Inflammatory bowel disease (IBD) is a chronic and multifactorial disease of the gastrointestinal tract. The exact etiology of IBD remains complex and unclear involving an inadequately defined relationship between microbial insult, genetic predisposition, altered intestinal barrier permeability, oxidative stress components and abnormal immune responses. The role of the co-stimulatory system made up of cluster of differentiation 40 protein (CD40) and its ligand (CD40L) in the response of the immune system to pathogens is now widely accepted. The implication of CD40/CD40L axis in immune system disorders due to its important role as signal transduction pathway among immune cells is well documented. Several studies have suggested that CD40/CD40L interactions regulate oxidative stress; this can affect various signaling pathways leading to IBD development. Hence, CD40/CD40L signaling pathway may become a new target for IBD treatment. This review will cover the general contribution of the CD40/CD40L dyad in the development of IBD in order to facilitate future approaches aiming to elucidate the immunological mechanisms that control gut inflammation.

Platelets are megakaryocyte-derived fragments lacking nuclei and prepped to maintain primary hemostasis by initiating blood clots on injured vascular endothelia. Pathologically, platelets undergo the same physiological processes of activation, secretion, and aggregation yet with such pronouncedness that they orchestrate and make headway the progression of atherothrombotic diseases not only through clot formation but also via forcing a pro-inflammatory state. Indeed, nuclear factor-κB (NF-κB) is largely implicated in atherosclerosis and its pathological complication in atherothrombotic diseases due to its transcriptional role in maintaining pro-survival and pro-inflammatory states in vascular and blood cells. On the other hand, we know little on the functions of platelet NF-κB, which seems to function in other non-genomic ways to modulate atherothrombosis. Therein, this review will resemble a rich portfolio for NF-κB in platelets, specifically showing its implications at the levels of platelet survival and function. We will also share the knowledge thus far on the effects of active ingredients on NF-κB in general, as an extrapolative method to highlight the potential therapeutic targeting of NF-κB in coronary diseases. Finally, we will unzip a new horizon on a possible extra-platelet role of platelet NF-κB, which will better expand our knowledge on the etiology and pathophysiology of atherothrombosis.

Anxiety can either impair or enhance performance depending on the context. Increased sensitivity to threat seems to be an important feature of sensory processing in anxiety since anxious individuals tend to be more attentive to threatening visual stimuli. Evidence of anxiety effects in olfaction is rare; though alterations of olfactory performance in psychiatric patients and some effects of trait and state anxiety on olfactory performance have been reported. Our main objective was thus to investigate whether olfactory processing speed varies as a function of trait anxiety levels. We additionally investigated a possible preferential bias for unpleasant odors in highly anxious participants. Thirty-eight healthy adults participated in a simple odor detection task, where response times (RTs) and anxiety levels were measured. We compared RTs to a pleasant and an unpleasant food odor between high- and low-trait anxiety participants. We found that high-trait anxiety participants detected both odors faster than low-trait anxiety participants, independently of odor pleasantness. Moreover, trait anxiety levels significantly correlated with reaction times to both odors, indicating that trait anxiety but not odor pleasantness influences olfactory detection speed. These findings provide new insights into olfactory processing in healthy adults showing how various levels of trait anxiety affect the olfactory modality.

Background CD40 ligand (CD40L) is a thromboinflammatory molecule that predicts cardiovascular events. CD40L is a strong activator of nuclear factor kappa B (NF‐κB) in platelets that primes and enhances platelet activation in response to thrombotic stimuli. In addition to its classical receptor CD40, CD40L binds αIIbβ3, α5β1, and αMβ2 in various cell types. However, the function of the different CD40L receptors on platelets remains unexplored. The present study aims to identify the receptors of CD40L, involved in platelet NF‐κB activation, their downstream signaling and their implication in platelet aggregation. Methods and Results We showed that platelets express CD40, αIIbβ3, and α5β1 and release CD40L in response to sCD40L stimulation. sCD40L alone dose‐dependently induced platelet NF‐κB activation; this effect was absent in CD40 −/− mouse platelets and inhibited by the CD40 blockade, but was unaffected by the αIIbβ3 or α5β1 blockade in human platelets. sCD40L/CD40 axis activates transforming growth factor‐β‐activated kinase 1 upstream of NF‐κB. In functional studies, sCD40L alone did not affect platelet aggregation but potentiated the aggregation response in the presence of suboptimal doses of thrombin; this effect was abolished by CD40, transforming growth factor‐β‐activated kinase 1, and NF‐κB inhibitors. Conclusions CD40L primes platelets via signaling pathways involving CD40/transforming growth factor‐β‐activated kinase 1/NF‐κB, which predisposes platelets to enhanced activation and aggregation in response to thrombotic stimuli.