RESUMEN
Cannabis allergy is a relatively new phenomenon described in the 1970s. Its increased frequency has been observed over the last years due to the increasing therapeutic and recreational use of cannabis-based products. Sensitization possibly leading to allergy symptoms can occur not only through the smoking of cannabis, but also through ingestion, the inhalation of pollen, or direct contact. The severity of symptoms varies from benign pruritus to anaphylaxis. There is scant information available to support clinicians throughout the entire therapeutic process, starting from diagnosis and ending in treatment. In this review, we present six cases of patients in whom molecular in vitro testing revealed sensitization to cannabis extract and/or cannabis-derived nsLTP molecules (Can s 3). Based on these cases, we raise important questions regarding this topic. The article discusses current proposals and highlights the importance of further research not only on cannabis allergy but also on asymptomatic sensitization to cannabis allergens, which may be ascertained in some percentage of the population.
Asunto(s)
Alérgenos , Cannabis , Inmunoglobulina E , Humanos , Alérgenos/inmunología , Alérgenos/efectos adversos , Cannabis/efectos adversos , Hipersensibilidad/inmunología , Hipersensibilidad/diagnóstico , Inmunoglobulina E/sangre , Inmunoglobulina E/inmunologíaRESUMEN
Vascular endothelium is a semi-permeable barrier that regulates the flow of nutrients, ions, cytokines and immune cells between blood and tissues. Barrier properties of endothelium, its ability to regenerate and the potential for secretion of inflammatory mediators play a crucial role in maintaining local tissue homeostasis. The lung vascular endothelial cells were shown to be infected by human rhinovirus (HRV) and generate antiviral, inflammatory and cytopathic responses. The current study reveals that in the long-time manner, the lung vascular endothelium may efficiently limit the HRV replication via the IFN-dependent 2'-5'-oligoadenylate synthetase 1 activation. This leads to the restoration of integrity accompanied by the up-regulation of adherens and tight junctions, increase of metabolic activity and proliferation rate. Secondly, HRV16-infected cells show delayed and transient up-regulation of the expression of vascular endothelial growth factor (VEGF), fibroblast growth factor, angiopoietin 1 and 2, and neuropilin-1, as well as VEGF receptors. The lung vascular endothelium infected with HRV may limit the infection, recover in time, and regain barrier properties and metabolic functions, thus leading to the restoration of integrated barrier tissue.
Asunto(s)
Rhinovirus , Factor A de Crecimiento Endotelial Vascular , 2',5'-Oligoadenilato Sintetasa , Angiopoyetina 1/metabolismo , Antivirales , Citocinas/metabolismo , Células Endoteliales , Endotelio Vascular , Factores de Crecimiento de Fibroblastos/metabolismo , Humanos , Mediadores de Inflamación/metabolismo , Interferones , Pulmón , Neuropilina-1/metabolismo , Receptores de Factores de Crecimiento Endotelial Vascular/metabolismo , Factor A de Crecimiento Endotelial Vascular/metabolismo , Replicación ViralRESUMEN
The effect of rhinovirus on airway epithelium is very well described. However, its influence on the vascular endothelium is unknown. The current study assesses the effect of rhinovirus HRV16 on the antiviral and inflammatory response in the human vascular endothelial cells (ECs). HRV16 increased IFN-ß, RANTES, and IP-10 mRNA expression and protein release. HRV16 copy number in ECs reached maximal value 10 h after incubation. Increase in virus copies was accompanied by the enhancement of Toll- and RIG-I-like receptors: TLR3, RIG-I, and MDA5. Additionally, HRV16 increased OAS-1 and PKR mRNA expression, enzymes responsible for virus degradation and inhibition of replication. ICAM-1 blockade decreased HRV16 copy number in ECs and inhibited IFN-ß, RANTES, IP-10, OAS1, PKR, TLR3, RIG-I, and MDA5 mRNA expression increase upon subsequent induction with HRV16. The vascular endothelium may be infected by human rhinovirus and generate antiviral and inflammatory innate response. Results of the study indicate the possible involvement of the vascular endothelium in the immunopathology of rhinoviral airway infections.
Asunto(s)
Endotelio Vascular/inmunología , Infecciones por Picornaviridae/inmunología , Rhinovirus/inmunología , Quimiocina CCL5/genética , Quimiocina CCL5/inmunología , Proteína 58 DEAD Box/genética , Proteína 58 DEAD Box/inmunología , Endotelio Vascular/virología , Células Endoteliales de la Vena Umbilical Humana/inmunología , Células Endoteliales de la Vena Umbilical Humana/virología , Humanos , Interferón beta/genética , Interferón beta/inmunología , Infecciones por Picornaviridae/genética , Infecciones por Picornaviridae/virología , Receptores Inmunológicos , Rhinovirus/genética , Receptor Toll-Like 3/genética , Receptor Toll-Like 3/inmunologíaRESUMEN
Irritable bowel syndrome (IBS), with the prevalence of 10%-20 % of the population has become an emerging problem worldwide. IBS is a functional gastrointestinal (GI) disorder characterized by abdominal pain or discomfort and altered bowel habits. The etiology of IBS contains genetic, psychological, and immunological factors, and has not been fully elucidated; of note, recent studies also point at environmental pollution and its role in the development of functional GI diseases. In this review we focus on several environmental factors, such as bacterial contamination, air pollution, radiation and even stress as potential triggers of IBS. We discuss associated disturbances in homeostasis, such as changes in intestinal microbiome and related pathophysiological mechanisms. Based on the effect of environmental factors on the GI tract, we also propose novel targets in IBS treatment.