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Hypersensitivity to Hymenoptera venom, occurring in approximately 3-5% of the population in Europe and the United States, is an important and difficult medical problem due to the fact that reactions after stings may pose a direct threat to life. In most cases, allergic reactions after stings are IgE-dependent, which is confirmed by the presence of specific IgE antibodies in the skin and/or serum against venom allergens. Diagnosing of hypersensitivity to Hymenoptera venom is often very difficult. This article presents the case of a patient who, as a result of her first bee sting, suffered a toxic-inflammatory reaction despite the presence of specific IgE antibodies to icarapine (rApi m10) detected in in vitro diagnostics. After a few years, the second sting, this time by a wasp, led to an anaphylactic reaction with abdominal symptoms predominating. Despite the lack of sIgE to wasp venom allergens in in vitro tests, hypersensitivity was confirmed in intradermal tests using wasp venom extract. After the final diagnosis was made, the patient was qualified for „ultra-rush” specific alergen immunotherapy using wasp venom extract. In each case, it is necessary to perform extensive diagnostics to confirm the immunological background of the reaction, which is also necessary to determine indications for the implementation of specific allergen venom immunotherapy. [ABSTRACT FROM AUTHOR]

According to the newest research human lung microvascular endothelial cells express receptors that respiratory viruses can bind to in order to infect said cells. Furthermore, endothelial cells express PRR receptors, responsible for generation of non specific immune response. Cytokines produced by endothelium besides their immunoprotective capabilities, can also take part in pathologies exacerbating symptoms of chronic diseases such as asthma. There are few scientific reports regarding the potential of endothelial cells to produce inflammatory and antiviral cytokines, as well as PRRs' role in these processes. Aim The aim of the study was to evaluate the generation of inflammatory and antiviral responses of endothelial cells in vitro, after stimulation with TLR agonist - poly(I:C). Material and methods Level of mRNA expression was studied for proinflammatory cytokines - IL-6, IL-8, RANTES, as well as for antiviral proteins - IFN-γ, OAS1, PKR. The expression of mRNA was evaluated using Real time PCR. Results Our studies suggest that TLR3 receptor is the key receptor involved in immune mechanisms generated by endothelium. This receptor shows great capability to induce expression of mRNA coding proinflammatory and antiviral proteins. Poly(I:C) in vitro stimulated HMVEC L cells with great effect, mimicking viral infection. Moreover poly(I:C) stimulation led to an increased expression of mRNA for all tested genes. Conclusions Literature data and our research shows, that endothelial cells are well adapted to recognition of viral RNA, resulting in generation of inflammatory and antiviral response. [ABSTRACT FROM AUTHOR]

Human rhinovirus 16 (HRV16) may induce inflammatory and antiviral responses in the human lung vascular endothelium (ECs) and impair its barrier functions after infection. However, ECs may regain barrier and metabolic functions. Mechanisms of limitation of HRV16 infection in the lung vascular endothelium are unknown. Human lung vascular endothelium (HMVEC-L) was infected with HRV16. IFN-β, OAS-1, and PKR expression was assessed by real-time PCR, flow cytometry, and confocal microscope. To prove the significance of IFN-β in the limitation of HRV16 replication, HMVEC-Ls were preincubated with anti-IFN-β Abs. To prove the involvement of OAS-1 and PKR in the IFNdependent limitation of HRV16 replication, HMVEC-Ls were transfected with respective siRNA. HRV16 stimulated IFN-β production and activated intracellular mechanisms of antiviral immunity based on OAS-1 and PKR activation. Blocking of IFN-β contributed to the inhibition of intracellular mechanisms of antiviral immunity (OAS-1, PKR) and boosted replication of HRV16. Effective OAS-1 silencing by siRNA caused the increase of HRV16 copy numbers after HRV16 infection. siRNA upregulated the other genes related to the antiviral response. The infected lung vascular endothelium may limit the HRV16 infection. This limitation may be associated with the induction of IFN-β-dependent intracellular mechanisms based on OAS-1 and PKR activity. [ABSTRACT FROM AUTHOR]

