Exploring the potential immunomodulatory effects of gallic acid on milk phagocytes in bovine mastitis caused by Staphylococcus aureus

• DOI: 10.3389/fvets.2023.1255058
• Publication Date: 2023-09-17T15:04:53Z
• Authors: Raktham Mektrirat; Phongsakorn Chuam...; Dussaniya Navathong; Thofun Khumma; Anyaphat Srithana...; Witaya Suriyasath...
• Keywords: 2. Zero hunger; Staphylococcus aureus; 0303 health sciences; Veterinary medicine; apoptosis; immunomodulation; 3. Good health; 03 medical and health sciences; milk phagocyte; SF600-1100; Veterinary Science; gallic acid; bovine mastitis; anti-inflammatory

Bovine mastitis caused by Staphylococcus aureus may exacerbate resulting in significant economic losses and impacting milk quality. To date, the use of gallic acid, a phenolic compound naturally occurring various plants, holds promise due to its potent anti-oxidant anti-inflammatory effects many pieces literature, thus, making it subject interest bovine innate immunity research. Here we used acid assess potential immunomodulation on phagocytes vitro challenges with mastitis-causing bacteria. Our findings indicated that cells exposed showed no harm cell viability but might maintain longevity during bacterial infection. Gallic acid-treated displayed reduced migration, phagocytosis, killing ability, while showing an increase ROS production, all which are undoubtedly linked intracellular abilities cells. Nonetheless, extracellular structure called neutrophil traps (NETs) was significantly released after receiving representing killing. We also reported neutralizes inflammation regulating specific pro-inflammatory genes (IL1B, IL6, TNF) ROS-generating (CYBA, LAMP1, RAC1), subsequently preventing tissue damage. Regarding apoptosis-related proteins, increased production caspase-3 Bcl-2 family proteins could potentially promote cells, implicated mechanism combating invasion udder The novel role highlights immunomodulatory properties contributes our understanding bacterial-host interactions, provides valuable molecular insights.