Antimicrobial Cationic Peptides
Amino Acid Sequence
Molecular Sequence Data
Microbial Sensitivity Tests
Sequence Homology, Amino Acid
Multiple Chemical Sensitivity
Transfer of a cathelicidin peptide antibiotic gene restores bacterial killing in a cystic fibrosis xenograft model. (1/295)Recent studies suggest that the gene defect in cystic fibrosis (CF) leads to a breach in innate immunity. We describe a novel genetic strategy for reversing the CF-specific defect of antimicrobial activity by transferring a gene encoding a secreted cathelicidin peptide antibiotic into the airway epithelium grown in a human bronchial xenograft model. The airway surface fluid (ASF) from CF xenografts failed to kill Pseudomonas aeruginosa or Staphylococcus aureus. Partial reconstitution of CF transmembrane conductance regulator expression after adenovirus-mediated gene transfer restored the antimicrobial activity of ASF from CF xenografts to normal levels. Exposure of CF xenografts to an adenovirus expressing the human cathelicidin LL-37/hCAP-18 increased levels of this peptide in the ASF three- to fourfold above the normal concentrations, which were equivalent in ASF from CF and normal xenografts before gene transfer. The increase of LL-37 was sufficient to restore bacterial killing to normal levels. The data presented describe an alternative genetic approach to the treatment of CF based on enhanced expression of an endogenous antimicrobial peptide and provide strong evidence that expression of antimicrobial peptides indeed protects against bacterial infection. (+info)
The human cationic antimicrobial protein (hCAP18), a peptide antibiotic, is widely expressed in human squamous epithelia and colocalizes with interleukin-6. (2/295)Peptide antibiotics are widespread in nature and, by providing a rapid first line of defense, may be key players in the innate immune system. Although epithelia are the main barriers shielding the internal environment from microorganisms, the role for peptide antibiotics in epithelial protection is unclear. We recently reported that the human cationic antimicrobial protein hCAP18, the precursor of the antimicrobial peptide called LL-37, is not expressed by normal human keratinocytes but is induced in various inflammatory skin disorders. In the present study we demonstrate that hCAP18 is consistently expressed at both mRNA and protein levels in squamous epithelia of the mouth, tongue, esophagus, cervix, and vagina in humans. The gene for hCAP18 contains promoter elements that are potentially regulated by interleukin-6, and our data further show a colocalization between interleukin-6 and hCAP18 expression in these tissues. Our finding that hCAP18 is widely produced in squamous epithelia suggests a role for this peptide in epithelial antimicrobial defense. Furthermore, colocalization with interleukin-6 indicates a potential local mechanism for the upregulation of hCAP18 at the epithelial surfaces. (+info)
Structure and organization of the human antimicrobial peptide LL-37 in phospholipid membranes: relevance to the molecular basis for its non-cell-selective activity. (3/295)The antimicrobial peptide LL-37 belongs to the cathelicidin family and is the first amphipathic alpha-helical peptide isolated from human. LL-37 is considered to play an important role in the first line of defence against local infection and systemic invasion of pathogens at sites of inflammation and wounds. Understanding its mode of action may assist in the development of antimicrobial agents mimicking those of the human immune system. In vitro studies revealed that LL-37 is cytotoxic to both bacterial and normal eukaryotic cells. To gain insight into the mechanism of its non-cell-selective cytotoxicity, we synthesized and structurally and functionally characterized LL-37, its N-terminal truncated form FF-33, and their fluorescent derivatives (which retained structure and activity). The results showed several differences, between LL-37 and other native antimicrobial peptides, that may shed light on its in vivo activities. Most interestingly, LL-37 exists in equilibrium between monomers and oligomers in solution at very low concentrations. Also, it is significantly resistant to proteolytic degradation in solution, and when bound to both zwitterionic (mimicking mammalian membranes) and negatively charged membranes (mimicking bacterial membranes). The results also showed a role for the N-terminus in proteolytic resistance and haemolytic activity, but not in antimicrobial activity. The LL-37 mode of action with negatively charged membranes suggests a detergent-like effect via a 'carpet-like' mechanism. However, the ability of LL-37 to oligomerize in zwitterionic membranes might suggest the formation of a transmembrane pore in normal eukaryotic cells. To examine this possibility we used polarized attenuated total reflectance Fourier-transform infrared spectroscopy and found that the peptide is predominantly alpha-helical and oriented nearly parallel with the surface of zwitterionic-lipid membranes. This result does not support the channel-forming hypothesis, but rather it supports the detergent-like effect. (+info)
