) ligand 4 (CCL4), nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF), was observed with cells isolated from the degenerative discs of eight patients versus non-infected controls. Expression levels did, however, depend on gene target, multiplicity and period of infection and, notably, donor response. Pre-treatment of cells with clindamycin prior to infection significantly reduced the production of pro-inflammatory mediators. This study confirms that C. acnes can stimulate the expression of IL-1 beta and other host molecules previously associated with pathological changes in disc tissue, including neo-innervation. While still controversial, the role of C. acnes in DDD remains biologically credible, and its ability to cause disease likely reflects a combination of factors, particularly individualised response to infection.