Interaction of caffeine with the SOS response pathway in Escherichia coli

Abstract

BackgroundPrevious studies have highlighted the antimicrobial activity of caffeine, both individually and in combination with other compounds. A proposed mechanism for caffeine’s antimicrobial effects is inhibition of bacterial DNA repair pathways. The current study examines the influence of sub-lethal caffeine levels on the growth and morphology of SOS response pathway mutants of Escherichia coli.MethodsGrowth inhibition after treatment with caffeine and methyl methane sulfonate (MMS), a mutagenic agent, was determined for E. coli mutants lacking key genes in the SOS response pathway. The persistence of caffeine’s effects was explored by examining growth and morphology of caffeine and MMS-treated bacterial isolates in the absence of selective pressure.ResultsCaffeine significantly reduced growth of E. coli recA- and uvrA-mutants treated with MMS. However, there was no significant difference in growth between umuC-isolates treated with MMS alone and MMS in combination with caffeine after 48 h of incubation. When recA-isolates from each treatment group were grown in untreated medium, bacterial isolates that had been exposed to MMS or MMS with caffeine showed increased growth relative to controls and caffeine-treated isolates. Morphologically, recA-isolates that had been treated with caffeine and both caffeine and MMS together had begun to display filamentous growth.ConclusionsCaffeine treatment further reduced growth of recA- and uvrA-mutants treated with MMS, despite a non-functional SOS response pathway. However, addition of caffeine had very little effect on MMS inhibition of umuC-mutants. Thus, growth inhibition of E. coli with caffeine treatment may be driven by caffeine interaction with UmuC, but also appears to induce damage by additional mechanisms as evidenced by the additive effects of caffeine in recA- and uvrA-mutants.

Membrane rigidity regulates E. coli proliferation rates

“…Also well-known is the accumulation of inviable cells in cultures treated with bilayer compacters such as nicotine 79 , or caffeine 80 . Although this bactericidal action is classically explained as a lethal genetic effect of fatty compounds 76 , 81 , our experiments reveal causality between lipid compaction and decreased growth rates under effective membrane stiffening.…”

Coffea Canephora Extract as Antibacterial Agent against Escherichia coli

“…Gene uvrA, uvrB dan uvrC work to excision nucleotide repair, especially uvrC which changes damage nucleotide with correct nucleotide. The study showed caffeine only inhibits uvrC gene with decrease synthesis trans-lesion in DNA cell 16 .…”

“…The research found caffeine inhibit DNA replication which need gen repaired by gen recA, recB, recC 15 AlkA, YzaB, Ogt, KsgA. In other study, Whitney and Weir showed caffeine potentiates methyl methane sulfonate (MMS) inhibit Escherichia coli with disrupt SOS Pathway in Escherichia coli 16 . SOS Pathway is mechanism DNA repair to prevents further damage 17 .…”

Capturing antibacterial natural products with in�silico techniques

“…A search on PubMed revealed that two of the highly indexed phytochemicals (caffeine and ricinine) have already been tested experimentally and confirmed as antibacterial agents ( 35 ). Caffeine has been reported to exert physiological effects on various organisms at µM concentrations and to act as an antimicrobial agent ( 36 , 37 ). Ricinine had high nematocidal activity ( 38 ) and notable activity against ants ( 39 ).…”