On this regard, concerns increase when doubts arise regarding the applicability of hyperthermia on NSCLC given the potential interaction of IL-6 with NSCLC.
Moreover, it can be hypothesized that CINC-1 is placed upstream TNF-α, IL-1β, and IL-6 among the prostaglandin-dependent fever-mediator cascade and amidst the prostaglandin-independent synthesis pathway of fever.
Compared to controls, exposure to IL-6 resulted in significant maternal temperature increase [mean temperature difference 0.558°C (95% CI, 0.417-0.698; P < .0001)].
During mild SI, H<sub>2</sub> reduced plasma surges of proinflammatory cytokines (TNF-α and IL-6) while caused an increase in plasma IL-10 (anti-inflammatory cytokine) and prevented fever.
Post-XRT findings included a second wave of fever and increased CRP and IL6, beginning 21 days after CAR T cells, which is late for cytokine-release syndrome from CAR T-cell therapy alone on this trial.
The univariate analysis revealed a statistically significant difference between groups in preoperative fever (p = 0.032), stone burden (p < 0.001), C-reactive protein (p = 0.011), PCT (p < 0.001) and interleukin-6 (p = 0.035) levels.
Here, we also found that transcription factor MADS, NFY, HSF, MYB/C and WRKY might play a crucial role in male fertility under the high temperature condition.
Secondary endpoints include the number of occurrences of accompanying symptoms during attacks; the time until a fever attack occurs; the duration of fever attacks; serum C-reactive protein and serum amyloid A; 36-item Short Form Health Survey; general evaluation by a physician (100-mm visual analogue scale); body temperature; the percentage of subjects who achieve FMF 50 at 12 weeks and 24 weeks; and pharmacodynamic assessment, including the measurement of serum TCZ level and soluble IL-6 receptor.
The gilts infected with PRRSV had elevated plasma interleukin-6 levels and developed transient febrile and anorectic responses lasting approximately 21 days.
Hyperthermia (42 °C) significantly prevented these changes, i.e., increases in IL-6, α-SMA, and collagen, as induced by TGF-β1 in a time-dependent manner.
To evaluate the intracranial inflammatory response in patients with acute-stage KD, we measured the levels of cytokines (interleukin [IL]-6 and tumor necrosis factor [TNF]-α) and pentraxin-3 (PTX3) in the cerebrospinal fluid of patients with KD (<i>n</i> = 7) and compared the levels to those of the age- and sex-matched febrile control patients (bacterial meningitis [<i>n</i> = 5], enteroviral meningitis [<i>n</i> = 10], nonspecific viral illness without central nervous system involvement [<i>n</i> = 10]).
High-throughput gene profile analysis identifies nine differentially expressed genes that are closely immune-related upon mild heat, accompanied by IL-6 upregulation, a pyrogenic cytokine usually found during fever.
Because the patient was under anti-IL-6 therapy at the onset, some symptoms typically seen in DIHS were absent, such as fever and leukocyte count abnormalities.
Although a majority of patients will achieve a complete response following a single infusion of CD19-targeted CAR-modified T cells (CD19 CAR T cells)<sup>2-4</sup>, the broad applicability of this treatment is hampered by severe cytokine release syndrome (CRS), which is characterized by fever, hypotension and respiratory insufficiency associated with elevated serum cytokines, including interleukin-6 (IL-6)<sup>2,5</sup>.