The human antibacterial cathelicidin, hCAP-18, is bound to lipoproteins in plasma. (4/295)Cathelicidins are a family of antibacterial and lipopolysaccharide-binding proteins. hCAP-18, the only human cathelicidin, is a major protein of the specific granules of human neutrophils. The plasma level of hCAP-18 is >20-fold higher than that of other specific granule proteins relative to their levels within circulating neutrophils. The aim of this study was to elucidate the background for this high plasma level of hCAP-18. Plasma was subjected to molecular sieve chromatography, and hCAP-18 was found in distinct high molecular mass fractions that coeluted with apolipoproteins A-I and B, respectively. The association of hCAP-18 with lipoproteins was validated by the cofractionation of hCAP-18 with lipoproteins using two different methods for isolation of lipoproteins from plasma. Furthermore, the level of hCAP-18 in delipidated plasma was <1% of that in normal plasma. Immunoprecipitation of very low, low, and high density lipoprotein particles with anti-apolipoprotein antibodies resulted in coprecipitation of hCAP-18. The binding of hCAP-18 to lipoproteins was mediated by the antibacterial C-terminal part of the protein. The binding of hCAP-18 to lipoproteins suggests that lipoproteins may play an important role as a reservoir of this antimicrobial protein. (+info)
Novel cathelicidins in horse leukocytes(1). (5/295)Cathelicidins are precursors of defense peptides of the innate immunity and are widespread in mammals. Their structure comprises a conserved prepropiece and an antimicrobial domain that is structurally varied both intra- and inter-species. We investigated the complexity of the cathelicidin family in horse by a reverse transcription-PCR-based cloning strategy of myeloid mRNA and by Southern and Western analyses. Three novel cathelicidin sequences were deduced from bone marrow mRNA and designated equine cathelicidins eCATH-1, eCATH-2 and eCATH-3. Putative antimicrobial domains of 26, 27 and 40 residues with no significant sequence homology to other peptides were inferred at the C-terminus of the sequences. Southern analysis of genomic DNA using a probe based on the cathelicidin-conserved propiece revealed a polymorphic DNA region with several hybridization-positive fragments and suggested the presence of additional genes. A null eCATH-1 allele was also demonstrated with a frequency of 0.71 in the horse population analyzed and low amounts of eCATH-1-specific mRNA were found in myeloid cells of gene-positive animals. A Western analysis using antibodies to synthetic eCATH peptides revealed the presence of eCATH-2 and eCATH-3 propeptides, but not of eCATH-1-related polypeptides, in horse neutrophil granules and in the secretions of phorbol myristate acetate-stimulated neutrophils. These results thus suggest that eCATH-2 and eCATH-3 are functional genes, whereas eCATH-1 is unable to encode a polypeptide. (+info)
Augmentation of innate host defense by expression of a cathelicidin antimicrobial peptide. (6/295)Antimicrobial peptides, such as defensins or cathelicidins, are effector substances of the innate immune system and are thought to have antimicrobial properties that contribute to host defense. The evidence that vertebrate antimicrobial peptides contribute to innate immunity in vivo is based on their expression pattern and in vitro activity against microorganisms. The goal of this study was to investigate whether the overexpression of an antimicrobial peptide results in augmented protection against bacterial infection. C57BL/6 mice were given an adenovirus vector containing the cDNA for LL-37/hCAP-18, a human cathelicidin antimicrobial peptide. Mice treated with intratracheal LL-37/hCAP-18 vector had a lower bacterial load and a smaller inflammatory response than did untreated mice following pulmonary challenge with Pseudomonas aeruginosa PAO1. Systemic expression of LL-37/hCAP-18 after intravenous injection of recombinant adenovirus resulted in improved survival rates following intravenous injection of lipopolysaccharide with galactosamine or Escherichia coli CP9. In conclusion, the data demonstrate that expression of an antimicrobial peptide by gene transfer results in augmentation of the innate immune response, providing support for the hypothesis that vertebrate antimicrobial peptides protect against microorganisms in vivo. (+info)
