A possible reason why free endotoxin/LPS was not increased in the serum of patients with ALS, in contrast to a previous report41, is that LPS is bound in the sCD14/LBP complex which may then be interacting with TLR-4 on the surface of cells not expressing mCD14, such as endothelial or epithelial cells, and thus exacerbating a pro-inflammatory response. Here, TLR4 is linked to amyotrophic lateral sclerosis.