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Nanomaterials ◽  
2022 ◽  
Vol 12 (2) ◽  
pp. 226
Author(s):  
Jie Tang ◽  
Larry Cai ◽  
Chuanfei Xu ◽  
Si Sun ◽  
Yuheng Liu ◽  
...  

Recent advancements in the field of in vitro transcribed mRNA (IVT-mRNA) vaccination have attracted considerable attention to such vaccination as a cutting-edge technique against infectious diseases including COVID-19 caused by SARS-CoV-2. While numerous pathogens infect the host through the respiratory mucosa, conventional parenterally administered vaccines are unable to induce protective immunity at mucosal surfaces. Mucosal immunization enables the induction of both mucosal and systemic immunity, efficiently removing pathogens from the mucosa before an infection occurs. Although respiratory mucosal vaccination is highly appealing, successful nasal or pulmonary delivery of nucleic acid-based vaccines is challenging because of several physical and biological barriers at the airway mucosal site, such as a variety of protective enzymes and mucociliary clearance, which remove exogenously inhaled substances. Hence, advanced nanotechnologies enabling delivery of DNA and IVT-mRNA to the nasal and pulmonary mucosa are urgently needed. Ideal nanocarriers for nucleic acid vaccines should be able to efficiently load and protect genetic payloads, overcome physical and biological barriers at the airway mucosal site, facilitate transfection in targeted epithelial or antigen-presenting cells, and incorporate adjuvants. In this review, we discuss recent developments in nucleic acid delivery systems that target airway mucosa for vaccination purposes.


Author(s):  
Rinu Sivarajan ◽  
David Komla Kessie ◽  
Heike Oberwinkler ◽  
Niklas Pallmann ◽  
Thorsten Walles ◽  
...  

To study the interaction of human pathogens with their host target structures, human tissue models based on primary cells are considered suitable. Complex tissue models of the human airways have been used as infection models for various viral and bacterial pathogens. The Gram-negative bacterium Bordetella pertussis is of relevant clinical interest since whooping cough has developed into a resurgent infectious disease. In the present study, we created three-dimensional tissue models of the human ciliated nasal and tracheo-bronchial mucosa. We compared the innate immune response of these models towards the B. pertussis virulence factor adenylate cyclase toxin (CyaA) and its enzymatically inactive but fully pore-forming toxoid CyaA-AC-. Applying molecular biological, histological, and microbiological assays, we found that 1 µg/ml CyaA elevated the intracellular cAMP level but did not disturb the epithelial barrier integrity of nasal and tracheo-bronchial airway mucosa tissue models. Interestingly, CyaA significantly increased interleukin 6, interleukin 8, and human beta defensin 2 secretion in nasal tissue models, whereas tracheo-bronchial tissue models were not significantly affected compared to the controls. Subsequently, we investigated the interaction of B. pertussis with both differentiated primary nasal and tracheo-bronchial tissue models and demonstrated bacterial adherence and invasion without observing host cell type-specific significant differences. Even though the nasal and the tracheo-bronchial mucosa appear similar from a histological perspective, they are differentially susceptible to B. pertussis CyaA in vitro. Our finding that nasal tissue models showed an increased innate immune response towards the B. pertussis virulence factor CyaA compared to tracheo-bronchial tissue models may reflect the key role of the nasal airway mucosa as the first line of defense against airborne pathogens.


Author(s):  
Sholly. CK

Black fungus is also known as Mucormycosis, and it is occasional but threatening infection. Black fungus is caused by getting into exposure with fungus spores in the surroundings. It can also form in the skin after the fungus enters through a cut, scrape, burn, or another type of skin trauma. Fungi live in the environment, particularly in soil and decaying organic matter such as leaves, compost piles, rotten wood, particularly in soil, compost, and animal dung. This fungal infection is caused by a type of mould known as 'mucromycetes’. It should be noted that this rare fungal infection affects persons who have health issues or who use drugs that weaken the body's ability to fight the infections. There are different types of mucormycosis Trusted Source, including rhino cerebral (sinus and brain), pulmonary (lung), gastrointestinal, and cutaneous (skin) mucormycosis. The COVID-19 generates a sudden change in the interior environment of the host for the fungus, and the medical treatment administered unknowingly promotes fungal development. COVID-19 causes harm to the airway mucosa and blood vessels. It also causes a rise in serum iron, which is required for the fungus to grow. Broad-spectrum antibiotics not only kill potentially harmful bacteria but also beneficial commensals. Although antifungals such as Voriconazole prevent Aspergillosis, Mucor survives and grows due to a lack of resistance. Long-term ventilation decreases immunity, and there is conjecture that the humidifier water that is delivered along with the oxygen transfers the fungus. It is ubiquitous and found in soil and air and even in the nose and mucus of healthy people. It affects the sinuses, the brain and the lungs and can be life-threatening in diabetic or severely immunocompromised individuals, such as cancer patients or people with HIV/AIDS. Doctors believe mucormycosis, which has an overall mortality rate of 50%, may be being triggered by the use of steroids, a life-saving treatment for severe and critically ill Covid-19 patients. Steroids reduce inflammation in the lungs for Covid-19 and appear to help stop some of the damage that can happen when the body's immune system goes into overdrive to fight off coronavirus. But they also reduce immunity and push up blood sugar levels in both diabetics and non-diabetic Covid-19 patients. It’s thought that this drop in immunity could be triggering these cases of mucormycosis.


2021 ◽  
Vol 21 (3) ◽  
pp. 97-102
Author(s):  
Elena L. Bolkhovitina ◽  
Julia D. Vavilova ◽  
Andrey O. Bogorodskiy ◽  
Ivan S. Okhrimenko ◽  
Valentin I. Borshchevskiy ◽  
...  

