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Introduction For patients treated with cisatracurium, it has been shown that proinflammatory cytokines (IL-1, IL-6, and IL-8) significantly went down during the 48 h of molecule administration as compared to placebo [1].
Additionally, it has been shown that proinflammatory cytokines disrupt the BTB and result in increased BTB permeability [13] [15].
It has been shown that proinflammatory and fibrogenic cytokine pathways are activated within the first 24 48 hr following pulmonary insult resulting from SARS-CoV infection [44].
It has been shown that proinflammatory cytokines might be responsible for the progression of arthritis [ 6].
It has been shown that proinflammatory cytokines are suppressed by progesterone (P).
It has been shown that proinflammatory cytokines alter the expression of genes involved in insulin signaling through activation of NF-κB.
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It was shown that proinflammatory adipocytokines (e.g., TNF α) could promote adipocyte dedifferentiation through downregulation of PPARγ.
Interestingly, in human bronchial cells it was shown that proinflammatory cytokines IL-1 β and IL-17A were potent inducers of MUC5B mRNA expression.
It has been shown that the proinflammatory cytokines TNF-α and IL-1β increase the expression of Fc α receptors in mesangial cells.
It has been shown that the proinflammatory cytokines determine the susceptibility of human CD8 T cells to Fas-mediated activation-induced cell death through modulation of FasL and c-FLIP(S) expression [ 34].
Furthermore, extremely obese patients undergoing emergent surgery develop sepsis and septic shock more often than normal weight patients [ 10], and it has been shown that sepsis-induced proinflammatory states correlate with the amount of total body fat [ 11– 13].
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