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Retinoids in Hidradenitis Suppurativa/Acne Inversa
Published in Ayse Serap Karadag, Berna Aksoy, Lawrence Charles Parish, Retinoids in Dermatology, 2019
Uwe Wollina, Piotr Brzezinski, André Koch
HS pathogenesis is not completely understood. HS is not primarily infectious. The major contributors to the ongoing inflammatory process are a disturbed innate and adaptive immunologic response for bacterial control, a dramatically changed microbiome of skin surface and subcutaneous lesions, activation of Th17 cells, impaired interleukin-22 signaling pathway, and formation of bacterial biofilms (4–7). A minority of patients suffer from syndromic HS (Table 20.2) (8).
Clinical Implications of Interkingdom Fungal and Bacterial Biofilms
Published in Chaminda Jayampath Seneviratne, Microbial Biofilms, 2017
Gordon Ramage, Lindsay E. O’Donnell, Ryan Kean, Eleanor Townsend, Ranjith Rajendran
The CF lung is a site of intense interkingdom interaction, where P. aeruginosa is a primary participant. It has been shown that P. aeruginosa is able to selectively form biofilms on hyphae and kill C. albicans, but not the yeast form [224]. Presumably this occurs through the release of a phenazine toxin [225,226]. It has also been shown to inhibit the morphological transition through a 3-oxo-C12 homoserine lactone [227], a phenomenon replicated in studies of A. fumigatus biofilm [228]. Recent evidence from a murine model demonstrated that lung tissue injury caused by P. aeruginosa infection is alleviated if preceded by a short-term C. albicans colonisation [229]. This was a result of C. albicans activating interleukin-22 (IL-22) producing innate lymphoid cells, which provided protection from P. aeruginosa–induced injury [230]. Given the dynamic relationship between these organisms, it is not surprising that release of the QS molecule farnesol by C. albicans impacts P. aeurginosa by inhibiting its quinolone signalling, which controls pyocyanin production [231]. These studies highlight the ongoing and dynamic battle within a polymicrobial environment such as the CF lung, which clearly plays a crucial role in the overall pathogenesis of disease [150]. Elegant studies in a Drosophila infection model of polymicrobial infection demonstrate this point; they showed that microorganisms of the CF airways were able to influence the outcome of an infection depending on the presence or absence of P. aeruginosa [232,233].
Lung Disease and Ventilator Strategies in Necrotizing Enterocolitis
Published in David J. Hackam, Necrotizing Enterocolitis, 2021
Jegen Kandasamy, Namasivayam Ambalavanan
In addition to the confounding factors of extreme prematurity (i.e., both NEC and BPD are increasingly more common with lower gestational ages and greater immaturity for a given gestational age), the association between NEC and BPD likely reflects the fact that patients with NEC are often critically ill with abdominal distension, which impairs breathing, and this results in a need for prolonged mechanical ventilation. Prolonged ventilation then leads to ventilation-induced lung injury (VILI). It is possible that systemic inflammation and alterations in the gut microbiota associated with the development of NEC also contribute to lung injury and predispose to the development of BPD. This paradigm reflects the preterm infant equivalent of the “gut–lung axis” dysregulation that has been proposed in lung disorders in adults and older children (4). There is literature from mouse models that pulmonary epithelial toll-like receptor 4 (TLR4) activation leads to lung injury in the NEC model (5, 6), in addition to intestinal injury (7). Sensing of commensal bacteria by intestinal mucosal dendritic cells also leads to an influx of interleukin-22 (IL-22) producing group 3 innate lymphoid cells into the lungs of newborn mice (8). Dysregulation of this process by intestinal luminal pathogens may disturb lung innate immunity. Infants with NEC often receive prolonged courses of antimicrobials, and there is evidence that microbial depletion using broad-spectrum antimicrobials may increase susceptibility to VILI (5), which may also contribute to BPD in the setting of NEC. On the other hand, probiotic supplementation that has been shown to reduce NEC does not reduce the risk of BPD (9). Regardless of the exact mechanisms involved, NEC results in lung injury and is associated with chronic lung disease such as BPD and its long-term respiratory sequelae.
The role of microbiota in allogeneic hematopoietic stem cell transplantation
Published in Expert Opinion on Biological Therapy, 2021
Chia-Chi Chang, Eiko Hayase, Robert R. Jenq
Allo-HSCT is an important therapy that connects three promising areas of current clinical research: personalized cancer therapy, stem cell therapeutics and immune-modulating techniques [1]. The influence of the microbiome on disease pathophysiology, in particular on acute GVHD after allo-HSCT, has been explored by many researchers over several decades. Microbiota-derived metabolites can directly or indirectly influence allogeneic immune responses (Figure 1) [95]. The gut microbiome can vary depending on patient age in children pre-HSCT and gradually develops together with the host immune system [96]. The co-evolution between gut bacteria and their hosts can confer a mutually beneficial relationship to maintain homeostasis [97]. For example, SCFAs and tryptophan metabolites, serve as messengers to induce immune activation and modulate mucosal immunity in the host [95,98]. SCFAs can further shape the cytokine profiles and drive colonic regulatory T cells (Tregs) differentiation [60,99]. Tryptophan metabolites promote Th17 cell differentiation through Stat1 activation in the presence of AhR ligands [100]. AhR was reported to drive gut innate lymphoid (ILC)-22 development, which produce interleukin-22 as an early host defense against pathogenic infections [101,102]. A comprehensive understanding of how microbiota-derived metabolites modulate the human immune system will help guide the design of microbiota-based therapies in the allo-HSCT setting. Whether administration of live organisms is feasible and effective in controlling inflammation and regulating GVHD will require additional studies.
Interleukin-22 promotes the migration and invasion of oral squamous cell carcinoma cells
Published in Immunological Medicine, 2020
Shihoko Komine-Aizawa, Sohichi Aizawa, Chika Takano, Satoshi Hayakawa
Interleukin 22 (IL-22) is a member of the IL-10 cytokine superfamily produced by activated helper T cells and innate lymphocytes. The IL-22 receptor consists of IL-22 receptor 1 (IL-22R1) and IL-10 receptor 2 (IL-10R2). While IL-10R2 is widely expressed in various cells, IL-22R1 expression is restricted to epithelial cells. Therefore, IL-22 is considered to mediate the crosstalk between immune cells and tissue epithelial cells [1]. For instance, IL-22 induces the secretion of antimicrobial peptides from epithelial cells to protect mucosal surfaces from pathogens [2]. In human keratinocytes, the retardation of epidermal differentiation and the induction of proinflammatory-associated gene expression are caused by IL-22 [3,4]. Moreover, IL-22 promotes the migration of keratinocytes and induces hyperplasia of the reconstituted human epidermis.
CircRAB3B suppresses proliferation, motility, cell cycle progression and promotes the apoptosis of IL-22-induced keratinocytes depending on the regulation of miR-1228-3p/PTEN axis in psoriasis
Published in Autoimmunity, 2021
Jiajing Lu, Xin Xu, Ying Li, Ning Yu, Yangfeng Ding, Yuling Shi
Psoriasis is an inflammation-associated cutaneous disorder featured by the hyper-proliferation and aberrant migration of keratinocytes [1]. The therapeutic strategies for psoriasis contain physiotherapy and topical/systemic therapy [2]. However, psoriasis is easy to relapse, which limits the therapeutic efficacy. Interleukin-22 (IL-22) belongs to IL-10 cytokine family, and it facilitates the growth and motility and suppresses terminal differentiation of keratinocytes [3–5]. In this study, we investigated the pathogenesis of psoriasis using IL-22-induced keratinocytes to identify novel potential therapeutic targets.