Elevated levels of the pro-inflammatory cytokine tumor necrosis factor-α (TNFα) inhibit erythropoiesis and cause anemia in patients with cancer and chronic inflammatory diseases.
Therefore, our data suggest that TNF-<i>α</i> stimulates the expression of hepcidin in IBD patients, resulting in aggravated anemia and that blockage of TNF-<i>α</i> or the caspase-3/8 and NF-<i>κ</i>B pathways could downregulate hepcidin expression.
Only the anti-anticardiolipin autoantibodies were associated with moderate/severe anaemia and, possibly by reacting with the parasite glycosylphosphatidylinositol (a powerful stimulator of TNF production), may have indirectly contributed to decrease the TNF levels, which could be involved in the malarial vivax anaemia of these children and adolescents.
This case-control study aimed to study the levels of hepcidin and other proinflammatory markers (IL-6, TNF-α, hs-CRP) and their relation with anemia in iron- and erythropoietin-naïve, non-dialysis CKD (stage 3 - 5) patients.
After adjusting for eGFR, albuminuria, and other traditional cardiovascular risk factors, anemia (1.37, 95% CI 1.09, 1.72, <i>P</i>=0.006), insulin resistance (1.16, 95% CI 1.04, 1.28, <i>P</i>=0.006), hemoglobin A1c (1.27, 95% CI 1.14, 1.41, <i>P</i><0.001), interleukin-6 (1.15, 95% CI 1.05, 1.25, <i>P</i>=0.002), and tumor necrosis factor-α (1.10, 95% CI 1.00, 1.21, <i>P</i>=0.05) were all significantly and directly associated with incidence of heart failure.
We have followed 67 RA patients and 64 PsA patients for 1 year to evaluate the effects of TNF-α inhibitors on disease activity and on inflammatory anemia.
Taken together, our studies demonstrate that decreased expression of DMT1 in intestinal mucosa leads to compromised absorption and transportation of iron and that blockade of TNF could rescue anemia and promote DMT1 expression in gut mucosa.
We hypothesized that in H. pylori infected children increased gastric concentrations of IL-1β and/or TNF-α, both potent inhibitors of gastric acid secretion that is essential for iron absorption, are predictors for low blood concentrations of ferritin and haemoglobin, markers of early depletion of iron stores and anaemia, respectively.
Significant improvements in anemia and disease activity, and reductions in serum hepcidin-25 levels were observed within 2 weeks in both groups, and these effects were more pronounced in the tocilizumab group than in the TNF-α inhibitors group.
Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand (TRAIL) and apoptin (VP3) of chicken anemia virus can selectively induce apoptosis in human tumor cell lines by two different pathways.
This study investigated putative functional single nucleotide polymorphisms (SNPs) and haplotypes across the major histocompatibility complex (MHC) class III region, including TNF and its immediate neighbors nuclear factor of kappa light polypeptide gene enhancer in B cells (lkappaBL), inhibitor-like 1 and lymphotoxin alpha (LTA), in relation to nutritional iron status and anemia, in a cohort of 780 children across a malaria season.
Ingestion of naturally acquired malarial pigment (hemozoin [PfHz]) by monocytes promoted the overproduction of IL-10 and TNF-alpha relative to the production of IL-12, which correlated with an enhanced severity of malarial anemia.
Healthy, malaria-exposed children had elevated levels of circulating bicyclo-PGE2/TNF-alpha, compared with children with malarial anemia (P<.01), with systemic bicyclo-PGE2 and TNF-alpha significantly associated with hemoglobin concentrations (r=0.745; P<.01).
In the patients with RA and amyloidosis, those with anemia had significantly higher TNFalpha and sTNFRI levels than did those without anemia, and circulating TNFalpha and sTNFRI levels correlated negatively with hemoglobin concentrations.
Repeat infection stimulated a wide variety of responses; most included expression of tumor necrosis factor-alpha, a cytokine that has been associated with inflammatory and host-destructive effects (weight loss, fever, anemia).
By contrast, the frequency of the TNF-alpha -238A allele, which has been associated with severe malarial anemia, was found to be similar to the frequency previously reported in comparison populations in Africa and elsewhere.
Since cytokines are of crucial significance in this process, we decided to examine the role of stem cell factor (SCF), granulocyte macrophage colony stimulating factor (GM-CSF), interleukin 3 (IL-3), granulocyte colony stimulating factor (G-CSF), and interleukin 1 alpha (IL-1 alpha), known for their stimulatory effects on in vitro hematopoiesis; and transforming growth factor beta (TGF beta), interferon gamma (IFN gamma) and tumor necrosis factor alpha (TNF-alpha), known for their inhibitory effect, in the anemia of GCA.