A5088283502- Antimicrobial Peptides and Activities
- Dermatology and Skin Diseases
- Psoriasis: Treatment and Pathogenesis
- Immune Response and Inflammation
- Wound Healing and Treatments
- IL-33, ST2, and ILC Pathways
- Biochemical and Structural Characterization
- Pressure Ulcer Prevention and Management
- Asthma and respiratory diseases
- Pediatric health and respiratory diseases
- Lipid Membrane Structure and Behavior
- RNA Research and Splicing
- Bacteriophages and microbial interactions
- Urticaria and Related Conditions
- Peptidase Inhibition and Analysis
- Gut microbiota and health
- Probiotics and Fermented Foods
- Neuropeptides and Animal Physiology
- Skin Protection and Aging
- Osteoarthritis Treatment and Mechanisms
- Acne and Rosacea Treatments and Effects
- Antimicrobial Resistance in Staphylococcus
- T-cell and B-cell Immunology
- Inflammasome and immune disorders
- Bayesian Methods and Mixture Models
Nanchang University
2024-2025
East China Normal University
2015-2024
First Affiliated Hospital of Jiangxi Medical College
2024
Hunan University
2024
Guangdong Ocean University
2024
Beijing University of Posts and Telecommunications
2022
South China Agricultural University
2022
Kyushu University
2021
University of Cape Town
2017
National Taichung University of Science and Technology
2017
Abstract NF-κB is constitutively activated in psoriatic epidermis. However, how promotes keratinocyte hyperproliferation psoriasis largely unknown. Here we report that the activation triggered by inflammatory cytokines induces transcription of microRNA (miRNA) miR-31, one most dynamic miRNAs identified skin patients and mouse models. The genetic deficiency miR-31 keratinocytes inhibits their hyperproliferation, decreases acanthosis reduces disease severity Furthermore, protein phosphatase 6...
Summary Staphylococcus aureus is a leading cause of hospital‐associated and, more recently, community‐associated infections caused by highly virulent methicillin‐resistant strains (CA‐MRSA). S. survival in the human host largely defined ability to evade attacks antimicrobial peptides (AMPs) and other mechanisms innate defence. Here we show that AMPs induce resistance CA‐MRSA via aps AMP sensor/regulator system, including (i) d ‐alanylation teichoic acids, (ii) incorporation...
To survive during colonization or infection of the human body, microorganisms must circumvent mechanisms innate host defense. Antimicrobial peptides represent a key component defense, especially in phagocytes and on epithelial surfaces. However, it is not known how clinically important group Gram-positive bacteria sense antimicrobial to coordinate directed defensive response. By determining genome-wide gene regulatory response beta-defensin 3 nosocomial pathogen Staphylococcus epidermidis,...
Antimicrobial peptides play an important role in host defense against pathogens. Recently, phenol-soluble modulins (PSMs) from Staphylococcus epidermidis (S. epidermidis) were shown to interact with lipid membranes, form complexes, and exert antimicrobial activity. Based on the abundance innocuity of cutaneous resident S. epidermidis, we hypothesized that their PSMs contribute defense. Here show delta-toxin (PSMgamma) is normally present epidermis sparsely dermis human skin using...
Summary Antimicrobial peptides (AMPs) represent a key component of innate host defence against bacterial pathogens. Bacterial resistance mechanisms usually depend on the characteristic positive charge AMPs. However, several human cell types also produce anionic AMPs, to which are poorly understood. Here we demonstrate that skin commensal and leading nosocomial pathogen Staphylococcus epidermidis senses efficiently inactivates AMP dermcidin. Dermcidin induced differential expression global...
T helper 17 (TH17) cells and interleukin-17A (IL-17A) produced by them are critical in autoinflammatory diseases, such as psoriasis. IL-17A has been shown to signal through IL-17 receptor A/IL-17 C (IL-17RA/IL-17RC) complex drive inflammatory responses. However, a psoriasis model, we found that Il17rc deficiency did not completely ameliorate the disease, suggesting another receptor. In search for IL-17A-interacting receptor, IL-17RD directly bound but IL-17F or IL-17A/F heterodimer formed...
Staphylococcus epidermidis (S. epidermidis) plays a critical role in modulating cutaneous inflammatory responses skin. Although S. has been shown to co-colonize with Propionibacterium acnes (P. acnes) acne lesions, it is unclear whether involved the regulation of P. acnes-induced responses. In this study, we demonstrated that inhibited inflammation induced expression interleukin-6 and tumor necrosis factor-α via activation toll-like receptor (TLR) 2 both keratinocytes mouse ears....
Dysregulated inflammatory responses are known to impair wound healing in diabetes, but the underlying mechanisms poorly understood. Here we show that antimicrobial protein REG3A controls TLR3-mediated inflammation after skin injury. This control is mediated by REG3A-induced SHP-1 protein, and acts selectively on TLR3-activated JNK2. In diabetic mouse skin, hyperglycaemia inhibits expression of IL-17-induced IL-33 via glucose glycation. The decrease cutaneous reduces epidermal keratinocytes....
Abstract Aberrant RNA splicing in keratinocytes drives inflammatory skin disorders. In the present study, we found that helicase DDX5 was downregulated from lesions patients with atopic dermatitis and psoriasis, mice keratinocyte-specific deletion of Ddx5 ( ∆KC ) were more susceptible to cutaneous inflammation. Inhibition expression induced by cytokine interleukin (IL)-17D through activation CD93–p38 MAPK–AKT–SMAD2/3 signaling pathway led pre-messenger events favored production...
Skin injury always results in fibrotic, non-functional scars adults. Although multiple factors are well-known contributors to scar formation, the precise underlying mechanisms remain elusive. This review aims elucidate intricacies of wound healing process, summarize known driving skin cells wounds toward a scarring fate, and particularly discuss impact fibroblast heterogeneity on formation. To end, we explore potential therapeutic interventions used treatment wounds.
Abstract Hyaline cartilage fibrosis is typically considered an end-stage pathology of osteoarthritis (OA), which results in changes to the extracellular matrix. However, mechanism behind this largely unclear. Here, we found that RNA helicase DDX5 was dramatically downregulated during progression OA. deficiency increased phenotype by upregulating COL1 expression and downregulating COL2 expression. In addition, loss aggravated degradation inducing production cartilage-degrading enzymes....
Abstract Mast cells (MC) express cathelicidin antimicrobial peptides that act as broad-spectrum antibiotics and influence the immune defense of multiple epithelial surfaces. We hypothesized MC help protect against skin infection through expression cathelicidin. The susceptibility MC-deficient mice (Kit Wsh−/−) to invasive group A streptococcus (GAS) was compared with control mice. Following s.c. injection GAS, had 30% larger lesions, 80% more lesional bacteria, spleens positive for bacteria....
Mast cells (MCs) are well-known effectors of allergic reactions and considered sentinels in the skin mucosa. In addition, through their production cathelicidin, MCs have capacity to oppose invading pathogens. We therefore hypothesized that could act as against viral infections using antimicrobial peptides. this study, we demonstrate react vaccinia virus (VV) degranulate a membrane-activated pathway leads peptide discharge inactivation. This finding was supported mouse model infection....