SMAP-29: a potent antibacterial and antifungal peptide from sheep leukocytes. (7/295)SMAP-29 is a cathelicidin-derived peptide deduced from sheep myeloid mRNA. The C-terminally amidated form of this peptide was chemically synthesized and shown to exert a potent antimicrobial activity. Antibiotic-resistant clinical isolates highly susceptible to this peptide include MRSA and VREF isolates, that are a major worldwide problem, and mucoid Pseudomonas aeruginosa associated with chronic respiratory inflammation in CF patients. In addition, SMAP-29 is also active against fungi, including Cryptococcus neoformans isolated from immunocompromised patients. SMAP-29 causes significant morphological alterations of the bacterial surfaces, as shown by scanning electron microscopy, and is also hemolytic against human, but not sheep erythrocytes. Its potent antimicrobial activity suggests that this peptide is an excellent candidate as a lead compound for the development of novel antiinfective agents. (+info)
Biological activities of lipopolysaccharides of Proteus spp. and their interactions with polymyxin B and an 18-kDa cationic antimicrobial protein (CAP18)-derived peptide. (8/295)The saccharide constituents of lipopolysaccharides (LPS) of Proteus spp. vary with the strain and contain unique components about which little is known. The biological activities of LPS and lipid A from S- and R-forms of 10 Proteus strains were examined. LPS from all S-form Proteus strains was lethal to D-(+)-galactosamine (GalN)-loaded, LPS-responsive, C3H/HeN mice, but not to LPS-hypo-responsive C3H/HeJ mice. P. vulgaris 025 LPS evoked strong anaphylactoid reactions in N-acetylmuramyl-L-alanyl-D-isoglutamine (MDP)-primed C3H/HeJ mice. LPS from S- and R-form Proteus strains induced production of nitric oxide (NO) and tumour necrosis factor (TNF) by macrophages isolated from C3H/HeN but not C3H/HeJ mice. Lipid A from Proteus strains also induced NO and TNF production, although lipid A was less potent than LPS. The effects of LPS were mainly dependent on CD14; LPS-induced NO and TNF production in CD14+ J774.1 cells was significantly greater than in CD14-J7.DEF.3 cells. All LPS from Proteus strains, and especially from P. vulgaris 025, exhibited higher anti-complementary activity than LPS from Escherichia coli or Pseudomonas aeruginosa. Polymyxin B inactivated proteus LPS in a dose-dependent manner, but these LPS preparations were more resistant to polymyxin B than E. coli LPS. CAP18(109-135), a granulocyte-derived peptide, inhibited proteus LPS endotoxicity only when the LPS:CAP18(109-135) ratio was appropriate, which suggests that CAP18(109-135) acts through a different mechanism than polymyxin B. The results indicate that LPS from Proteus spp. are potently endotoxic, but that the toxicity is different from that of LPS from E. coli or Salmonella spp. and even varies among different Proteus strains. The variation in biological activities among proteus LPS may be due to unique components within the respective LPS. (+info)
The exact cause of rosacea is not known, but it is thought to be related to dysregulation of the immune system, genetic predisposition, and environmental triggers such as sun exposure, stress, and certain skincare products. The condition can worsen over time if left untreated, leading to permanent redness, thickening of the skin, and disfigurement.
Rosacea typically affects fair-skinned individuals, particularly women during their 30s and 40s, although it can also occur in men and people with darker skin tones. There is no cure for rosacea, but various treatments are available to manage its symptoms, including topical creams and gels, oral antibiotics, and laser therapy.
Lifestyle modifications, such as avoiding triggers, protecting the skin from the sun, and maintaining a healthy diet, can also help alleviate rosacea symptoms. It is essential to seek medical advice if you suspect you have rosacea, as early diagnosis and treatment can improve its management and minimize long-term consequences.
