Overview
IL-8 (CXCL8) is the primary neutrophil chemokine — it recruits neutrophils to infection sites and activates their antimicrobial functions (oxidative burst, degranulation, NET formation). In the WikiBiome context, IL-8 is notable for its vulnerability to gingipain degradation — P. gingivalis gingipains rapidly destroy IL-8, preventing neutrophil recruitment and enabling immune evasion.
Key Interactions
- Functional shielding: Mixed C. albicans + P. gingivalis biofilm caused near-complete IL-8 disappearance at 24h — gingipain RgpA rapidly degrades IL-8, and the fungal biofilm amplifies gingipain activity [1].
- GERD: Esophageal dysbiosis drives IL-8 via TLR2/TLR4 → NF-kB, contributing to esophageal inflammation [2] [3].
- Perinatal depression: Part of inflammatory biomarker profile [4].
Cross-References
- interleukin 6 — co-elevated pro-inflammatory cytokine
- tnf alpha — co-elevated; drives IL-8 transcription
- porphyromonas gingivalis — gingipains degrade IL-8 for immune evasion
- functional shielding — biofilm-mediated IL-8 destruction
- nf kappa b — transcriptional driver of IL-8