BACKGROUND: Airborne pathogens such as virus particles undergo elimination from the respiratory tract by mucociliary clearance and phagocytosis by immune cells. The data about phagocytic cell type infiltration and stimuli that attract phagocytic cells to conducting airway are required for the anti-virus immune response mechanism understanding and the treatment strategy development. AIM: To detect the role of the receptor-binding domain of SARS-CoV-2 in neutrophil immune response activation in conducting airway mucosa after 100 nm particles application. MATERIALS AND METHODS: C57BL/6 mice received an oropharyngeal application of fluorescent 100 nm particles suspended in the receptor-binding domain of SARS-CoV-2 solution. 24 hours after, conducting airways of mice were dissected and subjected for immunohistochemistry as whole-mounts. Three-dimensional images of conducting airway regions were obtained using confocal microscopy. Quantitative image analysis was performed to estimate the ingestion activity of neutrophils in conducting airway mucosa. RESULTS: Neutrophil migration to conducting airway mucosa was detected in case of the application of particles in receptor-binding domain solution, but not in phosphate buffer or bovine serum albumin solution. Receptor-binding domain solution alone also induced neutrophil migration to conducting airway mucosa. Infiltrating conducting airway wall mucosa neutrophils contributed to particles internalization. CONCLUSIONS: The receptor-binding domain of SARS-CoV-2 can activate the neutrophil-mediated response in conducting airway mucosa.


Author(s):  
Iriondo Cinta ◽  
Kari-Pekka Skarp ◽  
Mieke Veltman ◽  
Marjon Buscop-Van Kempen ◽  
Anne Boerema-De Munck ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Xiaokun Shen ◽  
Huiyun Zhang ◽  
Hua Xie ◽  
Liping Chen ◽  
Shinan Li ◽  
...  

Human regulatory T (Treg) cells play a central role in controlling allergic inflammation in the airways. A reduced number of peripheral Treg cells and decreased suppressive function have been previously reported in the pathogenesis of allergic asthma. However, the characteristic role of specific Treg cell subsets and their mechanisms in the pathogenesis of allergic asthma remain unclear. In this study, we examined the proportion of different Treg cell subsets in both healthy subjects and patients with allergic asthma using flow cytometry and single-cell RNA sequencing. The migration function of the cells was compared using cell sorting and Transwell experiments. Furthermore, two allergen-challenged mouse models and a cell transfer experiment were used to examine the role of these Treg subsets. We found that the proportion of CD25+Foxp3+CD127- Treg cells in the peripheral blood of patients with allergic asthma was lower than in those of healthy subjects. Furthermore, the circulating Treg cells expressed lower levels of CCR6 and IL-17 compared with healthy subjects. The chemokine from the airway mucosa, CCL20, was abundantly expressed, and Transwell experiments further proved that this chemokine promoted CCR6+ Treg cell migration in vitro. A mouse model induced by house dust mite (HDM) revealed that the number of CCR6+ Treg cells in the lung tissue increased remarkably. The incidence of allergic asthma may be related to an increase in Treg cells secreting IL-17 in the lung tissue. Recruited CCR6+ Treg cells are likely to differentiate into Th17-like cells under the Th17 environment present in the lungs. IL-17 derived from Th17-like cells could be associated with the pathology of allergic asthma by promoting Th17 responses, thereby favoring HDM-induced asthma exacerbations.


2021 ◽  
Vol 8 ◽  
Author(s):  
Mehdi Khosravi ◽  
Ruei-Lung Lin ◽  
Ashish P. Maskey ◽  
Subodh Pandey ◽  
An-Hsuan Lin ◽  
...  

Extensive evidence indicates that several types of temperature-sensitive ion channels are abundantly expressed in the sensory nerves innervating airway mucosa. Indeed, airway temperature is known to play an important role in regulating respiratory functions. However, the actual airway mucosal temperature and its dynamic changes during the respiratory cycle have not been directly measured. In previous studies, airway tissue temperature was often estimated by indirect measurement of the peak exhaled breath temperature (PEBT). In view of the poor thermal conductivity of air, we believe that the airway tissue temperature cannot be accurately determined by the exhaled air temperature, and this study aimed to test this hypothesis. We applied a miniature rapid-response temperature probe to measure directly the mucosal temperatures of trachea, major, lobar, and segmental bronchi in eight human subjects during a bronchoscopy procedure. Unlike the air temperature in the airway lumen, the mucosal temperature in these airway segments remained relatively stable and did not exhibit the phasic changes synchronous with respiratory cycles. The airway mucosal temperature increased progressively from the extra-thoracic trachea (35.7 ± 0.2°C) toward the segmental bronchus (36.9 ± 0.2°C). Most importantly, the temperatures measured directly at the mucosa of all these airway segments were substantially higher than the PEBT (31.7 ± 0.8°C). The recent findings of a close association between an increased PEBT and airway tissue inflammation have revealed the implication and potential of incorporating the PEBT measurement in the future clinical diagnosis of airway inflammation. Therefore, it is imperative to recognize this distinct difference in temperature between airway mucosa and exhaled air.


Author(s):  
Björn Corleis ◽  
Josalyn L. Cho ◽  
Samantha J Gates ◽  
Alice H Linder ◽  
Amy Dickey ◽  
...  
Keyword(s):  
T Cells ◽  

Author(s):  
E. Evonne Jean ◽  
Olivia Good ◽  
Juan M. Inclan Rico ◽  
Heather L. Rossi ◽  
De'Broski R. Herbert

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