Abstract:Nitric oxide (NO) is an active and critical nitrogen oxide in the microbe-driven nitrogen biogeochemical cycle, and is of great interest to medicine and the biological sciences. As a gas molecule prior to oxygen, NO respiration represents an early form of energy generation via various reactions in prokaryotes. Major enzymes for endogenous NO formation known to date include two types of nitrite reductases in denitrification, hydroxylamine oxidoreductase in ammonia oxidation, and NO synthases (NOSs). While the f… Show more
“…In fact, such wrinkled morphology is likely to be the result of biofilm formation as reported 25 , which partly accounts for the roles of these bacteria in disease prevention and better health of the host organisms 26 , 27 . Consistently, increased NO levels are found to induce biofilm formation by Bacillus subtilis 23 , 28 . Figure 4 Scanning electron microscopy (SEM) images of Caco2-HT29 epithelial layer and THP1 cells cocultured on the opposite side of the 3D Flipwell membrane.…”
Section: Resultsmentioning
confidence: 53%
“…In fact, such wrinkled morphology is likely to be the result of biofilm formation as reported 25 , which partly accounts for the roles of these bacteria in disease prevention and better health of the host organisms 26,27 . Consistently, increased NO levels are found to induce biofilm formation by Bacillus subtilis 23,28 .…”
Section: Sep Treatment Of Co-cultures Elevated the Thickness And Inte...mentioning
confidence: 55%
“…SEP effectively reprograms tumor associated macrophages from the immuno-suppressive M2-type (alternatively activated) to immuno-stimulatory M1-type (classically activated), while also strongly suppressing breast tumor cell growth 19 , 20 . Here, we tested the effects of SEP on colon epithelial Caco2 and mucus-producing HT-29/MTX cells, THP-1 macrophages and Gram-positive commensal Bacillus subtilis , where SEP could activate both mammalian and bacterial NOS isoforms to produce NO 23 . We also made comparisons between mono-cultures and co-cultures.…”
Gut mucosa consists of stratified layers of microbes, semi-permeable mucus, epithelium and stroma abundant in immune cells. Although tightly regulated, interactions between gut commensals and immune cells play indispensable roles in homeostasis and cancer pathogenesis in the body. Thus, there is a critical need to develop a robust model for the gut mucosal microenvironment. Here, we report our novel co-culture utilizing 3D Flipwell system for establishing the stratified layers of discrete mucosal components. This method allows for analyzing synchronous effects of test stimuli on gut bacteria, mucus, epithelium and immune cells, as well as their crosstalks. In the present report, we tested the immuno-stimulatory effects of sepiapterin (SEP, the precursor of the cofactor of nitric oxide synthase (NOS)—BH4) on the gut mucosal community. We previously reported that SEP effectively reprogrammed tumor-associated macrophages and inhibited breast tumor cell growth. In our co-cultures, SEP largely promoted mucus integrity, bacterial binding, and M1-like polarization of macrophages. Conversely, these phenomena were absent in control-treated cultures. Our results demonstrate that this novel co-culture may serve as a robust in vitro system to recapitulate the effects of pharmacological agents on the gut mucosal microenvironment, and could potentially be expanded to test the effects outside the gut.
“…In fact, such wrinkled morphology is likely to be the result of biofilm formation as reported 25 , which partly accounts for the roles of these bacteria in disease prevention and better health of the host organisms 26 , 27 . Consistently, increased NO levels are found to induce biofilm formation by Bacillus subtilis 23 , 28 . Figure 4 Scanning electron microscopy (SEM) images of Caco2-HT29 epithelial layer and THP1 cells cocultured on the opposite side of the 3D Flipwell membrane.…”
Section: Resultsmentioning
confidence: 53%
“…In fact, such wrinkled morphology is likely to be the result of biofilm formation as reported 25 , which partly accounts for the roles of these bacteria in disease prevention and better health of the host organisms 26,27 . Consistently, increased NO levels are found to induce biofilm formation by Bacillus subtilis 23,28 .…”
Section: Sep Treatment Of Co-cultures Elevated the Thickness And Inte...mentioning
confidence: 55%
“…SEP effectively reprograms tumor associated macrophages from the immuno-suppressive M2-type (alternatively activated) to immuno-stimulatory M1-type (classically activated), while also strongly suppressing breast tumor cell growth 19 , 20 . Here, we tested the effects of SEP on colon epithelial Caco2 and mucus-producing HT-29/MTX cells, THP-1 macrophages and Gram-positive commensal Bacillus subtilis , where SEP could activate both mammalian and bacterial NOS isoforms to produce NO 23 . We also made comparisons between mono-cultures and co-cultures.…”
Gut mucosa consists of stratified layers of microbes, semi-permeable mucus, epithelium and stroma abundant in immune cells. Although tightly regulated, interactions between gut commensals and immune cells play indispensable roles in homeostasis and cancer pathogenesis in the body. Thus, there is a critical need to develop a robust model for the gut mucosal microenvironment. Here, we report our novel co-culture utilizing 3D Flipwell system for establishing the stratified layers of discrete mucosal components. This method allows for analyzing synchronous effects of test stimuli on gut bacteria, mucus, epithelium and immune cells, as well as their crosstalks. In the present report, we tested the immuno-stimulatory effects of sepiapterin (SEP, the precursor of the cofactor of nitric oxide synthase (NOS)—BH4) on the gut mucosal community. We previously reported that SEP effectively reprogrammed tumor-associated macrophages and inhibited breast tumor cell growth. In our co-cultures, SEP largely promoted mucus integrity, bacterial binding, and M1-like polarization of macrophages. Conversely, these phenomena were absent in control-treated cultures. Our results demonstrate that this novel co-culture may serve as a robust in vitro system to recapitulate the effects of pharmacological agents on the gut mucosal microenvironment, and could potentially be expanded to test the effects outside the gut.