The symptoms of candidiasis, cutaneous may include:
* Redness and swelling on the affected area
* Itching and burning sensation
* Thickening and discoloration of the skin
* Cracks or fissures in the skin
Candidiasis, cutaneous can be diagnosed through a physical examination and may require additional tests such as a skin scraping or biopsy to confirm the diagnosis. Treatment typically involves antifungal medications and good wound care. In severe cases, hospitalization may be required.
Prevention is key in avoiding candidiasis, cutaneous. Good hygiene practices such as frequent handwashing, keeping the skin clean and dry, and avoiding sharing personal items can help reduce the risk of infection. Additionally, managing underlying conditions such as diabetes and taking antibiotics only when necessary can also help prevent candidiasis, cutaneous.
There are several types of food hypersensitivity, including:
1. Food Allergy: An immune system reaction to a specific food that can cause symptoms ranging from mild hives to life-threatening anaphylaxis. Common food allergies include reactions to peanuts, tree nuts, fish, shellfish, milk, eggs, wheat, and soy.
2. Non-Allergic Food Hypersensitivity: Also known as non-IgE-mediated food hypersensitivity, this type of reaction does not involve the immune system. Symptoms can include bloating, abdominal pain, diarrhea, and headaches. Common culprits include gluten, dairy, and high-FODMAP foods.
3. Food Intolerance: A condition where the body cannot properly digest or process a specific food. Symptoms can include bloating, abdominal pain, diarrhea, and gas. Common food intolerances include lactose intolerance, fructose malabsorption, and celiac disease.
4. Food Aversion: An emotional response to a specific food that can cause avoidance or dislike of the food. This is not an allergic or physiological reaction but rather a psychological one.
The diagnosis of food hypersensitivity typically involves a thorough medical history, physical examination, and diagnostic tests such as skin prick testing or blood tests. Treatment options for food hypersensitivity depend on the type and severity of the reaction and may include avoidance of the offending food, medication, or immunotherapy.
The diagnosis of MCS is based on a combination of medical history, physical examination, and laboratory tests. There is no specific diagnostic test for MCS, and the condition can be difficult to diagnose because its symptoms are similar to those of other conditions. Treatment for MCS typically involves avoiding exposure to chemicals and managing symptoms through lifestyle changes, stress reduction techniques, and medication.
MCS is a controversial condition, and some researchers question whether it is a valid medical diagnosis. However, many health professionals recognize MCS as a legitimate condition that affects thousands of people worldwide.
There are several types of chemical sensitivity, including:
* Irritant-induced sensitivity: This type of sensitivity occurs when an individual becomes sensitive to a specific chemical after repeated exposure to it.
* Allergic contact sensitivity: This type of sensitivity occurs when an individual develops an allergic reaction to a specific chemical.
* Idiopathic environmental intolerance: This type of sensitivity occurs when an individual experiences adverse reactions to multiple chemicals, without any known cause.
There are several risk factors for developing MCS, including:
* Previous exposure to toxic chemicals
* Genetic predisposition
* Age (MCS is more common in younger adults)
* Gender (women are more likely to develop MCS than men)
* Stress and psychological factors
There are several ways to prevent or reduce the risk of developing MCS, including:
* Avoiding exposure to toxic chemicals
* Using protective gear and equipment when working with chemicals
* Properly disposing of chemical waste
* Following safety protocols when handling chemicals
* Reducing stress and managing psychological factors.
There are several ways to diagnose MCS, including:
* Medical history and physical examination
* Allergy testing (such as skin prick testing or blood tests)
* Environmental exposure assessment
* Physiological testing (such as heart rate and blood pressure monitoring)
* Neuropsychological testing (such as cognitive function and mood assessment).
There are several treatment options for MCS, including:
* Avoiding exposure to triggers
* Medications (such as antihistamines or antidepressants)
* Immunotherapy (such as allergy shots)
* Cognitive behavioral therapy (CBT)
* Alternative therapies (such as acupuncture or herbal supplements).
It is important to note that MCS is a complex and controversial condition, and there is ongoing debate about its cause and validity. However, for those who suffer from the condition, it can have a significant impact on their quality of life, and it is important to seek medical attention if symptoms persist or worsen over time.
There are several theories about what might cause fibromyalgia, including:
1. Overactive nerve endings: Some research suggests that people with fibromyalgia may have overactive nerve endings that amplify pain signals.
