Nitric oxide (NO) is one of the critical components of the vasculature, regulating key signaling pathways in health. In macrovessels, NO functions to suppress cell inflammation as well as adhesion. In this way, it inhibits thrombosis and promotes blood flow. It also functions to limit vessel constriction and vessel wall remodeling. In microvessels and particularly capillaries, NO, along with growth factors, is important in promoting new vessel formation, a process termed angiogenesis. With age and cardiovascular disease, animal and human studies confirm that NO is dysregulated at multiple levels including decreased production, decreased tissue half-life, and decreased potency. NO has also been implicated in diseases that are related to neurotransmission and cancer although it is likely that these processes involve NO at higher concentrations and from nonvascular cell sources. Conversely, NO and drugs that directly or indirectly increase NO signaling have found clinical applications in both age-related diseases and in younger individuals. This focused review considers recently reported advances being made in the field of NO signaling regulation at several levels including enzymatic production, receptor function, interacting partners, localization of signaling, matrix-cellular and cell-to-cell cross talk, as well as the possible impact these newly described mechanisms have on health and disease.

/pdf/nitric-oxide-what-s-new-to-no-31t6i4ym08.pdf

Nitric oxide: what’s new to NO?

According to our previous results, resveratrol (RSV, 3, 5, 4-trihydroxystilbene), a naturally polyphenolic phytoalexin, could attenuate myocardial ischemia/reperfusion injury through up-reg...

Resveratrol protects against isoproterenol induced myocardial infarction in rats through VEGF-B/AMPK/eNOS/NO signalling pathway.

Intranasal delivery of MSC-derived exosomes attenuates allergic asthma via expanding IL-10 producing lung interstitial macrophages in mice.

Coronary heart disease (CHD) is a group of diseases that include: no symptoms, angina, myocardial infarction, ischemia cardiomyopathy and sudden cardiac death. And it results from multiple risks factors consisting of invariable factors (e.g. age, gender, etc.) and variable factors (e.g. dyslipidemia, hypertension, diabetes, smoking, etc.). Meanwhile, CHD could cause impact not only localized in the heart, but also on pulmonary function, whole-body skeletal muscle function, activity ability, psychological status, etc. Nowadays, CHD has been the leading cause of death in the world. However, many clinical researches showed that exercise training plays an important role in cardiac rehabilitation and can bring a lot of benefits for CHD patients.

Exercise for Cardiovascular Disease Prevention and Treatment

Chronic helminth infection with Schistosoma (S.) mansoni protects against allergic airway inflammation (AAI) in mice and is associated with reduced Th2 responses to inhaled allergens in humans, despite the presence of schistosome-specific Th2 immunity. Schistosome eggs strongly induce type 2 immunity and allow to study the dynamics of Th2 versus regulatory responses in the absence of worms. Treatment with isolated S. mansoni eggs by i.p. injection prior to induction of AAI to ovalbumin (OVA)/alum led to significantly reduced AAI as assessed by less BAL and lung eosinophilia, less cellular influx into lung tissue, less OVA-specific Th2 cytokines in lungs and lung-draining mediastinal lymph nodes and less circulating allergen-specific IgG1 and IgE antibodies. While OVA-specific Th2 responses were inhibited, treatment induced a strong systemic Th2 response to the eggs. The protective effect of S. mansoni eggs was unaltered in mu MT mice lacking mature (B2) B cells and unaffected by Treg cell depletion using anti-CD25 blocking antibodies during egg treatment and allergic sensitization. Notably, prophylactic egg treatment resulted in a reduced influx of pro-inflammatory, monocyte-derived dendritic cells into lung tissue of allergic mice following challenge. Altogether, S. mansoni eggs can protect against the development of AAI, despite strong egg-specific Th2 responses.

https://onlinelibrary.wiley.com/doi/pdf/10.1111/pim.12579

Isolated Schistosoma mansoni eggs prevent allergic airway inflammation.

Our and others' previous studies have shown that Schistosoma japonicum (SJ) infection can inhibit allergic reactions. We recently reported that DCs played an important role in SJ infection-mediated inhibition of allergy, which was associated with enhanced IL-10 and T regulatory cell responses. Here, we further compared the role of CD8α(+) DC and CD8α(-) DC subsets for the inhibitory effect. We sorted CD8α(+) DC (SJCD8α(+) DC) and CD8α(-) DC (SJCD8α(-) DC) from SJ-infected mice and tested their ability to modulate allergic responses in vivo. The data showed that the adoptive transfer of SJCD8α(-) DC was much more efficient than SJCD8α(+) DC for the suppression of allergic airway eosinophilia, mucus overproduction, antigen-specific IgE responses, and Th2 cytokines (IL-4 and IL-5). More importantly, we found that the transfer of SJCD8α(-) DC, but not SJCD8α(+) DC, significantly increased IL-10 and TGF-β production following OVA exposure. As control, the transfer of DC subsets from naive mice had no significant effect on allergic inflammation. In addition, SJCD8α-DC expressed significantly higher IL-10 but lower IL-12, CD80 and CD86 than SJCD8α(+) DC, fitting a tolerogenic phenotype. The results suggest that CD8α(-) DC is the predominant DC subset which is involved in the parasitic infection-mediated inhibition of allergic inflammation and possibly through enhancing immunomodulatory cytokine (IL-10 and TGF-β) production.

CD8α¯ DC is the major DC subset which mediates inhibition of allergic responses by Schistosoma infection.

Objective: Exercise training (ET) provides a cardioprotective effect against pathological cardiac hypertrophy. Nitric oxide (NO) plays an important role in modula

Nitric Oxide Synthase Inhibition Abolishes Exercise-Mediated Protection against Isoproterenol-Induced Cardiac Hypertrophy in Female Mice

Allergic asthma is a chronic inflammatory disease mediated by Th2 cell immune responses. Currently, immunotherapies based on immune deviation are attractive, preventive, and therapeutic strategies for asthma. Many studies have shown that intracellular bacterial infections such as mycobacteria and their components can suppress asthmatic reactions by enhancing Th1 responses, while helminth infections and their proteins can inhibit allergic asthma via immune regulation. However, some helminth proteins such as SmP40, the major egg antigen of Schistosoma mansoni, are found as Th1 type antigens. Using a panel of overlapping peptides, we identified T-cell epitopes on SjP40 protein of Schistosoma japonicum, which can induce Th1 cytokine and inhibit the production of Th2 cytokines and airway inflammation in a mouse model of allergic asthma. These results reveal a novel form of immune protective mechanism, which may play an important role in the modulating effect of helminth infection on allergic asthmatic reactions.

https://onlinelibrary.wiley.com/doi/pdf/10.1002/eji.201545775

Novel T‐cell epitopes on Schistosoma japonicum SjP40 protein and their preventive effect on allergic asthma in mice

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CD8α¯ DC is the major DC subset which mediates inhibition of allergic responses by Schistosoma infection.

Nitric Oxide Synthase Inhibition Abolishes Exercise-Mediated Protection against Isoproterenol-Induced Cardiac Hypertrophy in Female Mice

Novel T‐cell epitopes on Schistosoma japonicum SjP40 protein and their preventive effect on allergic asthma in mice