![]() 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. ![]() 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. 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. 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. The occurrence of harmful algal blooms (HABs) has been increasingly found over the past decades across the world 1. In the United States, the presence of cyanobacterial HABs has been reported in numerous inland lakes and rivers 2– 4. 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. 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. HABs are well-known producers of diverse types of cyanotoxins in the water systems as secondary metabolites.
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