Lactoferrin and oral pathologies: a therapeutic treatment

2020 ◽  
pp. 1-10
Author(s):  
Luigi Rosa ◽  
Maria Stefania Lepanto ◽  
Antimo Cutone ◽  
Giusi Ianiro ◽  
Stefania Pernarella ◽  
...  
Keyword(s):  
Topical Administration ◽  
Protective Role ◽  
Pathogenic Microorganisms ◽  
Protective Function ◽  
Maxillary Bone ◽  
Abiotic Surfaces ◽  
Bone Damage ◽  
Aerobic And Anaerobic ◽  
Simultaneous Activity

The oral cavity is a non-uniform, extraordinary environment characterized by mucosal, epithelial, abiotic surfaces and secretions as saliva. Aerobic and anaerobic commensal and pathogenic microorganisms colonize the tongue, teeth, jowl, gingiva, and periodontium. Commensals exert an important role in host defenses, while pathogenic microorganisms can nullify this protective function causing oral and systemic diseases. Every day, 750–1000 mL of saliva, containing several host defense constituents including lactoferrin (Lf), are secreted and swallowed. Lf is a multifunctional iron-chelating cationic glycoprotein of innate immunity. Depending on, or regardless of its iron-binding ability, Lf exerts bacteriostatic, bactericidal, antibiofilm, antioxidant, antiadhesive, anti-invasive, and anti-inflammatory activities. Here, we report the protective role of Lf in different oral pathologies, such as xerostomia, halitosis, alveolar or maxillary bone damage, gingivitis, periodontitis, and black stain. Unlike antibiotic therapy, which is ineffective against bacteria that are within a biofilm, adherent, or intracellular, the topical administration of Lf, through its simultaneous activity against microbial replication, biofilms, adhesion, and invasiveness, as well as inflammation, has been proven to be efficient in the treatment of all known oral pathologies without any adverse effects.

Protective role of NO in hepatic microcirculatory dysfunction during endotoxemia

1994 ◽  
Vol 267 (6) ◽  
pp. G1135-G1141 ◽  
Author(s):  
J. Nishida ◽  
R. S. McCuskey ◽  
D. McDonnell ◽  
E. S. Fox
Keyword(s):  
Hepatic Injury ◽  
Protective Role ◽  
No Production ◽  
Leukocyte Adherence ◽  
In Vivo Microscopy ◽  
Hepatic Microcirculation ◽  
Protective Function ◽  
Microcirculatory Disturbances

Nitric oxide (NO) has been reported to have a protective function in attenuating hepatic injury during endotoxemia or sepsis. As a result, the role of NO in attenuating the hepatic microcirculatory alterations associated with endotoxemia was investigated in mice by in vivo microscopy. The livers were examined 2 h after intravenous injection of Escherichia coli 0111:B4 lipopolysaccharide (LPS) alone or in combination with inhibitors of the synthesis of NO, NG-nitro-L-arginine methyl ester or NG-monomethyl-L-arginine. In the animals treated with the combination of NO synthase inhibitors and LPS, leukocyte adherence was increased threefold above that in animals treated with LPS alone. This was accompanied by a 33% reduction in sinusoidal blood flow. Simultaneous administration of L-arginine, but not D-arginine, eliminated these microcirculatory disturbances. The results demonstrate that inhibition of LPS-stimulated NO production results in an early hepatic microvascular inflammatory response to a dose of endotoxin which by itself is scarcely inflammatory. This suggests that NO plays a significant role in stabilizing the hepatic microcirculation during endotoxemia, thereby helping to protect the liver from ischemia and leukocyte-induced oxidative injury.

scholarly journals A Contemporary View of Natriuretic Peptides in the SARS-CoV-2 Era

2021 ◽  
Vol 12 ◽  
Author(s):  
Speranza Rubattu ◽  
Giovanna Gallo ◽  
Massimo Volpe
Keyword(s):  
Viral Infection ◽  
Natriuretic Peptides ◽  
Pulmonary Inflammation ◽  
Protective Role ◽  
Protective Effects ◽  
Cardiac Damage ◽  
Protective Function ◽  
Therapeutic Benefits ◽  
Prognostic Implications

