IL-1 beta→Interleukin-11→Interleukin-1beta→NF-kappa B→NF-kappa B→JunD

• 19799718(IL-1+beta): Salivary interleukin-1beta concentration and the presence of multiple pathogens in periodontitis.

  An association was also found with the presence of multiple periodontal pathogens.

• 18433382(Interleukin-11): Interleukin-11, interleukin-1beta, interleukin-12 and the pathogenesis of inflammatory periodontal diseases.

  Because of the possible preventive effect of IL-11 on inflammation , IL-11 may be an important factor in the therapeutic modulation of periodontal disease.

• 17559635(Interleukin-1beta): Mitogen-activated protein kinases mediate interleukin-1beta-induced receptor activator of nuclear factor-kappaB ligand expression in human periodontal ligament cells.

  CONCLUSION : In human periodontal ligament cells , three types of MAPK inhibitor may abrogate RANKL expression and activity induced by interleukin-1beta , directly or indirectly through partial suppression of prostaglandin E2 synthesis.

• 14581482(NF-kappa B): Temporal control of NF-kappaB activation by ERK differentially regulates interleukin-1beta-induced gene expression.

  Thus , although NF-kappaB activation was essential for interleukin-1beta induction of each of the proteins studied , gene expression was differentially regulated by ERK and by the duration of NF-kappaB activation.

• 17005669(NF-kappa B): Human cytomegalovirus blocks tumor necrosis factor alpha- and interleukin-1beta-mediated NF-kappaB signaling.

  NF-kappaB is also utilized by many viral pathogens , like human cytomegalovirus (HCMV) , to activate their own gene expression programs , reflecting intricate roles for NF-kappaB in both antiviral defense mechanisms and viral physiology.

• 12820962(JunD): JunD mediates survival signaling by the JNK signal transduction pathway.

  The JNK/JunD pathway can collaborate with NF-kappaB to increase antiapoptotic gene expression.