Of Mice and Microflora

Treuting, Piper M.; Clifford, Charles B.; Sellers, Rani S.; Brayton, Cory

doi:10.1177/0300985811431446

Cited by 48 publications

(27 citation statements)

References 91 publications

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“…Consistent with prior studies (Treuting et al, 2012), we found little if any T.mu in the small intestine of T.mu -bearing animals prompting us to focus mainly on immune changes in the colonic mucosa (data not shown). To directly address whether the presence of T.mu was responsible for the expansion of gut tissue-resident immune cells and increased IgA levels, we colonized commercial B6 mice with purified T.mu .…”

Section: Resultssupporting

confidence: 90%

Host-Protozoan Interactions Protect from Mucosal Infections through Activation of the Inflammasome

Chudnovskiy

Mortha

Kana

et al. 2016

Cell

274

304

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While conventional pathogenic protists have been extensively studied, there is an underappreciated constitutive protist microbiota that is an integral part of the vertebrate microbiome. The impact of these species on the host and their potential contributions to mucosal immune homeostasis remain poorly studied. Here, we show that the protozoan Tritrichomonas musculis activates the host epithelial inflammasome to induce IL-18 release. Epithelial-derived IL-18 promotes dendritic cell-driven Th1 and Th17 immunity and confers dramatic protection from mucosal bacterial infections. Along with its role as a “protistic” antibiotic, colonization with T. musculis exacerbates the development of T cell driven colitis and sporadic colorectal tumors. Our findings demonstrate a novel mutualistic host-protozoan interaction that increases mucosal host defenses at the cost of an increased risk of inflammatory disease.

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Section: Resultssupporting

confidence: 90%

Host-Protozoan Interactions Protect from Mucosal Infections through Activation of the Inflammasome

Chudnovskiy

Mortha

Kana

et al. 2016

Cell

274

304

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“…66 These intraluminal protozoa were not associated with any clinical signs or evidence of host response or tissue damage.…”

Section: Resultsmentioning

confidence: 91%

“…P. pneumotropica is a gram-negative, non-spore-forming opportunistic pathogen with high prevalence in murine research colonies. 66 Transmission occurs through direct contact, although its true nature as a primary pathogen is questionable. Outbreaks of P. pneumotropica have been reported in numerous GEM and spontaneous immunodeficient mice.…”

Section: Discussionmentioning

confidence: 99%

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Pathology of Aging in NOD scid gamma Female Mice

et al. 2017

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In the past decade, NOD.Cg-Prkdcscid Il2rgtm1Wjl/SzJ (NSG, NOD scid gamma) mice have become a model of choice in several areas of biomedical research; however, comprehensive data on their spontaneous age-related pathology are not currently available in the literature. The prevalence of spontaneous morbidity affecting aged NSG female breeders enrolled in a parasitology study was documented with classification of neoplastic and non-neoplastic (inflammatory, metabolic, degenerative) lesions. Malignant mammary neoplasms were most commonly diagnosed, often accompanied by pulmonary metastases, while a low frequency of lymphoma and histiocytic sarcoma was documented. The major inflammatory conditions were suppurative pleuropneumonia and bronchopneumonia with abscess formation, from which Pasteurella pneumotropica was commonly isolated, followed by otitis media. Both inflammatory and degenerative lesions of the genital tract were identified, along with neoplasms such as endometrial yolk sac carcinomas and granulosa cell tumors. Novel conditions identified included renal tubular degeneration and necrosis associated with 2 concurrent types of intranuclear inclusions, focal or multifocal hyperostosis of the skull, and neuroendocrine tumors of the mesometrium. The majority of degenerative lesions that affected the genital tract, endocrine, and skeletal systems did not represent the actual underlying cause of death but, rather, were considered incidental findings. This study indicates that both inflammatory and neoplastic conditions contribute to morbidity and mortality in experimentally manipulated aged female NSG mice.

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“…The second mouse was diagnosed with pulmonary Pneumocystis murina infection, which is characterized by alveolar filling and distention by large macrophages, fungal organisms and debris. 28,29 Interestingly, only a small number of alveolar macrophages had intense immunostaining (Figure 1O) whereas many lacked arginase-I immunostaining.…”

Section: Resultsmentioning

confidence: 98%

Immunohistochemical detection of arginase-I expression in formalin-fixed lung and other tissues

Hochstedler

Leidinger

Maher-Sturm

et al. 2013

Journal of Histotechnology

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Arginases are a family of enzymes that convert L-arginine to L-ornithine and urea. Alterations in expression of the isoform arginase-I are increasingly recognized in lung diseases such as asthma and cystic fibrosis. To define expression of murine arginase-I in formalin-fixed tissues, including lung, an immunohistochemical protocol was validated in murine liver; a tissue that has distinct zonal arginase-I expression making it a useful control. In the lung, arginase-I immunostaining was observed in airway surface epithelium and this decreased from large to small airways; with a preferential staining of ciliated epithelium versus Clara cells and alveolar epithelia. In submucosal glands, the ducts and serous acini had moderate immunostaining, which was absent in mucous cells. Focal immunostaining was observed in alveolar macrophages, endothelial cells, pulmonary vein cardiomyocytes, pulmonary artery smooth muscle, airway smooth muscle and neurons of ganglia of the lung. Arginase-I immunostaining was also detected in other tissues including salivary glands, pancreas, liver, skin, and intestine. Differential immunostaining was observed between sexes in submandibular salivary glands; arginase-I was diffusely expressed in the convoluted granular duct cells of females, but was rarely noted in males. Strain specific differences were not detected. In one mouse with an incidental case of lymphoma, neoplastic lymphocytes lacked arginase-I immunostaining, in contrast to immunostaining detected in non-neoplastic lymphocytes of lymphoid tissues. The use of liver tissue to validate arginase-I immunohistochemistry produced consistent expression patterns in mice and this approach can be useful to enhance consistency of arginase-I immunohistochemical studies.

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Of Mice and Microflora

Cited by 48 publications

References 91 publications

Host-Protozoan Interactions Protect from Mucosal Infections through Activation of the Inflammasome

Host-Protozoan Interactions Protect from Mucosal Infections through Activation of the Inflammasome

Pathology of Aging in NOD scid gamma Female Mice

Immunohistochemical detection of arginase-I expression in formalin-fixed lung and other tissues

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