We additionally found that CBD also prevented the “pro-acne” LA-T combination from elevating the expression of TNFA (Figure 3A), a key cytokine in the pathogenesis of acne vulgaris (2, 24–30). These data suggested that CBD may exert antiinflammatory actions on human sebocytes (as had already been demonstrated for CBD in several other experimental models, such as diabetes, rheumatoid arthritis, etc.) (31). Therefore, in order to confirm the putative universal antiinflammatory action of the CBD on human sebocytes, we next assessed its effects by modeling both Gram-negative infections (applying the TLR4 activator LPS) and Gram-positive infections (using the TLR2 activator lipoteichoic acid [LTA]). We found that CBD completely prevented the above treatments from elevating TNFA expression (Figure 3). Moreover, CBD also normalized LPS-induced IL1B and IL6 expression (Figure 3B) (expression of these 2 cytokines was found not to be modulated by 24-hour LA-T or LTA treatment; data not shown). Taken together, these results strongly suggest that CBD’s universal sebostatic action is accompanied by substantial antiinflammatory effects, which would be very much desired in the clinical treatment of acne vulgaris (1, 2, 24–30).