2. Hormonal imbalance: Hormones such as cortisol and serotonin play a role in regulating pain and mood, and some studies suggest that hormonal imbalances might contribute to fibromyalgia.
3. Infections: Some research suggests that fibromyalgia may be triggered by a viral or bacterial infection, although more research is needed to confirm this theory.
4. Genetics: Fibromyalgia tends to run in families, which suggests that there may be a genetic component to the condition.
5. Environmental factors: Trauma, stress, and other environmental factors may also play a role in the development of fibromyalgia.
There is no single test for diagnosing fibromyalgia, and doctors must use a combination of physical examination, medical history, and other tests to rule out other conditions that might cause similar symptoms. Treatment for fibromyalgia typically involves a multidisciplinary approach, including medication, physical therapy, and lifestyle changes such as exercise and stress management.
Some common symptoms of fibromyalgia include:
* Widespread muscle pain and stiffness
* Fatigue and decreased energy
* Tender points on the body (areas that are painful to the touch)
* Brain fog and cognitive difficulties (such as memory loss and difficulty concentrating)
* Sleep disturbances (including insomnia and restless sleep)
* Headaches and migraines
* Digestive problems (such as irritable bowel syndrome)
* Numbness or tingling in the hands and feet
* Depression and anxiety
There is no cure for fibromyalgia, but treatment can help manage symptoms and improve quality of life. Some common medications used to treat fibromyalgia include:
* Pain relievers (such as acetaminophen or nonsteroidal anti-inflammatory drugs)
* Anti-seizure medications (which can help reduce pain and improve sleep)
* Antidepressants (which can help with mood issues and improve sleep)
* Muscle relaxants (which can help reduce muscle spasms and stiffness)
In addition to medication, physical therapy and lifestyle changes can also be helpful in managing fibromyalgia symptoms. These might include:
* Exercise programs that are tailored to the individual's needs and abilities
* Stress management techniques (such as meditation or yoga)
* Healthy sleep habits (such as establishing a consistent bedtime routine and avoiding caffeine and electronics before bedtime)
* A balanced diet and adequate hydration
* Massage therapy or other forms of relaxation techniques.
It's important to note that each person with fibromyalgia may respond differently to different treatments, so it may take some trial and error to find the right combination of medications and lifestyle changes that work best for an individual case. It's also important to work closely with a healthcare provider to monitor progress and adjust treatment plans as needed.
There are several types of milk hypersensitivity, including:
1. Immunoglobulin E (IgE)-mediated allergy: This is the most common type of milk hypersensitivity and occurs when the body produces antibodies called IgE to fight off the perceived threat of milk proteins. These antibodies can cause a range of symptoms, from mild hives and itching to severe anaphylaxis.
2. Non-IgE-mediated allergy: This type of milk hypersensitivity does not involve the production of IgE antibodies, but instead involves other immune mechanisms that can cause a range of symptoms, including gastrointestinal issues like diarrhea and abdominal pain.
3. Lactose intolerance: This is not an allergy, but rather an inability to digest lactose, a sugar found in milk. It can cause gastrointestinal symptoms like bloating, gas, and diarrhea.
Milk hypersensitivity can be diagnosed through a combination of medical history, physical examination, and diagnostic tests such as skin prick testing or blood tests. Treatment for milk hypersensitivity typically involves avoiding milk and products that contain it, but in severe cases, medications like epinephrine may be necessary to manage an allergic reaction.
There are several symptoms of RA, including:
1. Joint pain and stiffness, especially in the hands and feet
2. Swollen and warm joints
3. Redness and tenderness in the affected areas
4. Fatigue, fever, and loss of appetite
5. Loss of range of motion in the affected joints
6. Firm bumps of tissue under the skin (rheumatoid nodules)
RA can be diagnosed through a combination of physical examination, medical history, blood tests, and imaging studies such as X-rays or ultrasound. Treatment typically involves a combination of medications, including nonsteroidal anti-inflammatory drugs (NSAIDs), disease-modifying anti-rheumatic drugs (DMARDs), and biologic agents. Lifestyle modifications such as exercise and physical therapy can also be helpful in managing symptoms and improving quality of life.