The Coronaviridae family includes the seven known human coronaviruses (HCoV) that cause mild to moderate respiratory infections (HCo-V-229E, HCoV-NL63, HCoV-OC43, HCoV-HKU1) as well as severe illness and death (MERS-CoV, SARS-CoV, SARS-CoV-2). Severe infections induce inflammatory responses that are often intensified by host adaptive immune pathways. Proinflammatory responses are triggered by CoV entry mediated by host cell surface receptors. Interestingly, four of the seven strains use cell surface metallopeptidases as receptors. The entry receptors for specific coronaviruses are: aminopeptidase N (AP-N), dipeptidyl peptidase 4 (DPP4) and angiotensin-converting enzyme 2 (ACE2) for HCoV-229E, MERS-CoV, SARS-CoV and SARS-CoV2, respectively. In addition, these receptors perform many physiological functions, including the regulation of the circulatory and immune systems. Coronavirus receptors are also highly expressed in human tissues and organs (intestines, kidneys, heart, lungs). Additionally, some cytokines, chemokines, and other proteins and immune cells influence the modulation of the expression of coronavirus receptors. This review presents the biological role of receptor proteins in the regulation of human physiological systems, the impact of the immune response on susceptibility to coronavirus infections, and the potential effects of glucocorticosteroids (GCS) and specific allergen immunotherapy (AIT) used in the treatment of asthma and allergy on the suscpetibility to coronaviral infections. [ABSTRACT FROM AUTHOR]

The effect of RV-16 on the lung endothelium has not yet been fully defined. It has been suggested that infection of lung endothelial cells with RV-16 drives the production of proinflammatory cytokines. Aim The study's main objective was to investigate lung endothelial cells' antiviral response in vitro to RV-16 infection in the context of modulation the concentration of thymic stromal lymphopoietin (TSLP), which has not been assessed yet. TSLP has been also determined in cell cultures exposed to the virus and stimulated with IL-33 in the presence of antibodies towards the IL-33 receptor (ST2). Material and methods Human lung microvascular endothelial cells (HMVEC-L) were infected with RV-16 or infected with this virus and stimulated with IL-33 in the presence or absence of anti-ST2 antibodies. In the supernatant TSLP level was determined using an enzyme imunoassay (ELISA). Results The TLSP level in cell cultures infected with RV-16, at 72 hours of incubation, was significantly lower compared to the cell culture in medium alone. Stimulation of cells infected with RV-16 with IL-33, in the presence or absence of anti-ST2 antibodies, did not influence the TSLP production and secretion. Conclusions RV-16 infection of lung endothelial cells is associated with decreased TSLP synthesis and release. IL-33 does not significantly affect the response of RV-16-infected lung endothelial cells in the context of TSLP synthesis and release. [ABSTRACT FROM AUTHOR]