The heart releases natriuretic peptides (NPs) which represent an important hormonal axis with cardiorenal protective effects. In view of their properties, NPs have pathophysiologic, diagnostic and prognostic implications in several cardiovascular diseases (CVDs). Severe pulmonary inflammation, as induced by the SARS-COV2, may increase pulmonary pressure with potential influence on NPs release, whereby normal cardiovascular integrity becomes impaired. Moreover, pre-existing CVDs are strong negative prognostic factors since they exacerbate the effects of the viral infection and lead to worse outcomes. In this context, it may be expected that NPs exert a key protective role toward the virus infection whereas an impairment of NPs release contributes to the virus deleterious effects. In this review article we explore the potential involvement of NPs in the COVID-19 disease. To this aim, we will first focus on the interactions between NPs and the Ang II/ATIR arm of the renin-angiotensin-aldosterone system (RAAS) as well as with the protective ACE2/Ang (1-7) arm of the RAAS. Subsequently, we will review evidence that strongly supports the role of increased NT-proBNP level as a marker of cardiac damage and of worse prognosis in the COVID-19 affected patients. Finally, we will discuss the potential therapeutic benefits of these protective hormones toward the viral infection through their endothelial protective function, anti-inflammatory and anti-thrombotic effects. In conclusion, the potential implications of NPs in the SARS-CoV-2 infection, as discussed in our article, represent an important issue that deserves to be fully investigated.

scholarly journals Protective Role of Leaf Variegation in Pittosporum tobira under Low Temperature: Insights into the Physio-Biochemical and Molecular Mechanisms

2019 ◽  
Vol 20 (19) ◽  
pp. 4857
Author(s):  
Zhilu Zhang ◽  
Zhonghua Liu ◽  
Haina Song ◽  
Minghui Chen ◽  
Shiping Cheng
Keyword(s):  
Low Temperature ◽  
Molecular Mechanisms ◽  
Protective Role ◽  
Ros Scavenging ◽  
High Accumulation ◽  
Cold Response ◽  
Protective Function ◽  
Leaf Variegation ◽  
Pittosporum Tobira

Leaf variegation has been demonstrated to have adaptive functions such as cold tolerance. Pittosporum tobira is an ornamental plant with natural leaf variegated cultivars grown in temperate regions. Herein, we investigated the role of leaf variegation in low temperature responses by comparing variegated “Variegatum” and non-variegated “Green Pittosporum” cultivars. We found that leaf variegation is associated with impaired chloroplast development in the yellow sector, reduced chlorophyll content, strong accumulation of carotenoids and high levels of ROS. However, the photosynthetic efficiency was not obviously impaired in the variegated leaves. Also, leaf variegation plays low temperature protective function since “Variegatum” displayed strong and efficient ROS-scavenging enzymatic systems to buffer cold (10 °C)-induced damages. Transcriptome analysis under cold conditions revealed 309 differentially expressed genes between both cultivars. Distinctly, the strong cold response observed in “Variegatum” was essentially attributed to the up-regulation of HSP70/90 genes involved in cellular homeostasis; up-regulation of POD genes responsible for cell detoxification and up-regulation of FAD2 genes and subsequent down-regulation of GDSL genes leading to high accumulation of polyunsaturated fatty acids for cell membrane fluidity. Overall, our results indicated that leaf variegation is associated with changes in physiological, biochemical and molecular components playing low temperature protective function in P. tobira.

scholarly journals Protective role of neuronal and lymphoid cannabinoid CB2 receptors in neuropathic pain

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
David Cabañero ◽  
Angela Ramírez-López ◽  
Eva Drews ◽  
Anne Schmöle ◽  
David M Otte ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Immune Cells ◽  
Protective Role ◽  
Spontaneous Pain ◽  
Wild Type ◽  
Self Administration ◽  
Psychotropic Effects ◽  
Peripheral Immune Cells ◽  
Simultaneous Activity

