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Phytomedicines Targeting Antibiotic Resistance through Quorum Sensing and Biofilm Formation Associated with Acne Vulgaris
Published in Namrita Lall, Medicinal Plants for Cosmetics, Health and Diseases, 2022
Isa A. Lambrechts, Namrita Lall
Staphylococcus epidermidis produce Enterococcus faecalis surface proteins (Esp) that inhibit proteins involved in S. aureus biofilm production and growth. This serine protease enhances the antimicrobial activity of human beta-defensin-2 (hBD2) produced by keratinocytes due to inflammation but does not have antibacterial activity against Gram-positive bacteria alone. Furthermore, S. epidermidis releases antimicrobial molecules such as phenol-soluble modulins (PSMs) that cause membrane leakage and targets mostly Streptococcus pyogenes and S. aureus. Cutibacterium acnes, another commensal skin bacterium, can protect the skin from pathogens such as methicillin-resistant S. aureus (MRSA). Cutibacterium acnes protects the skin from pathogens through fermenting glycerol, a product of sebum triglyceride hydrolysis, lowering the pH and inhibiting MRSA growth (Schröder and Harder, 1999; Sanford and Gallo, 2013).
Dental Disease, Inflammation, Cardiovascular Disease, Nutrition and Nutritional Supplements
Published in Stephen T. Sinatra, Mark C. Houston, Nutritional and Integrative Strategies in Cardiovascular Medicine, 2022
Douglas G. Thompson, Gregori M. Kurtzman, Chelsea Q. Watkins
Utilizing modern salivary diagnostic tests or a combination of them can significantly enhance the practitioner’s knowledge about the initiators of the periodontal disease process. Just like the tests for oral pathogens, tests also exist for genetic mutations that may affect the disease process. These tests identify potential genetic mutations that may increase the risk of acquiring periodontal disease or reacting more severely to the disease if the patient already has it. Examples of some of the genes significant to this and other inflammatory disease processes are beta-defensin 1, CD14, toll-like receptor 4, tumor necrosis factor-alpha, interleukin-1, interleukin-6, interleukin-17A and matrix metallopeptidase 3. The Celsus OneTM (OralDNA® Labs, Eden Prairie, MN) test evaluates for mutations in eight gene markers related to a potential exaggerated inflammatory response: IL-1 composite genotype, IL-6, IL-17 A, beta-defensin 1, CD14, tumor necrosis factor-alpha, toll-like receptor 4 composite genotype and matrix metalloproteinase 3. These gene mutations are associated with an increased risk for more severe periodontal infections, as well as increased risk for periimplantitis (periodontal disease associated with dental implants), diabetes and cardiovascular disease (Figure 14.2).95,96
Host–Biofilm Interactions at Mucosal Surfaces and Implications in Human Health
Published in Chaminda Jayampath Seneviratne, Microbial Biofilms, 2017
Nityasri Venkiteswaran, Kassapa Ellepola, Chaminda Jayampath Seneviratne, Yuan Kun Lee, Kia Joo Puan, Siew Cheng Wong
In humans, a wide variety of proteins and peptides exhibit antimicrobial activity. Host-derived antimicrobial peptides (AMPs) form an essential part of the innate immune system. Defensins were the first natural antimicrobial peptides to be described in mammalian cells. Originally isolated from epithelial cells and neutrophils, they are small cationic peptides and function by binding to the bacterial plasma membrane. Defensins cause a disruption of the membrane integrity resulting in inhibition of DNA, RNA and protein synthesis. The nature of the interaction allows defensins to target both Gram-positive and Gram-negative bacteria, fungi and enveloped viruses. Two classes of defensins have been described in humans, alpha and beta. Both types consist of six conserved cysteine residues. Alpha-defensins are synthesised by polymorphonuclear leukocytes and Paneth cells. In contrast to alpha-defensins, beta-defensins are secreted by epithelial cells in the respiratory, gastrointestinal and urinary tracts. Defensins are secreted at low levels under normal physiological conditions but can be induced in response to microbial infections. Since their discovery, other functional roles have been ascribed to defensins [139]. For instance, alpha-defensins such as HNP1-3 have been demonstrated to function as chemoattractants for dendritic cells and naïve CD4 and CD8 T cells [140]. Alpha-defensins derived from human neutrophils have been shown to neutralise the anthrax lethal toxin [141], diphtheria toxin and Pseudomonas exotoxin A [141]. Recent investigations on human beta-defensin-3 have revealed its link to oral cancer [142].
