Dietary nitrate, from green-leafy vegetables, is reduced to nitrite in the oral cavity and to nitric oxide (NO) in the stomach. In the gut, NO increases mucosal blood flow, mucus thickness and prevents microbial infections. Gut microbiota is raising a great deal of interest since it has been recognized to be crucial to maintain gastrointestinal (GI) and systemic welfare. Dysbiosis (altered gut flora) is associated with increased epithelial permeability, deficient mucus production and with the activation of inflammatory pathways. These mechanisms elicit GI symptoms, such as heartburn, dyspepsia and diarrhea but are also related with the etiology of multi-organic disorders. Here we investigate whether dietary nitrate rescues GI physiology during dysbiosis. All animal interventions were in accordance with the ARRIVE guidelines. Four groups of Wistar rats (male, 200-250g) were maintained in the animal facilities for 7 days during which, in addition to food, they had access to 1) water, 2) an antibiotic cocktail (neomycin 5 mg/mL, bacitracin 5 mg/mL, imipenem 1.25 μg/mL), 3) antibiotic cocktail + sodium nitrate 10 mM, 4) sodium nitrate 10 mM. Animals were weighted daily. At the end of 7th day they were anesthetized (isoflurane) and euthanized. Ceca were collected and weighted. The stomach was isolated and occludin, claudin-5, ZO-1, mucin-1 (MUC-1) and myeloperoxidase (MPO) were analyzed by western blot and immunofluorescence (n=4, triplicate). Values are mean±SEM. Antibiotic exposure prevented weight gain in all animals when compared to controls. Nitrate prevented body weight loss under dysbiosis, suggesting a more efficient harvesting of nutrients. Also, ceca from animals with altered gut flora contained more fecal material than the ones from animals treated with nitrate under the same circumstances (18.47±0.99 g vs 14.7±71.12 g, p=0.0481). Dysbiosis reduced MUC-1 expression but supplementation with nitrate recovered this protein to control levels. The expression of tight junction proteins occludin and claudin-5 was slightly decreased when GI microflora was disrupted, but the reactivity of both proteins was recovered by nitrate (occludin: 5.83±0.46 vs 8.24±1.12, p=0.046; claudin-5: 3.59±0.36 vs 3.88±0.25, p=0.51). No differences were observed for ZO-1. Nitrate prevented MPO overexpression under dysbiosis (115.70±5.36 vs 61.00±19.00, p=0.04; % of control) suggesting the prevention of an over stimulated inflammatory status in the gut. NO is crucial for the gastroprotective mechanisms aforementioned, either by direct interaction with heme proteins or by triggering post-translational modifications. This data suggests that dietary nitrate may ensure gastric epithelial integrity and mucus production during dysbiosis and therefore its consumption may be recommended when antibiotics are prescribed to treat infections.