Cannabinoid CB2 receptor (CB2) agonists are potential analgesics void of psychotropic effects. Peripheral immune cells, neurons and glia express CB2; however, the involvement of CB2 from these cells in neuropathic pain remains unresolved. We explored spontaneous neuropathic pain through on-demand self-administration of the selective CB2 agonist JWH133 in wild-type and knockout mice lacking CB2 in neurons, monocytes or constitutively. Operant self-administration reflected drug-taking to alleviate spontaneous pain, nociceptive and affective manifestations. While constitutive deletion of CB2 disrupted JWH133-taking behavior, this behavior was not modified in monocyte-specific CB2 knockouts and was increased in mice defective in neuronal CB2 knockouts suggestive of increased spontaneous pain. Interestingly, CB2-positive lymphocytes infiltrated the injured nerve and possible CB2transfer from immune cells to neurons was found. Lymphocyte CB2depletion also exacerbated JWH133 self-administration and inhibited antinociception. This work identifies a simultaneous activity of neuronal and lymphoid CB2that protects against spontaneous and evoked neuropathic pain.

scholarly journals Protective role of neuronal and lymphoid cannabinoid CB2 receptors in neuropathic pain

2020 ◽  
Author(s):  
David Cabañero ◽  
Angela Ramírez-López ◽  
Eva Drews ◽  
Anne Schmöle ◽  
David M. Otte ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Immune Cells ◽  
Protective Role ◽  
Spontaneous Pain ◽  
Cb2 Receptor ◽  
Self Administration ◽  
Psychotropic Effects ◽  
Peripheral Immune Cells ◽  
Simultaneous Activity

AbstractCannabinoid CB2 receptor (CB2r) agonists are potential painkillers void of psychotropic effects. Peripheral immune cells, neurons and glia express CB2r, however the involvement of CB2r from these cells in neuropathic pain remains unresolved. We explored spontaneous neuropathic pain through on-demand self-administration of the selective CB2r agonist JWH133 in wild-type and knockout mice lacking CB2r in neurons, monocytes or constitutively. Operant self-administration reflected drug-taking to alleviate spontaneous pain, nociceptive and affective manifestations. While constitutive deletion of CB2r disrupted JWH133-taking behavior, this behavior was not modified in monocyte-specific CB2r knockouts and was increased in mice defective in neuronal CB2r knockouts suggestive of increased spontaneous pain. Interestingly, CB2r-positive lymphocytes infiltrated the injured nerve and possible CB2r transfer from immune cells to neurons was found. Lymphocyte CB2r depletion also exacerbated JWH133 self-administration and inhibited antinociception. This work identifies a simultaneous activity of neuronal and lymphoid CB2r that protects against spontaneous and evoked neuropathic pain.

Use of genetically altered animal models in understanding the role of metallothionein in cadmium toxicity

2000 ◽  
Vol 72 (6) ◽  
pp. 1023-1026 ◽  
Author(s):  
Curtis D. Klaassen ◽  
Supratim Choudhuri
Keyword(s):  
Liver Injury ◽  
Knockout Mice ◽  
Metal Binding ◽  
Cadmium Toxicity ◽  
Kidney Injury ◽  
Protective Role ◽  
Low Molecular Weight ◽  
Bone Damage ◽  
Cd Exposure

Acute Cd exposure produces liver injury, whereas chronic Cd exposure damages the kidney but not the liver. Previous experiments suggest that the low-molecular-weight, metal-binding protein metallothionein (MT) in liver protects against liver injury, but is responsible for the kidney injury observed after chronic Cd exposure. Thus, prior to the development of MT-transgenic and MT-knockout mice models, MT's role was always assumed to be a toxicological paradox, hepatoprotection but nephrotoxicity. The development of MT-transgenic and MT-knockout mice models has reconfirmed MT's protective role against Cd-induced hepatotoxicity, but it has challenged MT's suggested role in Cd-induced nephrotoxicity. In this communication, recent data using these genetically altered mice models indicate that MT protects against not only the Cd-induced hepatotoxicity, but also nephrotoxicity, hematotoxicity, immunotoxicity, and bone damage.

scholarly journals A Potential Probiotic for Diarrhea: Clostridium tyrobutyricum Protects Against LPS-Induced Epithelial Dysfunction via IL-22 Produced By Th17 Cells in the Ileum

