Docosahexaenoic Acid Inhibits Helicobacter pylori Growth In Vitro and Mice Gastric Mucosa Colonization

Abstract

H. pylori drug-resistant strains and non-compliance to therapy are the major causes of H. pylori eradication failure. For some bacterial species it has been demonstrated that fatty acids have a growth inhibitory effect. Our main aim was to assess the ability of docosahexaenoic acid (DHA) to inhibit H. pylori growth both in vitro and in a mouse model. The effectiveness of standard therapy (ST) in combination with DHA on H. pylori eradication and recurrence prevention success was also investigated. The effects of DHA on H. pylori growth were analyzed in an in vitro dose-response study and n in vivo model. We analized the ability of H. pylori to colonize mice gastric mucosa following DHA, ST or a combination of both treatments. Our data demonstrate that DHA decreases H. pylori growth in vitro in a dose-dependent manner. Furthermore, DHA inhibits H. pylori gastric colonization in vivo as well as decreases mouse gastric mucosa inflammation. Addition of DHA to ST was also associated with lower H. pylori infection recurrence in the mouse model. In conclusion, DHA is an inhibitor of H. pylori growth and its ability to colonize mouse stomach. DHA treatment is also associated with a lower recurrence of H. pylori infection in combination with ST. These observations pave the way to consider DHA as an adjunct agent in H. pylori eradication treatment.

Identification of self-growth-inhibiting compounds lauric acid and 7-(Z)-tetradecenoic acid from Helicobacter pylori

“…The inhibitory effect of polyunsaturated fatty acids on the growth of H. pylori, particularly docosahexaenoic acid and linolenic acids, was reported previously by Thompson et al (1994), Correia et al (2012Correia et al ( , 2013Correia et al ( , 2014 and Obonyo et al (2012). Docosahexaenoic acid pre-treated H. pylori cultures showed a reduction in IL-8 production, and a decrease of cyclooxygenase-2 and inducible nitric oxide synthase by adhesion to gastric epithelial cells.…”

The Effect of Oral Administration PUFAs on Oxidative Stress in Patients Infected by Helicobacter pylori with Dyspeptic Symptom

“…Several studies revealed that consumption of ω-3 PUFAs anti-inflammatory effects while consumption of ω-6 PUFAs produced strong inflammatory factors by locating in cell membrane and metabolization [35]. Correia et al have proved that inhibitory ability of ω-3 PUFAs in bacteria growth and its colonization solely depends on DHA in mice gastric [36,37]. It has been shown that 100 μM concentration of DHA reduces H. pylori growth while concentration greater than 250 μM inhibits the survival of H. pylori irreversibly.…”

A proposed role for diffusible signal factors in the biofilm formation and morphological transformation of Helicobacter pylori

“…The ability to initiate morphological changes in H. pylori has also been demonstrated for other fatty acids. Correia et al (46) investigated the influence of polyunsaturated docosahexaenoic acid (DHA) on the growth of H. pylori by observing bacterial viability using CFU/mL measurement and by analyzing the morphology of this pathogen. The exposure of H. pylori 26695 and SS1 to 100 μM DHA resulted in the conversion from the spiral to the coccoid form and the initiation of the VBNC state.…”

“…After bacterial proliferation in the gastric mucosa, microorganisms enter the stationary phase accompanied by a decrease in AI-2 concentration and an increase in DSFs autoinductive activity. This stage is promoted by another conversion of bacteria to the coccoid form (10,17,31,34,46). The spherical forms display enhanced survival capabilities as shown by the increased potential for autoaggregation, biofilm formation, and biocide resistance.…”

“…Saturated fatty acids, competing for the RpfC receptors, reduce the activation of processes conditioned by rpf genes, i.e. autoaggregative behavior and biofilm formation (35,38,39,45,46). Reduction of DSFs activity and an increase in AI-2 concentration results in the transformation of some coccoid H. pylori forms to the spiral morphotype, followed by chemorepulsion from the AI-2 source and migration in search of new niches in the gastric environment (6,17,(30)(31)(32)44).…”