Effects of parental omega-3 fatty acid intake on offspring microbiome and immunity.
The "Western diet" is characterized by increased intake of saturated and omega-6 (n-6) fatty acids with a relative reduction in omega-3 (n-3) consumption. These fatty acids can directly and indirectly modulate the gut microbiome, resulting in altered host immunity. Omega-3 fatty acids can also directly modulate immunity through alterations in the phospholipid membranes of immune cells, inhibition of n-6 induced inflammation, down-regulation of inflammatory transcription factors, and by serving as pre-cursors to anti-inflammatory lipid mediators such as resolvins and protectins. We have previously shown that consumption by breeder mice of diets high in saturated and n-6 fatty acids have inflammatory and immune-modulating effects on offspring that are at least partially driven by vertical transmission of altered gut microbiota. To determine if parental diets high in n-3 fatty acids could also affect offspring microbiome and immunity, we fed breeding mice an n-3-rich diet with 40% calories from fat and measured immune outcomes in their offspring. We found offspring from mice fed diets high in n-3 had altered gut microbiomes and modestly enhanced anti-inflammatory IL-10 from both colonic and splenic tissue. Omega-3 pups were protected during peanut oral allergy challenge with small but measurable alterations in peanut-related serologies. However, n-3 pups displayed a tendency toward worsened responses during E. coli sepsis and had significantly worse outcomes during Staphylococcus aureus skin infection. Our results indicate excess parental n-3 fatty acid intake alters microbiome and immune response in offspring.
Bacterial Pathogenesis Unit, Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America.
Ian A
IA
Myles
Bacterial Pathogenesis Unit, Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America.
Nathan B
NB
Pincus
Bacterial Pathogenesis Unit, Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America.
Natalia M
NM
Fontecilla
Bacterial Pathogenesis Unit, Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America.
Sandip K
SK
Datta
D000818:Animals; D041963:Bacteroidetes; D003106:Colon / Q000276:immunology / Q000382:microbiology; D060467:Disease Resistance; D004927:Escherichia coli Infections / Q000276:immunology; D015525:Fatty Acids, Omega-3 / Q000008:administration & dosage*; D005260:Female; D006090:Gram-Negative Bacteria; D006094:Gram-Positive Bacteria; D007113:Immunity, Innate; D008070:Lipopolysaccharides; D008297:Male; D055624:Methicillin-Resistant Staphylococcus aureus / Q000276:immunology; D051379:Mice; D008807:Mice, Inbred BALB C; D064307:Microbiota; D011247:Pregnancy; D039401:Prenatal Nutritional Physiological Phenomena / Q000276:immunology*; D018805:Sepsis / Q000276:immunology; D013207:Staphylococcal Skin Infections / Q000276:immunology / Q000382:microbiology
D015525:Fatty Acids, Omega-3; D008070:Lipopolysaccharides