J 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.

Základní údaje

Originální název

Pro-Inflammatory and Neurotrophic Factor Responses of Cells Derived from Degenerative Human Intervertebral Discs to the Opportunistic Pathogen Cutibacterium acnes

Autoři

CAPOOR, M. N., Anna KONIECZNA (203 Česká republika, domácí), A. MCDOWELL, Filip RŮŽIČKA (203 Česká republika, domácí), Martin SMRČKA (203 Česká republika, domácí), Radim JANČÁLEK (203 Česká republika, domácí), Karel MÁCA (203 Česká republika, domácí), Michael LUJC (203 Česká republika, domácí), Fatima AHMED (586 Pákistán), C. BIRKENMAIER, S. DUDLI a Ondřej SLABÝ (203 Česká republika, garant, domácí)

Vydání

International Journal of Molecular Sciences, Basel, MDPI, 2021, 1422-0067

Další údaje

Jazyk

angličtina

Typ výsledku

Článek v odborném periodiku

Obor

10608 Biochemistry and molecular biology

Stát vydavatele

Švýcarsko

Utajení

není předmětem státního či obchodního tajemství

Odkazy

Impakt faktor

Impact factor: 6.208

Kód RIV

RIV/00216224:14110/21:00121370

Organizační jednotka

Lékařská fakulta

UT WoS

000628279100001

Klíčová slova anglicky

Cutibacterium acnes; disc cells; co-culture; inflammation; neurotrophic factors; gene expression; intracellular

Příznaky

Mezinárodní význam, Recenzováno
Změněno: 5. 4. 2022 13:42, Mgr. Tereza Miškechová

Anotace

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.