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NMI and IFP35 serve as proinflammatory DAMPs during cellular infection and injury

Posted by ZK Xiahou, Xl Wang, J Shen, et al. on 2018-06-01 00:46:43


Damage-associated molecular patterns (DAMP) trigger innate immune response and exacerbate inflammation to combat infection and cellular damage. Identifying DAMPs and revealing their functions are thus of crucial importance. Here we report that two molecules, N-myc and STAT interactor (NMI) and interferon-induced protein 35 (IFP35) act as DAMPs and are released by activated macrophages during lipopolysaccharide-induced septic shock or acetaminophen-induced liver injury. We show that extracellular NMI and IFP35 activate macrophages to release proinflammatory cytokines by activating nuclear factor-kB through the Toll-like receptor 4 pathway. In addition, the serum levels of NMI are increased in patients who succumbed to severe inflammation. NMI deficiency reduces inflammatory responses and mortality in mouse models of sepsis and liver injury. We therefore propose that extracellular NMI and IFP35 exacerbate inflammation as DAMPs, making them potential therapeutic targets for clinical intervention.

Towards a TDP-43-Based Biomarker for ALS and FTLD

Posted by E Feneberg, E Gray, K Talbot, et al. on 2018-05-24 23:23:50


TDP-43 accumulates in nerve cells of nearly all cases of amyotrophic lateral sclerosis (ALS; the commonest form of motor neuron disease) and in the majority of Tau-negative frontotemporal lobar degeneration (FTLD). There is currently no biochemical test or marker of disease activity for ALS or FTLD, and the clinical diagnosis depends on the opinion of an experienced neurologist. TDP-43 has a key role in the pathogenesis of ALS/FTLD. Measuring TDP-43 in easily accessible biofluids, such as blood or cerebrospinal fluid, might reduce diagnostic delay and offer a readout for use in future drug trials. However, attempts at measuring disease-specific forms of TDP-43 in peripheral biofluids of ALS and FTLD patients have not yielded consistent results, and only some of the pathological biochemical features of TDP-43 found in human brain tissue have been detected in clinical biofluids to date. Reflecting on the molecular pathology of TDP-43, this review provides a critical overview on biofluid studies and future directions to develop a TDP-43-based clinical biomarker for ALS and FTLD.


TDP-43 Biomarker Cerebrospinal fluid Amyotrophic lateral sclerosis Frontotemporal dementia TARDBP


Platelet markers [soluble p selectin (sP-selectin) and soluble CD40 ligand (sCD40L)] are associated with platelet activation and cardiovascular risk. Both policosanol and 10-dehydrogingerdione are natural products with proven CETP inhibitory and antiatherogenic effects. Present work aimed mainly to investigate the levels of platelet activation biomarkers in the serum of dyslipidemic rabbits and the potential of these phytochemicals either alone or in a combination form to protect against atherogenicity. Additionally, this work clarified their effect on PCSK9, a key player in atherosclerosis progression. Daily administration of policosanol and/or 10-dehydrogingerdione at a dose level 10 mg/kg bw resulted in a CETP inhibitory activity, increasing HDL-C level. This protective effect was associated with improvement in lipid profile components and a reduction in PCSK9 level. Interestingly, this combination strengthened the CETP inhibitory activity of these phytochemicals, leading to a greater increase in serum HDL-C level than monotherapy. However, this combination did not enhance the reduction in PCSK9 level. Both drugs also decreased platelet activation and inflammation markers such as sCD40L, sP-selectin, and interferon-gamma (IFN-gamma), and their combination showed a synergistic effect. Therefore, such phytochemicals may be regarded as promising agents in the protection against atherothrombosis risk.


Atherogenesis CETP Dyslipidemia PCSK9 Policosano

Gingival crevicular fluid levels of human beta-defensin-1 in type 2 diabetes mellitus and periodontitis

Posted by D Yilmaz, F Caglayan, E Buber, et al. on 2018-05-24 20:24:40



Human beta-defensin (hBD)-1 is an important gatekeeper of the gingiva against constant bacterial challenge, and glucose levels are involved in its optimal expression. The aims of the study were to investigate hBD-1 levels in gingival crevicular fluid (GCF) and to compare these levels between type 2 diabetics with or without periodontitis and healthy individuals.

Materials and methods

Altogether, 81 subjects were included in the study: 21 subjects with type 2 diabetes mellitus (T2DM) suffering from generalized periodontitis (T2DM + GP), 18 systemically healthy generalized periodontitis patients (GP), 18 periodontally healthy T2DM subjects (T2DM+H), and 24 systemically and periodontally healthy subjects (control). Plaque index (PI), gingival index (GI), probing pocket depth (PPD), and clinical attachment level (CAL) were recorded, and GCF samples were collected. hBD-1 levels in GCF were measured using ELISA.


hBD-1 levels were significantly reduced in the T2DM + GP and GP groups. Although PI and GI scores were similar in both periodontally healthy groups, hBD-1 levels were lower in the T2DM + H group. In the whole population, hBD-1 levels correlated negatively with all periodontal parameters.


Both diabetes and periodontitis affect hBD-1 levels in GCF.

Clinical relevance

The altered levels of hBD-1 in GCF of diabetics might be associated with the susceptibility of diabetics to periodontitis.


Antimicrobial peptides Diabetes mellitus Periodontitis Gingival crevicular fluid


Liver fibrosis is a major health issue leading to high morbidity and mortality. The potential anti-fibrotic activity and the effect of mesalazine on osteopontin (OPN), an extra cellular matrix (ECM) component were evaluated in TAA-induced liver fibrosis in rats. For this purpose, forty-two adult male Wistar rats were divided into six groups. All animals, except the normal control, were intraperitoneally injected with TAA (200?mg/kg) twice per week for 6 weeks. In the hepato-protective study, animals were administered mesalazine (50 and 100?mg/kg, orally) for 4 weeks before induction of liver fibrosis then concomitantly with TAA injection. In the hepato-therapeutic study, animals were administered mesalazine for 6 weeks after TAA discontinuation with the same doses. In both studies, mesalazine administration improved liver biomarkers through decreasing serum levels of AST, ALT and total bilirubin when compared to fibrotic group with significant increase in total protein and albumin levels. Mesalazine significantly decreased hepatic MDA level and counteracted the depletion of hepatic GSH content and SOD activity. Additionally, it limits the elevation of OPN and TGF-beta1 concentrations and suppressed TNF-alpha as well as alpha-SMA levels in hepatic tissue homogenate. Histopathologically, mesalazine as a treatment showed a good restoration of the hepatic parenchymal cells with an obvious decreased intensity and retraction of fibrous proliferation, while as a prophylaxis it didnot achieve enough protection against the harmful effect of TAA, although it decreased the intensity of portal to portal fibrosis and pseudolobulation. Furthermore, mesalazine could suppress the expression of both alpha-SMA and caspase-3 in immunohistochemical sections. In conclusion, mesalazine could have a potential new indication as anti-fibrotic agent through limiting the oxidative damage and altering TNF-alpha pathway as an anti-inflammatory drug with down-regulating TGF-beta1, OPN, alpha-SMA and caspase-3 signaling pathways.

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