Abstract

Previous studies have indicated that interleukin (IL)‑1β has an important role in the development of allergic diseases. Therefore, the present study aimed to investigate the upstream pathway underlying IL‑1β production in an experimental model of allergy. BALB/c mice (female, 6‑8 weeks old) were sensitized to recombinant (r)Che a 2 by intraperitoneal injection of rChe a 2 adsorbed onto an alum gel suspension on days 0, 7, 14 and 21. In the control group, mice received an injection of 20 mM phosphate‑buffered saline absorbed onto alum via the same route. The allergic status of the mice was confirmed serologically by measuring allergen‑specific immunoglobulin (Ig)E levels. The protein expression levels of IL‑1β and the mRNA expression levels of inflammasome compartments were measured by enzyme‑linked immunosorbent assay and semi‑quantitative reverse transcription polymerase chain reaction, respectively. In addition, caspase‑1 activity was determined by fluorometric assay. Sensitized mice exhibited significantly increased levels of specific IgE (P<0.05). IL‑1β production and caspase‑1 activity were significantly higher in the sensitized mice compared with the control group. In addition, no significant differences were observed between the control and sensitized mice in the expression of genes associated with the inflammasome, including NLR family, pyrin domain containing 3; apoptosis‑associated speck‑like protein; and NLR family, apoptosis inhibitory protein 5. However, IL‑1β converting enzyme protease‑activating factor (IPAF) expression was significantly increased in sensitized mice compared with in the control group (P<0.05). These data indicate that caspase‑1 activation and IL‑1β expression are associated with the IPAF inflammasome. Therefore, based on this association, the IPAF inflammasome may be considered for IL‑1β production in the experimental model of allergy.

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.