Blocking HMGB1 activity during the first week of infection induced lower expression of TNFα, IFNγ and IL-17, denoting certain HMGB1 pro-inflammatory activity, but on day 14, when the oxidized form of HMGB1 was produced and its activity was blocked, a significant decrease in pulmonary bacilli loads was seen in coexistence with higher expression of pro-inflammatory cytokines. Here, HMGB1 is linked to infection.