Injury From Nematode Lung Migration Induces an IL-13-Dependent Hyaluronan Matrix.

A consistent feature of lung injury is a rapid and sustained accumulation of hyaluronan (HA). The rodent gut-dwelling nematode (Nb) induces tissue damage as it migrates through the lungs. Type 2 immune responses are essential for the repair of the lungs, hence Nb infection is a well-established model to study immune-mediated lung repair.

The IL-17A-neutrophil axis promotes epithelial cell IL-33 production during nematode lung migration.

The early migratory phase of pulmonary helminth infections is characterized by tissue injury leading to the release of the alarmin interleukin (IL)-33 and subsequent induction of type 2 immune responses. We recently described a role for IL-17A, through suppression of interferon (IFN)-γ, as an important inducer of type 2 responses during infection with the lung-migrating rodent nematode Nippostrongylus brasiliensis. Here, we aimed to investigate the interaction between IL-17A and IL-33 during the early lung migratory stages of N.

Instructional Cueing Alters Upper Limb Muscle Activity and Kinematics During Elastic Resistance Exercise.

Objective: The purpose of this study was to quantify the differences in upper limb muscle activity and kinematics when performing shoulder elastic resistance exercises with no cue, slouched posture, and corrected posture.

Design: Fifteen healthy participants completed four shoulder elastic resistance exercises (unilateral flexion, bilateral flexion, external rotation, and external rotation with towel) across three simulated body postures (no cue, corrected posture, and slouched posture). Surface electromyography was measured on 16 upper limb muscles and kinematics were collected.

IL-13 deficiency exacerbates lung damage and impairs epithelial-derived type 2 molecules during nematode infection.

IL-13 is implicated in effective repair after acute lung injury and the pathogenesis of chronic diseases such as allergic asthma. Both these processes involve matrix remodelling, but understanding the specific contribution of IL-13 has been challenging because IL-13 shares receptors and signalling pathways with IL-4. Here, we used infection as a model of acute lung damage comparing responses between WT and IL-13-deficient mice, in which IL-4 signalling is intact.

The magnitude of airway remodeling is not altered by distinct allergic inflammatory responses in BALB/c versus C57BL/6 mice but matrix composition differs.

Allergic airway inflammation is heterogeneous with variability in immune phenotypes observed across asthmatic patients. Inflammation has been thought to directly contribute to airway remodeling in asthma, but clinical data suggest that neutralizing type 2 cytokines does not necessarily alter disease pathogenesis. Here, we utilized C57BL/6 and BALB/c mice to investigate the development of allergic airway inflammation and remodeling.

IL-17A both initiates, via IFNγ suppression, and limits the pulmonary type-2 immune response to nematode infection.

Nippostrongylus brasiliensis is a well-defined model of type-2 immunity but the early lung-migrating phase is dominated by innate IL-17A production. In this study, we confirm previous observations that Il17a-KO mice infected with N. brasiliensis exhibit an impaired type-2 immune response.

Inflammasome-Independent Role for NLRP3 in Controlling Innate Antihelminth Immunity and Tissue Repair in the Lung.

Alternatively activated macrophages are essential effector cells during type 2 immunity and tissue repair following helminth infections. We previously showed that Ym1, an alternative activation marker, can drive innate IL-1R-dependent neutrophil recruitment during infection with the lung-migrating nematode, , suggesting a potential role for the inflammasome in the IL-1-mediated innate response to infection. Although inflammasome proteins such as NLRP3 have important proinflammatory functions in macrophages, their role during type 2 responses and repair are less defined.