Elevated Tear Human Neutrophil Peptides 1-3, Human Beta Defensin-2 Levels and Conjunctival Cathelicidin LL-37 Gene Expression in Ocular Rosacea
Published in Ocular Immunology and Inflammation, 2019
Nesrin Büyüktortop Gökçınar, Ayşe Anıl Karabulut, Zafer Onaran, Erhan Yumuşak, Fatma Azize Budak Yıldıran
The alpha- and beta-defensin family and cathelicidin are the main AMPs in humans.6 Ribonucleases, S100-alarmins (S100As), and liver-expressed antimicrobial peptides (LEAPs) are other less known families of AMPs.12 Alpha-defensins 1–4 are expressed in neutrophil granules and named as human neutrophil peptides (HNPs).13 Beta-defensins are produced by epithelial cells of the skin, ocular surface, urinary, gastrointestinal, and respiratory system.14 The only human cathelicidin, leucine leucine-37 (LL-37), is produced by many cell types such as myeloid cells, neutrophils, mast cells, monocytes, colon enterocytes, keratinocytes, and epithelial cells lining the oral cavity, ocular surface, respiratory, urogenital, and gastrointestinal tracts.13,14
Vitamin D receptor gene polymorphism and vitamin D supplementation on clinical/ treatment outcome in tuberculosis: current and future perspectives
Published in Expert Review of Anti-infective Therapy, 2022
Sonal Sekhar Miraj, Navya Vyas, Shilia Jacob Kurian, Tejaswini Baral, Levin Thomas, B Shrikar Reddy, Murali Munisamy, Mithu Banerjee, Mahadev Rao
Currently, the link between vitamin D and TB is a major area of interest. An association has been found between vitamin D deficiency (VDD) and increased susceptibility to as well as the severity of TB [2]. 1,25-Dihydroxy vitamin D, a vitamin D metabolite, which is biologically active, is a potent immunomodulatory molecule that works via vitamin D receptor (VDR) to stimulate macrophages to restrict the growth of Mycobacterium tuberculosis (MTB) in vitro [3] (Figure 1). Active metabolite also enhances innate immune response by inducing cathelicidin, an antimicrobial peptide (AMP), and intermediates of reactive oxygen species (ROS). Pathogen-associated molecular patterns (PAMPs) are present on the microbe surfaces that are recognized by toll-like receptors (TLRs) located on the antigen-presenting cells such as macrophages, dendritic cells, and polymorphonuclear cells, facilitating the adaptive immune system [4]. The TLRs on binding to the targets secrete cytokines and chemokines that induce the expression of AMPs. VDR can modulate the TLR activity and vice versa [5,6]. In various human cell lines such as neutrophils, myeloid cells, keratinocytes, and monocytes/macrophages, it is also demonstrated that vitamin D induces the transcription of cathelicidin and defensins that aid in phagocytosis [7,8]. Beta-defensins are upregulated in the presence of TLR2/1 mediated IL-1β, which has marked antimicrobial activity against MTB [9]. TLR activation in human macrophages enhances VDR expression and 25-hydroxyvitamin D 1-alpha-hydroxylase (VD1A hydroxylase, also known as CYP27B1) that can further induce cathelicidin. Moreover, 1,25-dihydroxy vitamin D promotes the differentiation of monocytes/macrophages and enhances their chemotactic and phagocytic capacity [4].
The expression of β-Defensin-2, IL-22, IL-22R1 and IL-10R2 in rat model of Klebsiella pneumonia and their correlation with histological grades
Published in Experimental Lung Research, 2020
Jianyong Fan, Yuan Luo, Yan Qin, Changgui Wu, Xinpeng Han, Haifeng Ouyang, Liyuan Zhang, Pei Cai, Nie Li
Defensins are strongly cationic peptides which have broad-spectrum anti-bacterial activities against various gram-positive and gram-negative bacteria, mycobacteria in the physiological condition. Among them, beta-defensin-2(βD2) is expressed by cells in lung, brain, and liver [7].Many studies indicated that pore formation on microbial membrane is the key mechanism defensins-mediated anti-bacterial activities [8]. Lehrer et al. [9] reported that defensins penetrated cell membrane of E. coli and induced cell death, suggesting that the anti-bacterial activities of defensins are based on the sensitive reaction of defensins expression to bacteria. In our study, we found elevated protein and gene expression of beta-defensin-2 in rat lungs at early stage of pneumonia. Expression of beta-defensin-2 reached peak at 3d and then decreased. These results demonstrate that rat β-defensin-2 is secreted by cells in lung tissue and is up-regulated by Klebsiella pneumonia-infection. In addition, the histological grades of pneumonia was significantly correlated with protein expression of β-defensin-2 and serum level of IL-22. Similarly, Routsias et al. [10, 11] observed that human defensin-2 showed high bactericidal activity against Acinetobacter baumannii, Pseudomonas aeruginosa, Enterococcus faecalis, Enterococcus faecium and Staphylococcus aureus. Morrison et al. [12] revealed that the number of Staphylococcus aureus in the urine and bladder from Detbl–/– mice was significantly higher than that from wild-type mice. It is also reported that polysaccharide capsular of K. pneumoniae could protect the pathogens and inhibit the expression of β-defensin-1, β-defensin-2 and β-defensin-3 [13], but the underlying mechanisms remain unclear. In the present study, we found no evidence that supported K. pneumoniae inhibited the expression of β-defensin-2 in rat lung. Further study will be performed to investigate the mechanism for the antimicrobial effect of beta-defensins. On the other hand, many factors including ion concentration and bacterial factors could regulate anti-bacterial activities of defensins and thus affect the pathogenesis of pneumonia. For example, human beta-defensin-1 lost its antimicrobial activity when the concentration of Na+ >150 mmol/L [14].