Except the mice with disabled CCR5 (-/- in the original abstract, which did not translate here; i.e. the knockout mice) showed increased mortality, so it really doesn't support leronlimab or other CCR5 targeted drug being effective in sepsis.

I think their experimental protocol is probably not a good model for sepsis. Would rather they used an anti-CCR5 antibody like leronlimab after systemic inflammation / sepsis sets in, versus genetic knockout with CCR5 turned off the entire time / course of sepsis induction. I mean, if knockout prevents monocytes from going to the site of infection, the organism is more likely to die due to spread of infection. But if one gives CCR5 after the infection is mostly under control regionally but there is a hyperinflammatory response in all the body's other organs, then shutting down CCR5 with an anti-CCR5 antibody like LL might be useful.