BATF promotes group 2 innate lymphoid cell–mediated lung tissue protection during acute respiratory virus infection

BATF regulates ILC2-mediated tissue repair and inflammation resolution during acute respiratory virus infection.

Alternaria alternata Accelerates Loss of Alveolar Macrophages and Promotes Lethal Influenza A Infection

Chronic inhalation of fungi and fungal components has been linked to the development of respiratory disorders, although their role with respect to the pathogenesis of acute respiratory virus infection remains unclear. Here, we evaluate inflammatory pathology induced by repetitive administration of a filtrate of the ubiquitous fungus, Alternaria alternata, and its impact on susceptibility to infection with influenza A. We showed previously that A. alternata at the nasal mucosae resulted in increased susceptibility to an otherwise sublethal inoculum of influenza A in wild-type mice. Here we demonstrate that A. alternata-induced potentiation of influenza A infection was not dependent on fungal serine protease or ribonuclease activity. Repetitive challenge with A. alternata prior to virus infection resulted proinflammatory cytokines, neutrophil recruitment, and loss of alveolar macrophages to a degree that substantially exceeded that observed in response to influenza A infection alone. Concomitant administration of immunomodulatory Lactobacillus plantarum, a strategy shown previously to limit virus-induced inflammation in the airways, blocked the exaggerated lethal response. These observations promote an improved understanding of severe influenza infection with potential clinical relevance for individuals subjected to continuous exposure to molds and fungi.

Quis Custodiet Ipsos Custodes? Regulation of Cell-Mediated Immune Responses Following Viral Lung Infections

Viral lung infections are leading causes of morbidity and mortality. Effective immune responses to these infections require precise immune regulation to preserve lung function after viral clearance. One component of airway pathophysiology and lung injury associated with acute respiratory virus infection is effector T cells, yet these are the primary cells required for viral clearance. Accordingly, multiple immune mechanisms exist to regulate effector T cells, limiting immunopathology while permitting clearance of infection. Much has been learned in recent years about regulation of T cell function during chronic infection and cancer, and it is now clear that many of these mechanisms also control inflammation in acute lung infection. In this review, we focus on regulatory T cells, inhibitory receptors, and other cells and molecules that regulate cell-mediated immunity in the context of acute respiratory virus infection.