There is no cure for RA, but early diagnosis and aggressive treatment can help to slow the progression of the disease and reduce symptoms. With proper management, many people with RA are able to lead active and fulfilling lives.
Virtual colony count
Transforming growth factor beta
Mesenchymal stem cell
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Publications by Schauber, Juergen
- The etiology of this disorder is unknown, although symptoms are exacerbated by factors that trigger innate immune responses, such as the release of cathelicidin antimicrobial peptides. (nih.gov)
- Here we show that individuals with rosacea express abnormally high levels of cathelicidin in their facial skin and that the proteolytically processed forms of cathelicidin peptides found in rosacea are different from those present in normal individuals. (nih.gov)
- These cathelicidin peptides are a result of a post-translational processing abnormality associated with an increase in stratum corneum tryptic enzyme (SCTE) in the epidermis. (nih.gov)
- In mice, injection of the cathelicidin peptides found in rosacea, addition of SCTE, and increasing protease activity by targeted deletion of the serine protease inhibitor gene Spink5 each increases inflammation in mouse skin. (nih.gov)
- We report that the bone marrow (BM) stroma-released LL-37, a member of the cathelicidin family of antimicrobial peptides, primes/increases the responsiveness of murine and human hematopoietic stem/progenitor cells (HSPCs) to an α-chemokine stromal-derived factor-1 (SDF-1) gradient. (nih.gov)
- Cathelicidins are a family of antimicrobial peptides which exhibit broad antimicrobial activities against antibiotic-resistant bacteria. (ac.ir)
- The cathelicidin family of antimicrobial peptides is an integral component of the innate immune response that exhibits activity against bacterial, fungal, and viral pathogens. (medscape.com)
- 7. Immunomodulatory and Anti-Inflammatory Activities of Chicken Cathelicidin-2 Derived Peptides. (nih.gov)
- 17. Cathelicidins PMAP-36, LL-37 and CATH-2 are similar peptides with different modes of action. (nih.gov)
- 11. Lehrer RI, Ganz T. Cathelicidins: a family of endogenous antimicrobial peptides. (bvsalud.org)
- Through skin biopsies, Gallo and his team found that people with rosacea had high levels of cathelicidins, peptides with antimicrobial and pro-inflammatory properties that protect the skin against infection. (nih.gov)
- Says Gallo, "Our findings help to show that antimicrobial peptides such as the cathelicidins, which are evolutionarily ancient elements of immune defense, play a critical role in inflammation. (nih.gov)
Serine protease activity1
- Cathelicidin, kallikrein 5, and serine protease activity is inhibited during treatment of rosacea with azelaic acid 15% gel. (bvsalud.org)
- 10. Chicken heterophils are recruited to the site of Salmonella infection and release antibacterial mature Cathelicidin-2 upon stimulation with LPS. (nih.gov)
- 18. Evidence of an antimicrobial-immunomodulatory role of Atlantic salmon cathelicidins during infection with Yersinia ruckeri. (nih.gov)
- A type of skin cell called a dermal fibroblast can make an antimicrobial compound called cathelicidin in response to infection by acne-causing bacteria. (nih.gov)
- 14. Differing effects of exogenous or endogenous cathelicidin on macrophage toll-like receptor signaling. (nih.gov)
- These findings confirm the role of cathelicidin in skin inflammatory responses and suggest an explanation for the pathogenesis of rosacea by demonstrating that an exacerbated innate immune response can reproduce elements of this disease. (nih.gov)
- Group A Streptococcal M1 protein sequesters cathelicidin to evade innate immune killing. (mpg.de)
- 12. Antimicrobial and immunomodulatory activities of an ovine proline/arginine-rich cathelicidin. (nih.gov)
- Considering the progressive antibiotic resistance, cathelicidin is a candidate for use as an alternative approach to treat and overcome the challenge of antimicrobial resistance. (ac.ir)
- Vitamin D stimulates the production of cathelicidin, a protein with natural antibiotic properties. (vitalitymagazine.com)
- Excess cathelicidin and kallikrein 5 (KLK5) have been hypothesized to play a role in the pathophysiology of rosacea . (bvsalud.org)
