RESUMEN
The pandemic COVID-19 abruptly exploded, taking most health professionals around the world unprepared. Italy, the first European country to be hit violently, was forced to activate the lockdown in mid-February 2020. At the time of the spread, a high number of victims were quickly registered, especially in the regions of Northern Italy which have a high rate of highly-polluting production activities. The need to hospitalize the large number of patients with severe forms of COVID-19 led the National Health System to move a large number of specialists from their disciplines to the emergency hospital departments for the treatment of COVID-19. Furthermore, the lockdown itself has limited the possibility for general practitioners and pediatricians to be able to make outpatient visits and/or home care for patients with chronic diseases. Among them, the patient with atopic diseases, such as asthma, rhinitis and atopic dermatitis, is worthy of particular attention as she/he is immersed in a studded negative scenario with the onset of spring, a factor that should not be underestimated for those who suffer from pollen allergy. The Italian Society of Asthma Allergology and Clinical Immunology, to quickly deal with the lack of references and specialist medical procedures, has produced a series of indications for immunologic patient care that are reported in this paper, and can be used as guidelines by specialists of our discipline.
Asunto(s)
Vacuna BCG , Infecciones por Coronavirus , Coronavirus , Pandemias , Neumonía Viral , Betacoronavirus , COVID-19 , Humanos , Sistema Inmunológico , SARS-CoV-2 , VacunaciónRESUMEN
Ultraviolet A (UVA) rays penetrate the dermis, influencing the function of different cells, including mast cells, able to produce angiogenic factors. We investigated vascular endothelial growth factor (VEGF) release and gene-expression from mast cells (MCs), after UVA irradiation in vitro. The release of VEGF-A by Human MCs-1 (HMC-1) was induced by calcium ionophore A23187 and phorbol 12 myristate 13 acetate (PMA). Half of the cells received increasing doses of UVA (5, 25 and 50 J/cm(2)), the unirradiated HMC-1 served as controls. VEGF release and VEGF's messenger ribonucleic acid (mRNA) were detected respectively by enzyme-linked immunoabsorbent assay (ELISA) and reverse transcription-polymerase chain reaction (RT-PCR) analysis. Results showed a UVA dose-dependent inhibitory effect on VEGF-A release from HMC-1. In particular, the release ability was reduced by 71.2% with 5 J/cm(2); 85% with 25 J/cm(2) and 86.3% with 50 J/cm(2). The VEGF-A RNA expression was reduced after UVA irradiation with 5 J/cm(2). We speculated that, at least in vitro and at our experimental conditions, UVA irradiation decreases mast cells-VEGF release and gene-expression.
Asunto(s)
Regulación de la Expresión Génica/efectos de la radiación , Factor A de Crecimiento Endotelial Vascular/biosíntesis , Calcimicina/farmacología , Ionóforos de Calcio/farmacología , Carcinógenos/farmacología , Línea Celular Tumoral , Relación Dosis-Respuesta en la Radiación , Regulación de la Expresión Génica/efectos de los fármacos , Humanos , Mastocitos , ARN Mensajero/biosíntesis , Acetato de Tetradecanoilforbol/farmacología , Rayos UltravioletaRESUMEN
Helicobacter pylori-derived peptide RpL1 aa 2-20 (Hp(2-20)) in addition to its antimicrobial action exerts several immunomodulatory effects in eukaryotic cells by interacting with formyl peptide receptors (FPRs). It has recently been shown that activation of FPRs facilitates intestinal epithelial cell restitution. We investigated whether Hp(2-20) induces healing of injured gastric mucosa and assessed the mechanisms underlying any such effect. We investigated the expression of FPRs in two gastric epithelial cell lines (MKN-28 and AGS) at mRNA and protein level. To determine whether FPRs were functional we performed chemotaxis experiments and proliferation assays and studied the Hp(2-20)-activated downstream signaling pathway. The effect of Hp(2-20) on mucosal healing was evaluated in rats after indomethacin-induced injury. Here we show that: (1) FPRs were expressed in both cell lines; (2) Hp(2-20) stimulated migration and proliferation of gastric epithelial cells; (3) this effect was specifically mediated by formyl peptide receptor-like 1 (FPRL1) and FPRL2 and was associated with activation of FPR-related downstream signaling pathways; (4) Hp(2-20) up-regulated the expression and secretion of vascular endothelial growth factor; and (5) Hp(2-20) accelerated healing of rat gastric mucosa after injury brought about by indomethacin at both the macroscopic and microscopic levels. In conclusion, by interacting with FRPL1 and FPRL2, H. pylori-derived Hp(2-20) induces cell migration and proliferation, as well as the expression of vascular endothelial growth factor, thereby promoting gastric mucosal healing. This study provides further evidence of the complexity of the relationship between H. pylori and human gastric mucosa, and it suggests that a bacterial product may be used to heal gastric mucosal injury.
