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Evans, S. E.

Publications and source records attributed to Evans, S. E..

21 records · Page 2Linked to original sources

Non-rainfall moisture: a key driver of carbon flux from standing litter in arid, semiarid, and mesic grasslands

Models assume that rainfall is the major source of moisture driving decomposition. Non-rainfall moisture (NRM: high humidity, dew, and fog) can also induce standing litter decomposition, but there have been few standard measurements of NRM-mediated decompositions across sites, and no efforts to extrapolate the contribution of NRM to larger scales to assess whether this mechanism can improve model predictions. Here we show that NRM is an important, year-round source of moisture in grassland sites with contrasting moisture regimes using field measurements and modeling. We first characterized NRM frequency and measured NRM-mediated decomposition in sites on the extreme dry and wet end of grassland systems: at two sites in the Namib Desert, Namibia (hyperarid desert) and at one site in Iowa, USA (tallgrass prairie). NRM was frequent at all sites (85-99% of hours that litter was likely to be wet were attributed to NRM) and tended to occur in cool, high-humidity periods for several hours or more at a time. NRM also caused respiration of standing litter at all sites when litter became sufficiently wet (>5% for fine litter and >13% for coarse), and contributed to mass loss, even in the Namib West site that had almost no rain. When we modeled annual mass loss induced by NRM and rain, and extrapolated our characterization of NRM decomposition to a final site with intermediate rainfall (Sevilleta, New Mexico, semiarid grassland), we found that models driven by rainfall alone underestimated mass loss, while including NRM produced estimates within the range of observed mass loss. Together these findings suggest that NRM is an important missing component in quantitative and conceptual models of litter decomposition, but there is nuance involved in modeling NRM at larger scales. Specifically, temperature and physical features of the substrate emerge as factors that affect the common microbial response to litter wetting under NRM across grasslands sites, and require further study. Hourly humidity can provide an adequate proxy of NRM frequency, but site-specific calibration with litter wetness is needed to accurately attribute decomposition to periods when NRM wets litter. Greater recognition of NRM-driven decomposition and its interaction with other processes (e.g. photodegradation) is needed, especially since fog, dew, and humidity are likely to shift under future climates.\n\nManuscript highlightsO_LINon-rainfall moisture (NRM; humidity, fog, dew) induces decomposition in grasslands\nC_LIO_LINRM decomposition depends on substrate type, and occurs at colder times than rain\nC_LIO_LIIncluding NRM (instead of rain alone) improved predictions of litter decomposition\nC_LI

ecology↗

Aerosolized TLR Agonists Suppress Acute Sendai Virus Lung Infection and Chronic Airway Disease in Mice

Respiratory viral infections play central roles in the initiation, exacerbation and progression of asthma in humans. An acute paramyxoviral infection in mice can cause a chronic lung disease that resembles human asthma. We sought to determine whether reduction of Sendai virus lung burden in mice by stimulating innate immunity with aerosolized Toll-like receptor (TLR) agonists could attenuate the severity of chronic asthma-like lung disease. Treatment with 1 {micro}M oligodeoxynucleotide (ODN) M362, an agonist of the TLR9 homodimer, and 4 {micro}M Pam2CSK4 (Pam2), an agonist of the TLR2/6 heterodimer, within a few days before or after Sendai virus challenge, resulted in a [~]75% reduction in lung Sendai virus burden five days after challenge. The reduction in acute lung virus burden was associated with marked reductions 49 days after viral challenge in eosinophilic and lymphocytic lung inflammation, airway mucous metaplasia, lumenal mucus occlusion, and hyperresponsiveness to methacholine. Mechanistically, ODN/Pam2 treatment attenuated the chronic asthma phenotype by suppressing IL-33 production by type 2 pneumocytes, both by reducing the severity of acute infection and by downregulating Type 2 (allergic) inflammation. These data suggest that treatment of susceptible human hosts with aerosolized ODN and Pam2 at the time of a respiratory viral infection might attenuate the severity of the acute infection and reduce progression of asthma.\n\nOne Sentence SummaryRespiratory viral infections can induce chronic airway disease, and we find that stimulating innate immunity within the lungs of mice reduces the severity of acute infection and development of a chronic asthma phenotype.

immunology↗

Inducible Lung Epithelial Resistance Requires Multisource Reactive Oxygen Species Generation to Protect against Bacterial Infections

Pneumonia remains a global health threat, in part due to expanding categories of susceptible individuals and increasing prevalence of antibiotic resistant pathogens. However, therapeutic stimulation of the lungs mucosal defenses by inhaled exposure to a synergistic combination of Toll-like receptor (TLR) agonists known as Pam2-ODN promotes mouse survival of pneumonia caused by a wide array of pathogens. This inducible resistance to pneumonia relies on intact lung epithelial TLR signaling, and inducible protection against viral pathogens has recently been shown to require increased production of epithelial reactive oxygen species (ROS) from multiple epithelial ROS generators. To determine whether similar mechanisms contribute to inducible antibacterial responses, the current work investigates the role of ROS in therapeutically-stimulated protection against Pseudomonas aerugnosa challenges. Inhaled Pam2-ODN treatment one day before infection prevented hemorrhagic lung cytotoxicity and mouse death in a manner that correlated with reduction in bacterial burden. The bacterial killing effect of Pam2-ODN was recapitulated in isolated mouse and human lung epithelial cells, and the protection correlated with inducible epithelial generation of ROS. Scavenging or targeted blockade of ROS production from either dual oxidase or mitochondrial sources resulted in near complete loss of Pam2-ODN-induced bacterial killing, whereas deficiency of induced antimicrobial peptides had little effect. These findings support a central role for multisource epithelial ROS in inducible resistance against bacterial pathogens and provide mechanistic insights into means to protect vulnerable patients against lethal infections.

immunology↗