“…You also increase your breathing rate to get more oxygen into your body. The results show that the post-VO 2max was significantly different from the pre-VO 2max and improved by 10.1% [41]. The NO Swimming Exercise-Induced Improvements in Cardiorespiratory Fitness (CRF) are Caused… DOI: http://dx.doi.org/10.5772/intechopen.109306 signaling pathway is an endogenously generated regulator of vascular via cGMP leading to smooth muscle relaxation which is the primary mechanism of NO-mediated physiology.…”
Section: No Functional Adaptations In the Oxygen Transport Systemmentioning
Cardiorespiratory fitness (CRF) is associated with referring to enhance oxygen transport capacity to respiratory systems and increasing oxygen transport circulatory to skeletal muscle to produce energy. The aim of this report on the health-related CRF in the oxygen transport system-mediated physiological nitric oxide (NO) functional adaptations. Therefore, we want to know that swimming exercise-induced improvements in CRF resulted in increased oxygen transport capacity during physical activity of the respiratory systems. Therefore, the oxygen circulatory transport system is related to NO signaling and has been associated with various pathophysiologic functions and neuronal activity. Besides mediating normal functions, NO is implicated in inflammation and hypertension disease states. Swimming exercise is a good way to increase the rate of metabolism. Swimming exercise improves heart rate and oxygen circulatory, and increases the rate of metabolism and burning of heat. In this context, this review summarizes the roles of NO in improvements in cardiorespiratory fitness.
“…These RNS molecules can interact with and inactivate bacterial DNA, proteins, and enzymes, thereby contributing to bacterial death at high concentrations of NO. 14,21 At low levels, NO correlates with low bacterial adhesion and biofilm dispersal, and NO has been identified as a key mediator of biofilm formation and dispersal conserved across microbial species. 11,22−24 The life cycle of biofilms consists of initial attachment, accumulation, maturation, and detachment (dispersal).…”
Nitric oxide (NO) releasing biomaterials are a promising approach against medical device associated microbial infection. In contrast to the bacteria-killing effects of NO at high concentrations, NO at low concentrations serves as an important signaling molecule to inhibit biofilm formation or disperse mature biofilms by regulating the intracellular nucleotide second messenger signaling network such as cyclic dimeric guanosine monophosphate (c-di-GMP) for many Gram-negative bacterial strains. However, Gram-positive staphylococcal bacteria are the most commonly diagnosed microbial infections on indwelling devices, but much less is known about the nucleotide messengers and their response to NO as well as the mechanism by which NO inhibits biofilm formation. This study investigated the cyclic nucleotide second messengers c-di-GMP, cyclic dimeric adenosine monophosphate (c-di-AMP), and cyclic adenosine monophosphate (cAMP) in both Staphylococcus aureus (S. aureus) Newman D2C and Staphylococcus epidermidis (S. epidermidis) RP62A after incubating with Snitroso-N-acetylpenicillamine (SNAP, NO donor) impregnated polyurethane (PU) films. Results demonstrated that NO release from the polymer films significantly reduced the c-di-GMP levels in S. aureus planktonic and sessile cells, and these bacteria showed inhibited biofilm formation. However, the effect of NO release on c-di-GMP in S. epidermidis was weak, but rather, S. epidermidis showed significant reduction in c-di-AMP levels in response to NO release and also showed reduced biofilm formation. Results strongly suggest that NO regulates the nucleotide second messenger signaling network in different ways for these two bacteria, but for both bacteria, these changes in signaling affect the formations of biofilms. These findings provide cues to understand the mechanism of Staphylococcus biofilm inhibition by NO and suggest novel targets for antibiofilm interventions.
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