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Hormone, metabolic peptide, and nutrient levels in the earliest phases of rheumatoid arthritis-contribution of free fatty acids to an increased cardiovascular risk during very early disease.
Tang, MW, Koopman, FA, Visscher, JP, de Hair, MJ, Gerlag, DM, Tak, PP
Clinical rheumatology. 2017;(2):269-278
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Abstract
Rheumatoid arthritis (RA) is a chronic autoimmune disease associated with changes in several hormones and metabolic peptides. Crosstalk between these factors and the immune system may be important for homeostasis during inflammation. Here, we studied the levels of hormones, metabolic peptides, and nutrients in individuals at risk for developing RA (at risk). In total, 18 hormones, metabolic peptides, and nutrients were measured in fasting serum samples from 45 autoantibody-positive individuals at risk, 22 RA patients, and 16 healthy subjects. Triglyceride (TG) levels were also measured in an independent validation cohort of 32 individuals at risk, 20 early arthritis patients, and 20 healthy controls. We found an elevated TG level in individuals at risk and significantly higher TG levels in RA patients compared to healthy controls. These results were confirmed in the validation cohort. Similarly, free fatty acid (FFA) levels showed an increase in individuals at risk and were significantly higher in RA patients compared to healthy controls. In RA patients, FFA levels were positively correlated with disease activity. Pancreatic polypeptide (PP) and norepinephrine levels were highly significantly increased in individuals at risk and RA patients compared to healthy controls. TG and FFA levels are increased in RA patients and positively correlated with disease activity parameters. The results presented here suggest a role for FFAs in the pathogenesis of RA. Furthermore, PP and norepinephrine may be a biomarker that could assist in the identification of individuals at risk.
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Convergence of hormones, inflammation, and energy-related factors: a novel pathway of cancer etiology.
Slattery, ML, Fitzpatrick, FA
Cancer prevention research (Philadelphia, Pa.). 2009;(11):922-30
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Abstract
Colorectal cancer (CRC) is a multifactorial disease with several hypothesized etiologic factors including inflammatory processes; hormones such as estrogen, androgen, and insulin; and energy-related factors. We present evidence that integrates these elements in a pathway we call the convergence of hormones, inflammation, and energy-related factors (CHIEF). First, given the physiology of the gut, substantial epidemiologic and molecular data support the hypothesis that activation of innate immunity in the normal gut mucosa by various environmental agents (commensal bacteria, dietary antigens, mucosal irritants, pathogens) and endogenous factors such as estrogen, androgens, and insulin levels provokes basal inflammation as an underlying factor of the association of insulin, estrogen, and energy-related factors with CRC. Second, critical genes involved in this pathway, e.g., phosphatase tensin homologue on chromosome 10 (PTEN) and serine threonine kinase 11 (STK11)/LKB1, are tumor suppressor genes often mutated in intestinal cancer or CRC. Third, laboratory experiments show that cellular PTEN and STK11/LKB1 tumor suppressor enzymes are vulnerable to inactivation by redox-active species, especially chemically reactive lipid mediators of inflammation and redox stress. Epidemiologic data further support the underlying proposal that CHIEF comprises important elements of CRC risk. Although this discussion of the CHIEF pathway focuses on CRC, we believe that this pathway may play an important role in the etiology of other cancers as well.
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Making sense of hormone crosstalk during plant immune responses.
Spoel, SH, Dong, X
Cell host & microbe. 2008;(6):348-51
Abstract
In response to biotic stress, crosstalk between plant hormonal signaling pathways prioritizes defense over other cellular functions. Some plant pathogens take advantage of this regulatory system by mimicking hormones that interfere with host immune responses to promote virulence. Here we discuss the various roles that crosstalk may play in response to pathogens with different infection strategies.
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Infusion of hypertonic saline before elective hysterectomy: effects on cytokines and stress hormones.
Kolsen-Petersen, JA, Bendtzen, K, Tonnesen, E
British journal of anaesthesia. 2008;(4):478-84
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Abstract
BACKGROUND Infusion of hypertonic saline provides early haemodynamic benefits and may affect the immune system. It is unknown if infusion of hypertonic saline affects plasma cytokines and stress hormones after surgery. METHODS Sixty-two women undergoing abdominal hysterectomy were randomized in a double-blind study to infusion of NaCl 7.5% (HS), NaCl 0.9% (NS4), both 4 ml kg(-1), or NaCl 0.9% 32 ml kg(-1) (NS32) over 20 min. Blood was collected at baseline, 1, 4, and 24 h after surgery (n=34) for the determination of interleukin (IL)-1beta, IL-6, IL-8, IL-10, IL-12, IL-1ra, and tumour necrosis factor-alpha. Serum cortisol and vasopressin were measured at these time points and 48 h after operation. Epinephrine and norepinephrine (n=26) were quantified at baseline, after infusion, 25 min after incision, 1, and 4 h after surgery. Finally, C-reactive protein was measured at baseline, 24, and 48 h after surgery. RESULTS Surgery and anaesthesia induced well-reported changes in the concentrations of cytokines and hormones. The concentration of norepinephrine briefly increased after infusion of HS and NS32 but not NS4 (P<0.05). Epinephrine was increased 25 min after incision in Group NS32 compared with the other groups (P<0.05). No other differences were found between the groups. CONCLUSIONS Infusion of a clinically relevant dose of hypertonic saline before hysterectomy appears to have limited effect on the postoperative concentration of selected plasma cytokines and the hormonal stress-response.