Retinoic acid (a vitamin A form) can make your white blood cells (neutrophils) fire up more defenses like reactive oxygen, NETs, and the antimicrobial peptide LL‑37, which helps kill tough bugs. It doesn’t stop MRSA from growing on its own, but it directly blocks group A Strep and, when applied to skin, shrinks lesions and bacterial load in mice. So, using retinoic acid topically might boost your body’s natural infection fight, especially against certain strep infections.

Vitamin A and its biologically active derivative, retinoic acid (RA), are important for many immune processes. RA, in particular, is essential for the development of immune cells, including neutrophils, which serve as a front-line defense against infection. While vitamin A deficiency has been linked to higher susceptibility to infections, the precise role of vitamin A/RA in host-pathogen interactions remains poorly understood. Here, we provided evidence that RA boosts neutrophil killing of methicillin-resistant <i>Staphylococcus aureus</i> (MRSA). RA treatment stimulated primary human neutrophils to produce reactive oxygen species, neutrophil extracellular traps, and the antimicrobial peptide cathelicidin (LL-37). Because RA treatment was insufficient to reduce MRSA burden in an in vivo murine model of skin infection, we expanded our analysis to other infectious agents. RA did not affect the growth of a number of common bacterial pathogens, including MRSA, <i>Escherichia coli</i> K1 and <i>Pseudomonas aeruginosa</i>; however, RA directly inhibited the growth of group A <i>Streptococcus</i> (GAS). This antimicrobial effect, likely in combination with RA-mediated neutrophil boosting, resulted in substantial GAS killing in neutrophil killing assays conducted in the presence of RA. Furthermore, in a murine model of GAS skin infection, topical RA treatment showed therapeutic potential by reducing both skin lesion size and bacterial burden. These findings suggest that RA may hold promise as a therapeutic agent against GAS and perhaps other clinically significant human pathogens.