Antiviral epithelial-macrophage crosstalk permits secondary bacterial infections.

Miscommunication of antiviral and antibacterial immune signals drives worsened morbidity and mortality during respiratory viral-bacterial coinfections. Extracellular vesicles (EVs) are a form of intercellular communication with broad implications during infection, and here we show that epithelium-derived EVs released during the antiviral response impair the antibacterial activity of macrophages, an innate immune cell crucial for bacterial control in the airway. Macrophages exposed to antiviral EVs display reduced clearance of as well as altered inflammatory signaling and anti-inflammatory metabolic reprogramming, thus revealing EVs as a source of dysregulated epithelium-macrophage crosstalk during coinfection.

Microbial and Immune Regulation of the Gut-Lung Axis during Viral-Bacterial Coinfection.

Viral-bacterial coinfections of the respiratory tract have long been associated with worsened disease outcomes. Clinical and basic research studies demonstrate that these infections are driven via complex interactions between the infecting pathogens, microbiome, and host immune response, although how these interactions contribute to disease progression is still not fully understood. Research over the last decade shows that the gut has a significant role in mediating respiratory outcomes, in a phenomenon known as the "gut-lung axis.

Clinical characteristics, outcomes, and seasonality of acute respiratory infection associated with single and codetected rhinovirus species among hospitalized children in Amman, Jordan.

Rhinovirus (RV)-specific surveillance studies in the Middle East are limited. Therefore, we aimed to study the clinical characteristics, outcomes, and seasonality of RV-associated acute respiratory infection among hospitalized young children in Jordan. We conducted a prospective viral surveillance study and enrolled children <2 years old admitted to a large public hospital in Amman, Jordan (2010-2013).

Extracellular vesicles promote transkingdom nutrient transfer during viral-bacterial co-infection.

Extracellular vesicles (EVs) are increasingly appreciated as a mechanism of communication among cells that contribute to many physiological processes. Although EVs can promote either antiviral or proviral effects during viral infections, the role of EVs in virus-associated polymicrobial infections remains poorly defined. We report that EVs secreted from airway epithelial cells during respiratory viral infection promote secondary bacterial growth, including biofilm biogenesis, by Pseudomonas aeruginosa.