Caulerpin Mitigates Helicobacter pylori-Induced Inflammation via Formyl Peptide Receptors

The identification of novel strategies to control Helicobacter pylori (Hp)-associated chronic inflammation is, at present, a considerable challenge. Here, we attempt to combat this issue by modulating the innate immune response, targeting formyl peptide receptors (FPRs), G-protein coupled receptors that play key roles in both the regulation and the resolution of the innate inflammatory response. Specifically, we investigated, in vitro, whether Caulerpin-a bis-indole alkaloid isolated from algae of the genus Caulerpa-could act as a molecular antagonist scaffold of FPRs. We showed that Caulerpin significantly reduces the immune response against Hp culture filtrate, by reverting the FPR2-related signaling cascade and thus counteracting the inflammatory reaction triggered by Hp peptide Hp(2-20). Our study suggests Caulerpin to be a promising therapeutic or adjuvant agent for the attenuation of inflammation triggered by Hp infection, as well as its related adverse clinical outcomes.

Automated summary

The study demonstrates that Caulerpin, a bis-indole alkaloid isolated from algae, can serve as a molecular antagonist of FPRs, reducing immune response against Hp culture filtrate by reverting FPR2-related signaling cascade and counteracting inflammatory reactions triggered by Hp peptide Hp(2-20). The findings suggest Caulerpin as a promising therapeutic or adjuvant agent for attenuating inflammation caused by Hp infection and its adverse clinical outcomes.