acute alcohol selectively reduced ERK MAPK levels with no significant effect on JNK and p38 MAPK. Our results overall indicate that, similar to the in vivo effects of acute alcohol on Kupffer cells (32), short-term alcohol exposure induces an “LPS hyporesponsive” state in human blood monocytes resulting in suppressed TNF-α production. Additionally, acute alcohol exposure could lead to LPS hyporesponsiveness in human peripheral blood monocytes limiting inflammation and favoring an increased susceptibility to infections similar to that described in septic shock patients (42).
