Innate immunity during human respiratory co-infections

Globally, respiratory tract infections remain the leading cause of both morbidity and mortality amongst the population. The burden is further increased by polymicrobial infections or viral and bacterial co-infections, “superinfections”, commonly exacerbating the existing conditions. It is well-documented that viruses dysregulate the innate immune response, increasing susceptibility, or exacerbating conditions caused from subsequent bacterial infections, and vice versa. Viral-bacterial co-infections of the respiratory tract illustrates a major but incompletely defined axis of the dysregulation of the innate immune response. Viral-bacterial co-infection engage both epithelial and myeloid pattern-recognition receptors such as NOD-like receptors and TLR-MyD88/TRIF and cause the downstream dysregulation of NF-κB, JAK-STAT, NLRP3 and IRF3/7. This results in the impairment of chemokines, I/III interferons, recruitment of phagocytes, and effector function (NETs, phagocytosis, and ROS), thus shifting the balance between immunopathology and pathogen clearance.Dissecting the mechanistical network on how co-infections perturbs the innate immune response, especially as a function of infection order and host background (immunosuppression, age, etc.) is key for identifying pathways that enhanced susceptibility, progression to ARDS and sepsis, and variable responses to antibiotics, antivirals and immunomodulators. Therefore, such insights will be critical for the design of host-direct therapies, timing of combined regimens and development of biomarkers that capture the innate immune state in patients with co-infections. We are interested in receiving manuscripts focusing on: - co-infections from bacteria-bacteria, which can include pathogens and/or commensals; bacterial-viral; viral-viral co-infections. - Articles may be host, pathogen, or host-pathogen focussed. - Clinical studies through to in vitro models are welcome, that include, but are not limited to observational, mechanistic data and pathway analyses that cover protein, transcriptomic and genomic datasets from host and/or pathogen. - We are interested in articles based on initial host-pathogen responses therefore focussing on innate immunity, rather than adaptive immunity, for this research topic. - We welcome articles investigating effects on respiratory epithelium, innate immune cells such as macrophages, as well as studies looking at crosstalk between epithelium-immune cells.. Topic editors: Caroline Weight, Muhammad Munir Source: https://www.frontiersin.org/research-topics/80929/innate-immunity-during-human-respiratory-co-infections