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Cough Formation in Viral Infections in Children
Published in Sunit K. Singh, Human Respiratory Viral Infections, 2014
O’Grady Kerry-Ann F., Ian M. Mackay, Anne B. Chang
Protracted bacterial bronchitis (PBB), a type of chronic airway inflammation in children, is a recent diagnostic clinical entity.66 PBB is associated with persistent bacterial infection in the airways66 and it is widely accepted that persistent bacterial infection is harmful to the airways.67 The organisms most commonly identified in the airways (sputum or bronchoalveolar lavage, BAL) of children with PBB are common respiratory bacteria, that is, nontypeable Haemophilus influenzae, S. pneumoniae, and Moraxella catarrhalis.66 However, transient viral ARIs in early childhood commonly precede PBB as the most common initiating event; more recent studies have found virus–bacteria coinfections in the BAL of children with PBB and wet cough.68 Disease mechanisms involved in PBB include neutrophilic inflammation, innate immunity upregulation in the airways,69and altered expression of both the toll-like receptor (TLR)-4 and the preprotachykinin gene, TAC1, that encodes substance P.70
Antifungal drug resistance: Significance and mechanisms
Published in Mahmoud A. Ghannoum, John R. Perfect, Antifungal Therapy, 2019
Sharvari Dharmaiah, Rania A. Sherif, Pranab K. Mukherjee
Transcriptional regulation of sterol biosynthesis genes plays a critical role in azole resistance and include zinc cluster proteins transcription factors (Zn2-Cys6 TFs) like TAC1 (transcriptional activator of CDR genes), MRR1/2 (multidrug resistance regulators that regulate MDR1), and UPC2 (activates the expression of related genes in response to sterol depletion through a conserved C-terminal domain) [152–162]. Recently, Hagiwara et al. [163] identified a novel Zn2-Cys6 Transcription Factor AtrR that co-regulates CYP51A and Cdr1B expression (by direct binding to both CYP51A and Cdr1B promoters) in A. fumigatus, A. oryzae, and A. nidulans, thus playing a critical role in azole resistance in these Aspegillus species. These investigators showed that while AtrR was responsible for the expression of CDR1B, SrbA was not involved in this process. Fluconazole-induced “microevolution” in C. albicans has also been suggested as a broader mechanism of resistance and comprises genomic rearrangements that result in gene amplification and loss of heterozygosity for resistance mutations (e.g., in mating type locus MTL), which further increases drug resistance and may also affect extended chromosomal regions with ancillary phenotypic effects [164]. For example, mutations in MTL allows the fungal cells to switch to the mating-competent opaque phenotype, allowing sexual recombination that may result in the generation of highly fluconazole-resistant strains with multiple resistance mechanisms.
STAT1 participates in the induction of substance P expression in airway epithelial cells by respiratory syncytial virus
Published in Experimental Lung Research, 2020
Yu-Long Luo, Sheng Wang, Zhi-Xin Fang, Yi-Chu Nie, Li-Ting Zhang, Chu-Qin Huang, Li Long, Ke-Fang Lai
Substance P (SP) is a tachykinin encoded by the TAC1 gene and is believed to be a transmitter of nociception related to noxious stimuli. SP is mainly expressed and secreted by neuronal cells, but non-neuronal cells such as immune cells, smooth muscle cells, endothelial cells, and airway epithelial cells are also sources of SP.1–4 SP activation of its specific receptors (neurokinin receptor 1/2/3) initiates G protein-mediated signaling events and induces diverse effects, including neuronal excitation, inflammation, cell migration, and proliferation in various types of cells in order to modulate pain, vascular permeability, smooth muscle contraction, mucus secretion, inflammation response, and tissue repair.5–8 In airway epithelium, viral infection, allergen stimulation, and smoking have been found to promote the expression of SP and its receptors and to inhibit enzymatic degradation, which are associated with enhanced airway inflammation and airway hyperresponsiveness.3,9,10 Antagonization of SP receptor is potential in treating these SP-induced inflammation.5 SP is also a facilitator of antiviral responses and acts as an antimicrobial to certain invasive microbes.11,12
The role of systemic corticosteroids in severe asthma and new evidence in their management and tapering
Published in Expert Review of Clinical Immunology, 2021
Francesco Menzella, Giulia Ghidoni, Matteo Fontana, Silvia Capobelli, Francesco Livrieri, Claudia Castagnetti, Nicola Facciolongo
In this regard, the results obtained by the U-BIOPRED cohort could open to new scenarios in terms of possible future application [114]. Three transcriptome-associated clusters (TACs) have been defined: Th2-high eosinophilic phenotype TAC1, and two non-Th2 phenotypes TAC2 and TAC3. The TAC1 phenotype is specific for severe asthma with oral corticosteroid dependency, frequent exacerbations and severe airflow obstruction. This innovative approach thus provides a new framework on how to phenotype asthma; it also offers a more precise and specific way to target certain treatments and consequently the chance to reduce the use of OCS.
Identification of vascular dementia and Alzheimer's disease hub genes expressed in the frontal lobe and temporal cortex by weighted co-expression network analysis and construction of a protein–protein interaction
Published in International Journal of Neuroscience, 2022
Xiaodou Tian, Yao Qin, Yuling Tian, Xiaoyan Ge, Jing Cui, Hongjuan Han, Long Liu, Hongmei Yu
TAC1SP is traditionally associated with increased vascular permeability and subsequent plasma protein exosmosis; therefore, it is considered to be the most effective initiator of neurogenic inflammation [46]. In a recent study, qRT-PCR was used to analyze the hippocampus of a large number of dead AD patients. This confirmed the downregulation of TAC1 and the upregulation of the gene encoding plasminogen activator inhibitor 1 (SERPINE1). Pathway analysis revealed dysregulation of neural network, cerebrovascular and amyloid clearance [47].