Asunto(s)
Proteínas Bacterianas/farmacología , Movimiento Celular/efectos de los fármacos , Proliferación Celular/efectos de los fármacos , Mucosa Gástrica/citología , Fragmentos de Péptidos/farmacología , Receptores de Formil Péptido/metabolismo , Cicatrización de Heridas/efectos de los fármacos , Animales , Línea Celular Tumoral , Células Epiteliales/efectos de los fármacos , Mucosa Gástrica/lesiones , Helicobacter pylori/química , Humanos , Indometacina , Ratas , Neoplasias Gástricas/patologíaRESUMEN
Background: Epidemiological studies show that BCG-vaccinated population seems to be more likely protected from COVID-19 infection, but WHO gave a stark warning on use of BCG vaccine without confirmed COVID-19 trials. The aim of the study is to evaluate whether TB vaccination, performed several years earlier, could confer protection against COVID-19. Methods: After the Ethical Committee authorization, professional orders were used to contact physicians with an online survey. Specialty, COVID-19 infection and previous BCG vaccination were recorded. Statistical data analysis was performed. Results: 1906 physicians answered the questionnaire, (M = 1068; F = 838; mean age 50.7 ± 13.3 years; range 24-87), more than half (1062; 55.7%) experienced BCG vaccination. Professional activity was recorded, and only 49 subjects (2.6%) of them were infected by SARS-CoV2. Among the group of infected people, asymptomatic form occurred in 12 subjects (24.5%); a pauci-symptomatic form in 24 subjects (49.0%); and a severe form (pneumonia and/or respiratory distress) in 13 (26.5%). Considering only the clinically relevant form of COVID-19, period prevalence was 2.2% (23/1062) in the vaccinated group and 1.7% (14/844) in the unvaccinated group (OR: 1.31, 95% C.I.: 0.68-2.63, p = 0.427). Conclusion: Our experience does not confirm the possible protective role of BCG vaccination, performed years earlier, against COVID-19. Although recent epidemiological studies point out in BCG-vaccinated population a lower prevalence of SARS-CoV2 infection, in our cohort of physicians no significant difference was found in terms of prevalence of COVID-19 infection. Our data underline the necessity to follow the WHO warning about the indiscriminate use of BCG vaccine, until clear evidence of protection by BCG vaccination against COVID-19 is fully demonstrated.
RESUMEN
Psoriasis is a chronic inflammatory disorder resulting from a combination of genetic and environmental factors, although the precise causal agents have not yet been identified. The immune system has a major role in the development of psoriasis, and the possibility exists that self antigens, antigens from microbial agents, or microbial superantigens initiate a vigorous immune response. Different subsets of T lymphocytes and dendritic cells, mast cells, and granulocytes participate in the pathogenesis; and several cytokines and chemokines have been identified in tissue lesions. Tumor necrosis factor-alpha, interleukin 17 (IL-17), and IL-23 are key cytokines with important pathogenetic roles in psoriasis. Angiogenesis is a prominent early event in lesional psoriatic skin. Potential targets in the treatment of this disorder include biologic agents aimed at blockade of cytokines, chemokines, and angiogenic factors.