2021 ◽  
Vol 12 ◽  
Author(s):  
Zhiping Xiao ◽  
Lujie Liu ◽  
Xun Pei ◽  
Wanjing Sun ◽  
Yuyue Jin ◽  
...  
Keyword(s):  
Th17 Cells ◽  
Intestinal Inflammation ◽  
Flow Cytometric Analysis ◽  
Protective Role ◽  
Regulatory Function ◽  
Clostridium Tyrobutyricum ◽  
Dependent Manner ◽  
Protective Function

Probiotics are clinically used for diarrhea and inflammatory bowel diseases in both humans and animals. Previous studies have shown that Clostridium tyrobutyricum (Ct) protects against intestinal dysfunction, while its regulatory function in the gut needs further investigation and the related mechanisms are still not fully elucidated. This study aims to further verify the protective function of Ct and reveal its underlying mechanisms in alleviating diarrhea and intestinal inflammation. Ct inhibited LPS-induced diarrhea and intestinal inflammation in the ileum. IL-22 was identified and the protective role of Ct in the ileum presented an IL-22-dependent manner according to the transcriptomic analysis and in vivo interference mice experiments. The flow cytometric analysis of immune cells in the ileum showed that Ct enhanced the proportions of Th17 cells in response to LPS. The results of in situ hybridization further verified that Ct triggered Th17 cells to produce IL-22, which combined with IL-22RA1 expressed in the epithelial cells. Moreover, Ct was unable to enhance the levels of short-chain fatty acids (SCFAs) in the ileum, suggesting that the protective role of Ct in the ileum was independent of SCFAs. This study uncovered the role of Ct in alleviating diarrhea and inflammation with the mechanism of stimulating Th17 cells in the lamina propria to produce IL-22, highlighting its potential application as a probiotic for diarrhea and inflammation in the ileum.

scholarly journals Stress Granule Formation Attenuates RACK1-Mediated Apoptotic Cell Death Induced by Morusin

2020 ◽  
Vol 21 (15) ◽  
pp. 5360
Author(s):  
Ye-Jin Park ◽  
Dong Wook Choi ◽  
Sang Woo Cho ◽  
Jaeseok Han ◽  
Siyoung Yang ◽  
...  
Keyword(s):  
Cell Death ◽  
Apoptotic Cell ◽  
Stress Granules ◽  
Protective Role ◽  
Stress Granule ◽  
Protein Kinase R ◽  
Granule Formation ◽  
Protective Function ◽  
Eif2α Phosphorylation

Stress granules are membraneless organelles composed of numerous components including ribonucleoproteins. The stress granules are characterized by a dynamic complex assembly in response to various environmental stressors, which has been implicated in the coordinated regulation of diverse biological pathways, to exert a protective role against stress-induced cell death. Here, we show that stress granule formation is induced by morusin, a novel phytochemical displaying antitumor capacity through barely known mechanisms. Morusin-mediated induction of stress granules requires activation of protein kinase R (PKR) and subsequent eIF2α phosphorylation. Notably, genetic inactivation of stress granule formation mediated by G3BP1 knockout sensitized cancer cells to morusin treatment. This protective function against morusin-mediated cell death can be attributed at least in part to the sequestration of receptors for activated C kinase-1 (RACK1) within the stress granules, which reduces caspase-3 activation. Collectively, our study provides biochemical evidence for the role of stress granules in suppressing the antitumor capacity of morusin, proposing that morusin treatment, together with pharmacological inhibition of stress granules, could be an efficient strategy for targeting cancer.

scholarly journals How are personality traits and physical activity involved in colorectal carcinogenesis? A cross-sectional study on patients undergoing colonoscopy

2017 ◽  
Vol 41 (S1) ◽  
pp. s503-s503
Author(s):  
M. Marchi ◽  
S. Alboni ◽  
C. Artoni ◽  
M. Galletti ◽  
N. Giambalvo ◽  
...  
Keyword(s):  
Physical Activity ◽  
Personality Traits ◽  
Cross Sectional Study ◽  
Protective Role ◽  
Colorectal Carcinogenesis ◽  
Sectional Study ◽  
Cross Sectional ◽  
Protective Function ◽  
Psychological Determinants

