Differential systemic MyD88-dependent versus MyD88- independent cytokine ratio by etiologic agent in adults with severe community-acquired pneumonia

Purpose: Classifying bacteria early, before cultures results are available, would improve the choice of initial antibiotics in patients with severe pneumonia. TLR2 and TLR4 transduce signal through the MyD88- dependent pathway to stimulate IL-8 and TNF-α production. TLR4 can also signal through a MyD88- independent pathway to stimulate RANTES and IFN-β production. As gram-negative bacteria primarily activate TLR4, while gram-positive bacteria also activate TLR2, differential cytokine expression would be expected depending on specific bacterial etiologies.