“…In IBD, for example, microbial dysbiosis is suspected to promote gut leakage and bacterial translocation which, in turn, induces an abnormal immune response and subsequently initiates a pro-inflammatory status [19,20]. Dysfunction of T-/B-cell memory and natural killer cells [21,22], chronic activation of innate antiviral signaling pathways (e.g., protein kinase R), different anti-oxidative (e.g., glutathione peroxidase, catalase) as well as increased inflammatory markers (e.g., C-reactive protein (CRP), tumor necrosis factor alpha (TNF-α)) [17,23], and increased activation of nuclear factor kappa beta (NF-κB) [24,25] are frequently described pathways in fatigue [1,26,27]. Interleukin (IL)-6, in particular, has been linked to fatigue and is even called the “sleep factor”, which could thus partly explain the characteristic tiredness [28] (p. 207).…”