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Induction of an Inflammatory Response in Primary Hepatocyte Cultures from Mice
Published on: March 10, 2017
Human peritoneal mesothelial cells synthesize interleukin-6: induction by IL-1 beta and TNF alpha
N Topley1, A Jörres, W Luttmann
1Institute of Nephrology, University of Wales College of Medicine, Cardiff Royal Infirmary, Wales, United Kingdom.
Insights
Human peritoneal mesothelial cells (HPMC) secrete interleukin-6 (IL-6), a key cytokine in CAPD peritonitis. Inflammatory cytokines like IL-1 beta and TNF alpha significantly increase HPMC IL-6 production.
Area of Science:
- Immunology
- Cell Biology
- Peritoneal Dialysis Research
Background:
- Elevated interleukin-6 (IL-6) levels are observed in the peritoneal cavity during continuous ambulatory peritoneal dialysis (CAPD) peritonitis.
- The cellular source and regulation of IL-6 in this context require further elucidation.
Purpose of the Study:
- To investigate human peritoneal mesothelial cells (HPMC) as a source of IL-6 during CAPD peritonitis.
- To characterize the IL-6 produced by HPMC and its regulation by other cytokines.
Main Methods:
- Assessed spontaneous and stimulated IL-6 release from HPMC.
- Utilized IL-1 beta and TNF alpha to stimulate HPMC.
- Employed ELISA and Western blot for IL-6 detection and characterization.
- Investigated the effect of anti-cytokine antibodies on IL-6 release.
Main Results:
- Unstimulated HPMC spontaneously released IL-6 in a time-dependent manner.
- IL-1 beta and TNF alpha significantly increased HPMC IL-6 production in a time- and dose-dependent fashion.
- Antibodies against IL-1 beta and TNF alpha inhibited IL-6 release, confirming their role.
Conclusions:
- HPMC are a significant source of IL-6 in the peritoneal cavity during CAPD peritonitis.
- IL-6 production by HPMC is upregulated by inflammatory cytokines IL-1 beta and TNF alpha.
- Targeting these cytokine pathways may offer therapeutic strategies for CAPD peritonitis.
Abstract:
Recent studies have demonstrated increased levels of IL-6 in the peritoneal cavity during CAPD peritonitis. The current investigation was initiated (i) to examine the human peritoneal mesothelial cell (HPMC) as a possible source of this secreted IL-6 and (ii) to characterize the released product and examine its regulation by other cytokines. Unstimulated HPMC under growth arrested conditions released IL-6 in a time dependent manner. After 24-hour HPMC IL-6 release (mean +/- SEM, N = 13) (expressed as pg/micrograms cell protein) was 1.67 +/- 0.33. Stimulation of HPMC with IL-1 beta or TNF alpha resulted in a time (increasing up to 48 hr) and dose dependent IL-6 generation. After 24 hours the levels induced by IL-1 beta and TNF alpha (both at 1000 pg/ml) were (mean +/- SEM, N = 13) 19.08 +/- 2.98 and 6.62 +/- 1.72, respectively. Stimulation with combinations of IL-1 beta and TNF alpha resulted in additive increases in IL-6 release. This release could be inhibited by co-incubation with anti-IL-1 beta and/or anti-TNF alpha antibodies. The level of released HPMC IL-6 measured by immunometric assay (ELISA) correlated directly with that detected in the 7TD1 IL-6 bioassay (r = 0.63; P < 0.001). Western blot analysis of concentrated HPMC supernatants using specific anti-IL-6 antibody demonstrated immunoreactive bands at 23 and 28 Kd following IL-1 beta or TNF alpha treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
