%0 Journal Article
%T Chloroquine regulates the lipopolysaccharide-induced inflammatory response in RAW264.7 cells.
%A Ota N
%A Endo S
%A Honma K
%A Iwayama K
%A Yamashita H
%A Tatsunami R
%A Sato K
%J Allergol Immunopathol (Madr)
%V 52
%N 4
%D 2024
%M 38970272
%F 2.094
%R 10.15586/aei.v52i4.1083
%X <B>OBJECTIVE: </B>Macrophage-induced inflammation plays a key role in defense against injury and harmful pathogens. Autophagy and the inflammatory response are associated; however, the relationship between the autophagy pathway and lipopolysaccharide (LPS)- induced inflammatory responses remains unknown. We aimed to determine the effect of autophagy on the LPS-induced myeloid differentiation factor 88 (MyD88)/nuclear transcription factor kB (NF-kB) pathway-mediated inflammatory response in RAW264.7 cells.<BR><B>METHODS: </B>To determine the effect of autophagy on the LPS-induced inflammatory response, using various in vitro assays, we determined the effect of autophagy inhibitors and inducers on the inflammatory response in RAW264.7 cells.<BR><B>RESULTS: </B>Chloroquine (CQ), an autophagy inhibitor, suppressed pro-inflammatory cytokines, including interleukin (IL)-1β, IL-6, and tumor necrosis factor α (TNFα) in LPS-stimulated RAW264.7 cells. CQ also affected inflammatory mediators such as myeloid differentiation factor 88 and NF-kB in LPS-stimulated RAW264.7 cells.<BR><B>CONCLUSIONS: </B>This study demonstrated that CQ regulates the LPS-induced inflammatory response in RAW264.7 cells. We propose that targeting the regulation of pro-inflammatory cytokine levels and inflammatory mediators using CQ is a promising therapeutic approach for preventing inflammatory injury. CQ serves as a potential therapeutic target for treating various inflammatory diseases.