- Patients with rosacea showed reduction in cathelicidin and KLK5 messenger RNA after treatment with AzA gel. (bvsalud.org)
- One theory is that people with rosacea don't effectively process a protein called cathelicidin. (health.com)
- excessive production of both cathelicidin (LL-37) and kallikrein-5 (KLK5), the predominant serine protease enzyme responsible for cleavage of LL-37 from an inactive precursor form, has been suggested to play a pathophysiologic role in rosacea. (jcadonline.com)
- In separate experiments, Gallo's team then injected mice with cathelicidins found in rosacea, added SCTE, and increased SCTE by turning off the gene that inhibits its activity. (nih.gov)
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- Cathelicidin-BF (Cath-BF) is a short antimicrobial peptide, which was originally extracted from the venom of Bungarus fasciatus. (ac.ir)
- 2020. A mouse model for vitamin D-induced human cathelicidin antimicrobial peptide gene expression. . (oregonstate.edu)
- [ 10 ] An inverse correlation between cathelicidin expression and serum immunoglobulin E levels in patients with AD and patients with KVE has also been found. (medscape.com)
- What we found was that there was a correlation between the vitamin D status of the children and the salivary AMP cathelicidin LL-37-but it was the opposite of what we'd anticipated," said Karczewski. (nih.gov)
- 15. Chicken cathelicidins as potent intrinsically disordered biocides with antimicrobial activity against infectious pathogens. (nih.gov)
- Conclusions: Cathelicidin attenuated hyperoxia-induced lung injury and caused a decrease in 8-OHdG and SOD1 protein expression, most likely by inhibiting oxidative stress in the lung. (tmu.edu.tw)
- [ 9 ] Skin from patients with KVE exhibited significantly lower levels of cathelicidin protein expression than skin from patients with AD. (medscape.com)
- Investigators also discovered that levels of stratum corneum tryptic enzyme or SCTE - the enzyme responsible for cleaving the inactive cathelicidins into their active form - were also elevated in people with the disease. (nih.gov)
- The importance of cathelicidins in antiviral skin host defense was confirmed by the observation of higher levels of HSV-2 replication in cathelicidin-deficient mouse skin compared with that seen in skin from their wild-type counterparts. (medscape.com)
- The team also found higher levels of cathelicidin in samples taken from acne lesions than in nearby healthy skin. (nih.gov)
- The team also found increased cathelicidin production in inflamed areas of the skin after retinoic acid treatment in people. (nih.gov)
- 1. Importance of Endosomal Cathelicidin Degradation To Enhance DNA-Induced Chicken Macrophage Activation. (nih.gov)
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- It decreased the number of fat cells produced by reactive adipogenesis but increased cathelicidin production. (nih.gov)
- Together, these results suggest that retinoids work in part by stimulating production of cathelicidin while suppressing fat cell production. (nih.gov)
- Vitamin D upregulates production of human cathelicidin, which has both antimicrobial and antiendotoxin activities. (doctorsaredangerous.com)
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- Cathelicidin treatment attenuated hyperoxia-induced lung injury as demonstrated by lower MLI and injury score and higher VEGF expression and vascular density. (tmu.edu.tw)
- 20. Avian cathelicidins: paradigms for the development of anti-infectives. (nih.gov)
- This research could assist in identifying new treatment options that specifically target the fibroblast's ability to produce cathelicidin," O'Neill says. (nih.gov)
- Methods and materials: Sprague Dawley rat pups were reared in either room air (RA) or hyperoxia (85% O2) and then randomly treated with low-dose (4 mg/kg) and high-dose (8 mg/kg) cathelicidin in 0.05 mL of normal saline (NS) administered intraperitoneally on postnatal days 1-6. (tmu.edu.tw)
- This study evaluated the therapeutic effects of cathelicidin in hyperoxia-induced lung injury in newborn rats. (tmu.edu.tw)
- Jiang, JS , Chou, HC & Chen, CM 2020, ' Cathelicidin attenuates hyperoxia-induced lung injury by inhibiting oxidative stress in newborn rats ', Free Radical Biology and Medicine , 卷 150, 頁 23-29. (tmu.edu.tw)