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BackgroundPulmonary epithelial-myoepithelial carcinoma (P-EMC) is a rare subset of salivary gland-type tumors of the lung. Because of its rarity and unproven malignant potential, the optimal therapy for P-EMC has not been defined. Here, we report a typical case of P-EMC and a review of the literature to consider appropriate treatment.Case presentationA 54-year-old woman presented with an abnormal lung shadow on a routine chest X-ray. A chest computed tomography (CT) scan verified an 18-mm endobronchial nodule on the middle lobe. We performed a bronchoscopic biopsy, and the patient was diagnosed with P-EMC. After confirming the absence of tumors in the salivary glands, she underwent a right middle lobectomy along with hilar and mediastinal lymph node dissections. Currently, the patient is doing well, without any sign of recurrence 3 years after surgery.ConclusionsAlthough a majority of P-EMC cases, as in our case, behave indolently, several poor progression cases have been reported. For distinguishing the minor malignancy cases from others, histological findings such as myoepithelial anaplasia could be a predictive factor. Complete resection is needed to evaluate the whole tumor, because P-EMCs often show histological heterogeneity. Moreover, incomplete excision may be a poor prognostic factor. Although lobectomies as well as lymph node dissections, sleeve lobectomies, or pneumonectomies are routinely performed for complete resection, further investigation is required to establish the optimal treatment strategy.

Human Mycoplasma pneumoniae (MP) pneumonia is characterized by alveolar infiltration with neutrophils and lymphocytes and lymphocyte/plasma cell infiltrates in the peri-bronchovascular area (PBVA). No mouse model has been able to mimic the pathological features seen in human MP pneumonia, such as plasma cell-rich lymphocytic infiltration in PBVA. To figure out the mechanism for inflammation by MP infection using a novel mouse model that mimics human MP pneumonia, mice were pre-immunized intraperitoneally with Th2 stimulating adjuvant, alum, alone or MP extracts with an alum, followed by intratracheal challenge with MP extracts. The toll-like receptor-2, which is the major receptor for mycoplasma cell wall lipoproteins, was strongly up-regulated in alveolar macrophages in a latter group after the pre-immunization but prior to the intratracheal challenge. Those findings demonstrated that acceleration of innate immunity by antecedent antigenic stimulation can be an important positive-feedback mechanism in lung inflammation during MP pneumonia.

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