Assuntos
Fístula Brônquica/microbiologia , Fístula/microbiologia , Linfadenopatia/microbiologia , Tuberculose Pulmonar/complicações , Idoso , Fístula Brônquica/imunologia , Fístula/imunologia , Humanos , Imunocompetência , Linfadenopatia/imunologia , Masculino , Mycobacterium tuberculosis , Tuberculose Pulmonar/imunologia , Tuberculose Pulmonar/microbiologiaRESUMO
This report presents a phenotypical characterization of the immune cell infiltrate in a rare case of endobronchial carcinoma. A patient initially treated for an adenocarcinoma of the esophagus developed an endobronchial carcinoma surrounded by gastric metaplasia distal to a suspected gastrobronchial fistula, 11 years after esophagectomy. Our hypothesis is that the sustained exposure of the bronchial mucosa to a mixed acid and pancreatobiliary refluxate led to chronic inflammation and promoted malignant transformation. We performed an immunohistochemical study of the tumor microenvironment evaluating the density of CD3(+), CD8(+) T lymphocytes, CD20(+) B lymphocytes, CD68(+) macrophages and FoxP3(+) regulatory T cells. Quantification of immune cell density was completed using a novel software-based analysis method. Our results suggest that, within all the tissues analyzed, FoxP3(+) regulatory T cells were present at their highest density in the malignant and metaplastic tissues. The endobronchial metaplasia biopsied several years prior to the detection of the endobronchial adenocarcinoma was already densely infiltrated by B cells and macrophages, when compared to the immune cell infiltrate of the endobronchial carcinoma. Altogether, these observations support the current understanding of carcinogenesis promoted by chronic inflammation.
Assuntos
Adenocarcinoma/imunologia , Fístula Brônquica/complicações , Fístula Brônquica/imunologia , Neoplasias Brônquicas/imunologia , Neoplasias Esofágicas/imunologia , Fístula Gástrica/complicações , Fístula Gástrica/imunologia , Inflamação/complicações , Mucosa Intestinal/patologia , Subpopulações de Linfócitos/metabolismo , Linfócitos do Interstício Tumoral/metabolismo , Adenocarcinoma/patologia , Adenocarcinoma/cirurgia , Antígenos CD/biossíntese , Fístula Brônquica/patologia , Neoplasias Brônquicas/complicações , Neoplasias Brônquicas/patologia , Broncopneumonia/etiologia , Broncopneumonia/imunologia , Broncoscopia , Contagem de Células , Doença Crônica , Progressão da Doença , Neoplasias Esofágicas/patologia , Neoplasias Esofágicas/cirurgia , Esofagectomia , Fatores de Transcrição Forkhead/biossíntese , Fístula Gástrica/patologia , Humanos , Imunofenotipagem , Subpopulações de Linfócitos/patologia , Linfócitos do Interstício Tumoral/patologia , Masculino , Metaplasia , Pessoa de Meia-Idade , Segunda Neoplasia Primária/patologia , Nódulo Pulmonar Solitário/imunologia , Nódulo Pulmonar Solitário/patologia , Nódulo Pulmonar Solitário/cirurgia , Estômago/patologia , Linfócitos T Reguladores/metabolismo , Linfócitos T Reguladores/patologiaRESUMO
The article presents the results of low-intensity laser application in complex treatment of 137 children with acute purulent destructive pneumonia complicated by pneumothorax with bronchial fistulas. A method of intracavitary laser therapy, developed in the clinic, allowed obliteration of bronchopleural fistulas without application of bronchial occlusion and other invasive techniques. Evaluation of the kallikrein-kinin system of blood revealed prominent reduction of kininogenesis in most (87%) patients upon admission (3 weeks after the onset of the disease), which is an important link of the pathogenesis of late stages of complicated acute purulent lung destruction in children. The study also demonstrated that low-intensity laser emission modulates pyoinflammatory process due to its effect on cell-mediated immunity, neutrophilic phagocytosis and the kallikrein-kinin system of blood. Intracavitary laser therapy is the treatment of choice in children with acute purulent destructive pneumonia complicated by pneumothorax with bronchial fistulas. Application of intracavitary laser therapy in complex therapy of complicated acute purulent lung destruction in children allowed discharge from the hospital 5 to 7 day earlier, and prevented lung inflammatory process chronization. None of the patients have died within last 10 years.