IntroductionInflammatory state of the large bowel is a key factor for the development of colorectal cancer (CRC). It has multifactorial aetiology, including psychological determinants. Physical activity may have a protective function against CRC via anti-inflammatory properties; on the contrary, personality traits correlate with an unhealthy and dangerous lifestyle.ObjectiveTo measure the association between personality traits, lifestyle and colonoscopy outcome.MethodsCross sectional study. Patients undergoing colonoscopy aged 40 or more, with a negative history for cancer or inflammatory bowel disease, were enrolled. Data collected: colonoscopy outcome, smoke, alcohol, physical activity, presence/absence of Metabolic Syndrome, personality traits assessed by the Temperament & Character Inventory (TCI).ResultsIn a sample of 53 subjects (females = 24, 45.3%), the mean age was 60.66 ± 9.08. At least one adenoma was found to 23 patients (43.3%). Twenty patients were smokers (37.74%), 36 (67.92%) drank alcohol at least weekly; approximately 60% reported regular physical activity. At the multivariate regression, the outcome was associated to: TCI Self Transcendence domain (ST) (OR = 1.36, P = 0.04) and physical activity (OR = 0.14, P = 0.03).ConclusionPeople with ST's characteristic personality traits and sedentary life style are more likely to have precancerous colorectal lesions. This confirms the protective role of physical activity, and suggests to further explore the role of personality in cancerogenesis.Disclosure of interestThe authors have not supplied their declaration of competing interest.

scholarly journals The Protective Role of Bacteroides fragilis in a Murine Model of Colitis-Associated Colorectal Cancer

mSphere ◽  
2018 ◽  
Vol 3 (6) ◽  
Author(s):  
Yun Kyung Lee ◽  
Parpi Mehrabian ◽  
Silva Boyajian ◽  
Wei-Li Wu ◽  
Jane Selicha ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Chemokine Receptor ◽  
Bacteroides Fragilis ◽  
Protective Role ◽  
Tumor Formation ◽  
Protective Function ◽  
Content Type ◽  
Colon Tumorigenesis ◽  
Tlr2 Signaling

ABSTRACT Many patients with chronic inflammation of the gut, such as that observed in inflammatory bowel disease (IBD), develop colorectal cancer (CRC). Recent studies have reported that the development of IBD and CRC partly results from an imbalanced composition of intestinal microbiota and that intestinal inflammation in these diseases can be modulated by the microbiota. The human commensal Bacteroides fragilis is best exemplified playing a protective role against the development of experimental colitis in several animal disease models. In this study, we found that gut inflammation caused by dextran sulfate sodium (DSS) treatment was inhibited by B. fragilis colonization in mice. Further, we reveal a protective role of B. fragilis treatment against colon tumorigenesis using an azoxymethane (AOM)/DSS-induced model of colitis-associated colon cancer in mice and demonstrate that the decreased tumorigenesis by B. fragilis administration is accompanied by inhibited expression of C-C chemokine receptor 5 (CCR5) in the gut. We show direct evidence that the inhibition of tumor formation provided by B. fragilis in colitis-associated CRC animals was dependent on the production of polysaccharide A (PSA) from B. fragilis and that Toll-like receptor 2 (TLR2) signaling was responsible for the protective function of B. fragilis. IMPORTANCE The incidence of colorectal cancer (CRC) is rapidly growing worldwide, and there is therefore a greater emphasis on studies of the treatment or prevention of CRC pathogenesis. Recent studies suggested that consideration of the microbiota is unavoidable to understand inflammation and tumorigenesis in the gastrointestinal tract. We demonstrate, using a mouse model of colitis-associated CRC, that human commensal B. fragilis protects against colon tumorigenesis. The protective role against tumor formation provided by B. fragilis is associated with inhibition of expression of the chemokine receptor CCR5 in the colon. The molecular mechanism for protection against CRC provided by B. fragilis is dependent on polysaccharide A production and is mediated by TLR2 signaling. Our results suggest that the commensal microorganism B. fragilis can be used to prevent inflammation-associated CRC development and may provide an effective therapeutic strategy for CRC.

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