However, two observations indicate that ACOD1 not only shows direct antimicrobial activity on C. burnetii but indeed has immunoregulatory effects in Q fever: firstly, we previously found in Myd88−/− mice that increased bacterial burden does not per se lead to stronger inflammatory responses; and secondly, the NMII burden in the spleen after intratracheal infection was not increased in Acod1−/− mice, but expression of Il6, IFNγ and Gbp1 was still significantly higher (Fig 4D). This evidence concerns the gene ACOD1 and infection.