The Influence of Caerulomycin A on the Intestinal Microbiota in SD Rats

• Main Authors: Hongwei Zhang, Mengmeng Lan, Guodong Cui, Weiming Zhu
• Format: Article
• Language: English
• Published: MDPI AG 2020-05-01
• Series: Marine Drugs
• Subjects: intestinal flora; 16S rDNA gene high-throughput sequencing; Caerulomycin A; colorectal cancer
• Online Access: https://www.mdpi.com/1660-3397/18/5/277

Caerulomycin A (CRM A) is the first example of natural caerulomycins with a 2,2′-bipyridyl ring core and 6-aldoxime functional group from <i>Streptomyces caeruleus</i> and recently from marine-derived <i>Actinoalloteichus</i><i> </i><i>cyanogriseus</i> WH1-2216-6. Our previous study revealed that CRM A showed anti-tumor activity against human colorectal cancer (CRC) both in vitro and in vivo. Because some intestinal flora can affect the occurrence and development of CRC, the influence of CRM A on the intestinal flora is worthy of study in Sprague–Dawley (SD) rats. The high throughput sequencing of the V3-V4 hypervariable region in bacterial 16S rDNA gene results showed that the CRM A affected the diversity of intestinal flora of the SD rats treated with CRM A for 2, 3 and 4 weeks. Further analysis indicated that the abundance of genera Prevotella_1, Prevotellaceae_UCG-001, and Lactobacillus were increased while the that of genera Alloprevotella and Ruminiclostridium_1 were decreased. For the CRC related intestinal flora, the abundance of genera <i>Bacteroides</i>,<i> Fusobacterium</i>, <i>Enterococcus</i>, <i>Escherichia-Shigella</i>, <i>Klebsiella</i>, <i>Streptococcus</i>, <i>Ruminococcus_2</i><i>,</i> and <i>Peptococcus</i> of SD rats treated with CRM A were decreased, while that of abundance of genera Bifidobacterium, Lactobacillus, Faecalibacterium, Blautia, Oscillibacter, and Clostridium were increased. The results indicated that CRM A could influence the intestinal flora by inhibiting some species of harmful flora and improving the beneficial bacteria in intestinal flora in the SD rats. The results may provide a new idea for revealing the mechanism of the anti-CRC activity of CRM A.