Alterations of the mycobiota composition associated with Crohn’s disease (CD) are challenging to link to defining elements of pathophysiology, such as poor injury repair. Using culture-dependent and -independent methods, we discovered that Debaryomyces hansenii preferentially localized to and was abundant within incompletely healed intestinal wounds of mice and inflamed mucosal tissues of CD human subjects. D. hansenii cultures from injured mice and inflamed CD tissues impaired colonic healing when introduced into injured conventionally raised or gnotobiotic mice. We reisolated D. hansenii from injured areas of these mice, fulfilling Koch’s postulates. Mechanistically, D. hansenii impaired mucosal healing through the myeloid cell–specific type 1 interferon–CCL5 axis. Taken together, we have identified a fungus that inhabits inflamed CD tissue and can lead to dysregulated mucosal healing.

Pneumonia virus of mice (PVM) is a natural rodent pathogen that replicates in bronchial epithelial cells and reproduces manyclinical and pathological features of the more severe forms of disease associated with human respiratory syncytial virus. In order to track virus-target cell interactions during acute infection in vivo, we developed rK2-PVM, bacterial artificial chromosomebased recombinant PVM strain J3666 that incorporates the fluorescent tag monomeric Katushka 2 (mKATE2). The rK2-PVM pathogen promotes lethal infection in BALB/c mice and elicits characteristic cytokine production and leukocyte recruitment to the lung parenchyma. Using recombinant virus, we demonstrate for the first time PVM infection of both dendritic cells (DCs; CD11c ؉ major histocompatibility complex class II ؉ ) and alveolar macrophages (AMs; CD11c ؉ sialic acid-binding immunoglobulin-like lectin F ؉ ) in vivo and likewise detect mKATE2 ؉ DCs in mediastinal lymph nodes from infected mice. AMs support both active virus replication and production of infectious virions. Furthermore, we report that priming of the respiratory tract with immunobiotic Lactobacillus plantarum, a regimen that results in protection against the lethal inflammatory sequelae of acute respiratory virus infection, resulted in differential recruitment of neutrophils, DCs, and lymphocytes to the lungs in response to rK2-PVM and a reduction from ϳ40% to <10% mKATE2 ؉ AMs in association with a 2-log drop in the release of infectious virions. In contrast, AMs from L. plantarum-primed mice challenged with virus ex vivo exhibited no differential susceptibility to rK2-PVM. Although the mechanisms underlying Lactobacillus-mediated viral suppression remain to be fully elucidated, this study provides insight into the cellular basis of this response. H uman respiratory syncytial virus (hRSV, family Paramyxoviridae, genus Pneumovirus) is a major cause of morbidity and death among infants and children worldwide and is recognized as a significant health concern among the elderly (1). The anti-hRSV antibody paluvizumab is highly effective when used as prophylaxis in infants identified as high risk (2), although there are many infants hospitalized with severe hRSV disease who are not identified in any of the high-risk cohorts (3). Treatment options for hRSV disease are primarily supportive. The antiviral agent ribavirin is currently recommended only for severely ill and immunocompromised children (4, 5). New antiviral agents that focus specifically on hRSV are in development (6)(7)(8), and the inflammatory responses characteristic of severe hRSV disease are also recognized as targets for therapeutic intervention (9, 10).Pneumonia virus of mice (PVM) is a rodent pathogen of the same family and genus as hRSV. PVM infection in inbred strains of mice reproduces many of the clinical and pathological features of the more severe forms of hRSV disease, which has facilitated the exploration of new therapeutic strategies in vivo (11,12). Similar to hRSV (13), PVM infects bronchial epi...

The Icelandic Purple Sandpiper Calidris maritima littoralis (C.L. Brehm, 1831) represents one member of a poorly understood subspecies complex. Currently, differences in size define two other subspecies: Calidris maritima belcheri Engelmoer & Roselaar, 1998, which breeds in north-eastern Canada along the Hudson Bay and James Bay, and Calidris maritima maritima (Brunnich, 1764), which breeds along the Arctic coasts elsewhere in northern Canada, Greenland, Svalbard, Scotland, and Fennoscandia, to northern central Siberia. There are large size differences amongst populations of C. m. maritima, however. As an Arctic/Alpine breeding bird, C. m. littoralis could provide an interesting perspective on the evolutionary changes following a northwards expansion of a species after glacial retreat. Considering the extent of the ice sheet in the northern hemisphere during the last glaciation, and the short period of time since it ended, the correct attribution of subspecies status for C. m. maritima may reflect either rapid diversification from a single population or ancestral splits of distinct evolutionary lineages that survived in isolation at southern latitudes. We applied morphometric subspecies criteria, diagnosability by Amadon's rule, and genetic analysis of five nuclear introns, and the mitochondrial DNA markers cytochrome oxidase c subunit I (COI) and NADH dehydrogenase subunit 2 (ND2), to geographically separate breeding populations in order to examine the subspecies status of the Icelandic population. The results do not provide support for the subspecies status of the Icelandic population because the nominate and Icelandic subspecies fail to uphold Amadon's rule, and genetic analyses indicate that the study populations derive from a single shared refugium.

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