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Acne vulgaris: A review of the pathophysiology, treatment, and recent nanotechnology based advances.Biochemistry and Biophysics Reports Dec 2023Globally, Acne Vulgaris is a widespread, chronic inflammatory condition of the pilosebaceous follicles. Acne is not fatal, but depending on its severity, it can leave... (Review)
Review
BACKGROUND
Globally, Acne Vulgaris is a widespread, chronic inflammatory condition of the pilosebaceous follicles. Acne is not fatal, but depending on its severity, it can leave the sufferer with scars, irritation, and significant psychological effects (including depression). In the current review, we have included various factors for acne and their treatment explained. It also narrated the current medicament and the new investigation dosage forms with clinical phases information provided.
MAIN BODY OF THE ABSTRACT
Acne's pathophysiology involves four important factors: excessive sebum production, hyperkeratinization of pilosebaceous follicles, hyperproliferation of propionibacterium acnes (P. acnes), and inflammation. Identifying both inflammatory (Papule, pustule, nodule, and cyst) and non-inflammatory (black heads, white heads) acne lesions is necessary for diagnosing and treating acne vulgaris.
SHORT CONCLUSION
In this review, traditional therapy approaches such as topical (i.e., retinoids and antibiotics), systemic (i.e., retinoids, antibiotics, and hormonal), and physical therapies are briefly discussed. In addition, we highlight the issues posed by P. acne's resistance to the antibiotics used in commercially available medications and the necessity for novel therapeutic techniques. Finally, we examined a few innovative acne therapies pending clinical trial approval and commercial acne medications.
PubMed: 38076662
DOI: 10.1016/j.bbrep.2023.101578 -
The Journal of Allergy and Clinical... Jul 2017Generalized pustular psoriasis (GPP) is a rare, debilitating, and often life-threatening inflammatory disease characterized by episodic infiltration of neutrophils into...
BACKGROUND
Generalized pustular psoriasis (GPP) is a rare, debilitating, and often life-threatening inflammatory disease characterized by episodic infiltration of neutrophils into the skin, pustule development, and systemic inflammation, which can manifest in the presence or absence of chronic plaque psoriasis (PV). Current treatments are unsatisfactory and warrant a better understanding of GPP pathogenesis.
OBJECTIVE
We sought to understand better the disease mechanism of GPP to allow improved targeted therapies.
METHODS
We performed a gene expression study on formalin-fixed paraffin-embedded GPP (n = 28) and PV (n = 12) lesional biopsies and healthy control (n = 20) skin. Differential gene expression was analyzed using gene ontology and enrichment analysis. Gene expression was validated with quantitative RT-PCR and immunohistochemistry, and a potential disease mechanism was investigated using primary human cell culture.
RESULTS
Compared with healthy skin, GPP lesions yielded 479 and PV 854 differentially expressed genes, respectively, with 184 upregulated in both diseases. We detected significant contributions of IL-17A, TNF, IL-1, IL-36, and interferons in both diseases; although GPP lesions furnished higher IL-1 and IL-36 and lower IL-17A and IFN-γ mRNA expression than PV lesions did. We detected prominent IL-36 expression by keratinocytes proximal to neutrophilic pustules, and we show that both neutrophils and neutrophil proteases activate IL-36. Suggesting another mechanism regulating IL-36 activity, the protease inhibitors serpin A1 and A3, which inhibit elastase and cathepsin G, respectively, were upregulated in both diseases and inhibited activation of IL-36.
CONCLUSIONS
Our data indicate sustained activation of IL-1 and IL-36 in GPP, inducing neutrophil chemokine expression, infiltration, and pustule formation, suggesting that the IL-1/IL-36 inflammatory axis is a potent driver of disease pathology in GPP.
Topics: Cells, Cultured; Cytokines; Humans; Keratinocytes; Neutrophils; Psoriasis; RNA, Messenger; Skin
PubMed: 28043870
DOI: 10.1016/j.jaci.2016.08.056 -
Frontiers in Medicine 2021Skin pathergy reaction (SPR) is a hyperreactivity response to needle induced trauma which is characterized by a papule or pustule formation, 24-48 h after sterile-needle... (Review)
Review
Skin pathergy reaction (SPR) is a hyperreactivity response to needle induced trauma which is characterized by a papule or pustule formation, 24-48 h after sterile-needle prick. It is affected by a wide array of factors, including the physical properties of the needles being used, number of pricks and disease related factors such as male gender, active disease. There is a great variation in reactivity among different populations with very low positivity rate in regions of low prevalence like Northern Europe, and higher prevalance mainly in communities living along the historical Silk Road, like Turkey, China and Middle Eastern countries. SPR is not constant during the disease course, has lost its sensitivity over decades and can be positive in various disorders including Sweet's syndrome, pyoderma gangrenosum, Crohn's diesease, A20 haploinsufficiency, deficiency of IL-1-receptor antagonist and few others. Nevertheless, it is a criteria included into many currently used diagnostic or classification criteria for Behçet's disease. Although, not being fully uncovered yet, available data points to the activation of both innate and adaptive immune system with an inflammatory response mediated by polymorphonuclears and T-cells. In addition to its utility in diagnosis of Behçet's Disease, SPR may serve as a model for investigating the inflammatory pathways involved in the etiopathogenesis of this complex disease.
PubMed: 34113630
DOI: 10.3389/fmed.2021.639404