Wstęp: Wirusy układu oddechowego w tym rinowirusy (HRV) są najczęstszymi czynnikami wywołującymi infekcje dolnych i górnych dróg oddechowych. Rinowirusy są odpowiedzialne za co najmniej połowę wszystkich przypadków przeziębienia oraz są najczęstszą przyczyną ciężkich zaostrzeń astmy u dzieci i dorosłych (60-80%). Zakażenia rinowirusowe występują w środowisku od wczesnej wiosny do późnej jesieni. Dodatkowo, sezonowe szczyty dla HRV oraz innych wirusów oddechowych często się nakładają, co zwiększa ryzyko kilkukrotnych infekcji tym samym bądź innym wirusem oddechowym w sezonie. Obecnie nie ma badań wskazujących na to, jak długo mogą utrzymywać się wrodzone mechanizmy oporności na ponowną infekcję wirusami oddechowymi w komórkach śródbłonka naczyń płucnych. Nie zostało również wyjaśnione, przez jaki okres czasu infekcja rinowirusowa poprzez indukcję odpowiedzi zapalnej i przeciwwirusowej może zabezpieczać komórki przed ponowną infekcją tym samym lub innym wirusem oddechowym. Cel: Głównym celem pracy było badanie długości utrzymywania się wrodzonych mechanizmów oporności na ponowną infekcję rinowiusem HRV16 w komórkach śródbłonka naczyń płucnych. Materiały i Metody: Ludzkie komórki śródbłonka naczyniowego płuc (HMVEC-L) inkubowano z HRV16 (MOI3) przez 3h. Następnie w 72h wymieniano podłoże i dodawano do komórek świeże medium. W 5 dobie od pierwotnego zakażenia, komórki ponownie infekowano wirusem HRV16 (MOI3) przez 3h i hodowano dalej przez 5, 24 i 72 godziny. Aktywność odpowiedzi zapalnej (IL-6, IL-8, RANTES, IP-10) i przeciwwirusowwej (IFNβ, IFNλ, OAS1, PKR) oceniono za pomocą real-time PCR, testu ELISA oraz cytometrii przepływowej. Wyniki: HRV16 w krótkim czasie po infekcji zwiększał ekspresję interferonów, enzymów OAS1 i PKR odpowiedzialnych za wewnątrzkomórkowe mechanizmy zahamowania replikacji wirusowej oraz chemokin i cytokin zapalnych. Po ponownej ekspozycji na HRV16 nie zaobserwowano zwiększonej aktywności odpowiedzi zapalnej i przeciwwirusowej, natomiast zaobserwowano wzrost ekspresji mRNA i białka dla enzymów OAS1 i PKR w porównaniu do pierwotnej infekcji. Podsumowanie: Zainfekowane komórki śródbłonka naczyń płucnych wykazują długoterminową zwiększoną aktywność wewnątrzkomórkowych mechanizmów walki przeciwwirusowej, w wyniku których komórki te mogą nie być podatne na ponowne zakażeniem tym samym bądź innym wirusem oddechowym. [ABSTRACT FROM AUTHOR]

It is postulated that vaccination against tuberculosis with Bacillus Calmette-Gue'rin (BCG) vaccine may translate into lower incidence of respiratory tract infections by modulating the release of pro-inflammatory cytokines by innate immune cells. This modulation may be due to epigenetic changes in these cells resulting in an increase in the production of pro-inflammatory cytokines such as IL-1β, IL-6 or TNF-α. It is not known whether the pulmonary vascular endothelium equipped with molecular pattern recognition receptors (PRRs) and with entry receptors for human coronaviruses can be infected by them, or whether BCG vaccination may modulate its susceptibility to infection with these viruses. This study analyzes the effect of the HCoV 229E human coronavirus on human pulmonary vascular endothelium. Moreover, the influence of BCG sonicates on susceptibility to HCoV 229E endothelial infection and the generation of antiviral and inflammatory responses was assessed. [ABSTRACT FROM AUTHOR]

Human rhinovirus 16 (HRV16) may induce inflammatory and antiviral responses in the human lung vascular endothelium (ECs) and impair its barrier functions after infection. However, ECs may regain barrier and metabolic functions. Mechanisms of limitation of HRV16 infection in the lung vascular endothelium are unknown. Human lung vascular endothelium (HMVEC-L) was infected with HRV16. IFN-β, OAS-1, and PKR expression was assessed by real-time PCR, flow cytometry, and confocal microscope. To prove the significance of IFN-β in the limitation of HRV16 replication, HMVEC-Ls were preincubated with anti-IFN-β Abs. To prove the involvement of OAS-1 and PKR in the IFN-dependent limitation of HRV16 replication, HMVEC-Ls were transfected with respective siRNA. HRV16 stimulated IFN-β production and activated intracellular mechanisms of antiviral immunity based on OAS-1 and PKR activation. Blocking of IFN-β contributed to the inhibition of intracellular mechanisms of antiviral immunity (OAS-1, PKR) and boosted replication of HRV16. Effective OAS-1 silencing by siRNA caused the increase of HRV16 copy numbers after HRV16 infection. siRNA upregulated the other genes related to the antiviral response. The infected lung vascular endothelium may limit the HRV16 infection. This limitation may be associated with the induction of IFN-β-dependent intracellular mechanisms based on OAS-1 and PKR activity., (© 2023 The Authors. APMIS published by John Wiley & Sons Ltd on behalf of Scandinavian Societies for Pathology, Medical Microbiology and Immunology.)