HABs are well-known producers of diverse types of cyanotoxins in the water systems as secondary metabolites. This eutrophication in combination with climate change and other forcing factors influences the excessive proliferation of cyanobacteria, which ultimately leads to bloom formation 5– 7. Anthropogenic activities such as the release of wastewater effluents, agricultural runoff containing fertilizers and pesticides, and urban runoff into water bodies can result in increased eutrophication. In the United States, the presence of cyanobacterial HABs has been reported in numerous inland lakes and rivers 2– 4. The occurrence of harmful algal blooms (HABs) has been increasingly found over the past decades across the world 1. In conclusion, the results show a first-ever characterization of the host resistome following microcystin-LR exposure and its connection to host immune status and antimicrobial resistance that can be crucial to understand treatment options with antibiotics in microcystin-exposed subjects in clinical settings. Microcystin-LR exposure also caused decreased TLR2, TLR4, and REG3G expressions, increased immunosenescence, and higher systemic levels of IL-6 in both wild-type and humanized mice. Increased abundance of these genes was positively associated with increased expression of PD1, a T-cell homeostasis marker, and pleiotropic inflammatory cytokine IL-6 with a concomitant negative association with immunosurveillance markers IL-7 and TLR2. Interestingly, the increased abundance of these genes was traced to resistance to common antibiotics such as tetracycline, macrolides, glycopeptide, and aminoglycosides, crucial for modern-day treatment of several diseases. Host resistome genotypes such as mefA, msrD, mel, ant6, and tet40 increased in diversity and relative abundance following microcystin-LR exposure.
We show that the mice exposed to microcystin-LR had an altered microbiome signature that harbored antibiotic resistance genes. We tested the hypothesis that prior exposure to the cyanotoxin microcystin-LR may alter the host resistome. A strong association between exposure to the common harmful algal bloom toxin microcystin and the altered host gut microbiome has been shown.