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Eosinophilic asthma has conventionally been proposed to be a T helper 2 driven disease but emerging evidence supports a central role of type 2 innate lymphoid cells (ILC2s). These are non-T, non-B cells that lack antigen specificity and produce more IL-5 and IL-13 than CD4 + T lymphocytes, on a cell per cell basis, in vitro. Although it is clear that ILC2s and CD4 + T cells work in concert with each other to drive type 2 immune responses, kinetic studies in allergic asthma suggest that ILC2s may act locally within the airways to "initiate" eosinophilic responses, whereas CD4 + T cells act locally and systemically to "perpetuate" eosinophilic inflammatory responses. Importantly, ILC2s are increased within the airways of severe asthmatics, with the greatest number of IL-5 + IL-13 + ILC2s being detected in sputum from severe asthmatics with uncontrolled eosinophilia despite high-dose steroid therapy. Although the precise relationship between ILC2s and steroid sensitivity in asthma remains unclear, controlling the activation of ILC2s within the airways may provide an effective therapeutic target for eosinophilic inflammation in airways diseases., (©2019 Society for Leukocyte Biology.)

Acute eosinophilic pneumonia is a rare entity characterized by rapidly progressive infiltration of eosinophils into the lungs and is often associated with drug exposure or infection. We report a case of a previously healthy 19-year-old woman who presented with acute progressive dyspnea. Chest radiograph revealed diffuse bilateral infiltrates. Based on the results of bronchoalveolar lavage fluid and her clinical course, she was diagnosed as having acute eosinophilic pneumonia. We suspect that the disease was related to smoking because she had started smoking 3 weeks before the onset of symptoms. Given the high prevalence of smoking and initiation of smoking in the military population, it is important for physicians taking care of this population to be aware of this disorder., (Reprint & Copyright © 2016 Association of Military Surgeons of the U.S.)

Induction of immunity to one pathogen in the lungs modifies the microenvironment and alters immunopathological changes that result from a second, unrelated pulmonary infection. However, it is unclear whether immunity generated at distant sites also affects lung immune responses. Here, we show that infection with the gut-restricted bacterium Citrobacter rodentium modifies immunopathological changes that result from pulmonary Cryptococcus neoformans infection. Th2 cytokine-driven pulmonary eosinophilia induced by C. neoformans infection was reduced, and the enhanced Th1 cytokine environment afforded more-rapid clearance of the fungus in C. rodentium-immune mice. The activated and intraepithelial (CD103+) T cell populations that expand after C. neoformans infection were diminished in C. rodentium-immune mice. T cell cross-reactivity was absent, but cross-reactive antibodies were detected. It is of importance to the "hygiene hypothesis" that these data indicate that an immune response induced by a gut-restricted pathogen can modify the immune outcome after pulmonary infection, suggesting that cell-phenotype modifications occur across mucosal sites.

Background: Tropical pulmonary eosinophilia (TPE) is a rare but serious manifestation of infection with the lymphatic filarial parasites Wuchereria bancrofti and Brugia malayi. Although endemicity is limited to the tropical and subtropical regions of Africa, South America, and Asia, immigration and travel practices have led to the diagnosis of TPE in areas of nonendemicity., Methods: We herein present a case series of all patients with TPE who presented to the Toronto General Hospital during 1990-2003., Results: Seventeen individuals presented with TPE during the study period, and all were of South Asian ancestry. All 17 received an incorrect diagnosis at presentation (median number of consultations before diagnosis, 2), the most frequent of which was asthma (76%). Eosinophil count, serum immunoglobulin E levels, and anti-filarial antibody titers were elevated in all patients. Ten of 14 patients had an abnormal chest radiograph finding, and 11 of 12 patients had abnormal results of pulmonary function tests., Conclusions: TPE is an important diagnostic consideration in patients with eosinophilia, respiratory symptoms, and history of exposure to this disease. In the untreated individual, TPE can lead to chronic and progressive respiratory compromise and death. Prompt recognition and treatment with diethylcarbamazine is therefore key to minimizing morbidity and mortality.

Severe respiratory syncytial virus (RSV) infection has been hypothesized to be a risk factor for the development of allergy and asthma, but epidemiologic studies in humans have been inconclusive. By use of a well-characterized murine model of RSV infection and allergic sensitization with ovalbumin, the effect of a preceding severe RSV infection on the development of the pulmonary allergic inflammatory response and airway hyperresponsiveness (AHR) was tested. The impact of prior allergic sensitization on RSV-induced illness, as measured by weight loss, also was evaluated. RSV infection before allergic sensitization decreased allergen-induced AHR, production of interleukin-13 in lung tissue, and lung eosinophilia. In contrast, allergic sensitization before RSV infection increased AHR and decreased RSV-related weight loss and lung levels of interferon-gamma but did not alter viral clearance. These data provide evidence that RSV-associated AHR occurs in hosts with allergic responses and that allergic inflammation is diminished when preceded by RSV infection.

Eosinophils have been shown to increase in tissues during many fibrotic conditions and consequently have been suggested to contribute to the development of fibrosis. This study tested the hypothesis that eosinophils are essential in the development of lung fibrosis in mice in response to bleomycin (BLM). Anti-IL-5 antibody was administered intraperitoneally into mice 2 h prior to endotracheal BLM inoculation and thereafter, every other day. Lung eosinophilia was evaluated by measurement of eosinophil peroxidase activity and confirmed by eosinophil counts in histologic sections. Lung fibrosis was evaluated by hydroxyproline content and confirmed by collagen staining in histological sections. Results demonstrated that BLM induced pronounced lung eosinophilia, which was maximal 7 days after BLM treatment and remained elevated through day 14, in C57B1/6 SCID mice and CBA/J mice. In contrast, eosinophilia was a minor component in the lungs of wildtype C57B1/6 mice after BLM treatment, although lung fibrosis developed similarly in all three strains of mice. Treatment with anti-IL-5 completely abrogated eosinophilia but failed to block pulmonary fibrosis induced by BLM in all mouse strains, including C57B1/6 SCID, wildtype C57B1/6 mice, and CBA/J mice. Analysis of cytokine mRNA by RNase-protection assay in C57B1/6 SCID mice indicated that BLM treatment caused enhanced expression of the cytokines, TNF-alpha, and IL-6 at days 3, 7, and 14 post-BLM inoculation, regardless of whether eosinophils were depleted by anti-IL-5. Finally, the importance of eosinophils in lung fibrosis was examined in IL-5 gene knockout mice (IL-5tm1Kopf). BLM treatment induced significant lung fibrosis in IL-5 knockout mice in the absence of eosinophilia. These findings indicate that eosinophils are not an absolute requirement for BLM-induced pulmonary fibrosis in the mouse.

We report a case of eosinophilic fasciitis, with the unusual features of pulmonary and pleural involvement. Similar cases which involve the lungs have been reported after exposure to L-tryptophan, but there is no relevant drug history in this case.