Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In chronic nonspecific diseases of the lungs lesions of the microcirculatory system of the visceral pleura are of generalized character. The most marked changes were observed in postcapillary and venular links of the microhemocirculation. A pronounced hypertrophy of the venular department and rearrangement of the postcapillary network were noted. The microcirculatory lymphatic system was found to be considerably developed. Along with the functioning lymphatic network there were seen emptying sclerosing lymphatic vessels. The changes in vascular terminals revealed were directly dependent upon the duration of the disease, character of expansion of the process in the lungs, degree of cardiopulmonary incompetence. Moreover, disorders of rheological properties of the blood and permeability of vessels were observed, these disorders being particularly pronounced in exacerbation of chronic pneumonia and cor pulmonale insufficiency of II-III degree. It may be assumed that changes in the microcirculation system in chronic nonspecific lung diseases may represent both an important link in the compensatory mechanisms at early stages of the disease and also a cause of deep irreversible metabolic disturbances in persisting and progressing process in the lungs.
 ...
PMID:[The morphology of the microcirculatory system of the visceral pleura in chronic non-specific lung diseases]. 122 Jun 48

A case of a large cell anaplastic carcinoma of the giant cell type in the lungs of a 5 year-old crossbred male Labrador is discussed. The dog was weak, depressed, febrile and markedly dyspnoeic. An intermittent moist cough and auscultable crackling rales were evident. Radiographic examination was indicative of pneumonia and pulmonic neoplasia. The dog died 36 hours after admission despite antibiotic and supportive therapy. At autopsy, the neoplasm appeared as numerous firm greyish-white nodules of varying size throughout all the lung lobes whilst in the right intermediate and diaphragmatic lobes the neoplasm was completely confluent. The microscopic features included: intra-alveolar composites of cells exhibiting considerable nuclear and cytoplasmic pleomorphism; the presence of numerous giant cells scattered throughout the tumour; the occurrence of tumour emboli within both venous and lymphatic vessels; and, metastatic foci in the bronchial and mediastinal lymph nodes. These features were considered to reflect a high degree of malignancy. Comparative and aetiological aspects of bronchogenic carcinomas in man and the dog are discussed.
 ...
PMID:A pulmonary giant cell carcinoma in a dog. 407 38

Twenty-three fatal sporadic cases of serogroup 1 Legionella pneumophila pneumonia have been analyzed. Bilateral consolidating fibrinopurulent pneumonia was evident in most cases. In four leukopenic immunosuppressed subjects, and acute fibrinoserous pneumonia with a remarkable lack on inflammation was present. The bacterium was found at extrathoracic sites in 27% of the cases. Involvement of the spleen (25%), bone marrow (13%), and kidneys (4.5%) suggests that hematogenous spread of the infection is not uncommon. Involvement of the hilar lymph nodes in 44% of the cases, and multiple peripheral lymph nodes in one case, suggest that lymphatic vessels may also be an important pathway of dissemination. We concluded that systemic spread of L pneumophila is not uncommon in seriously ill patients and we believe that some of the unusual extrathoracic manifestations of this disease may be related to bacteremia.
 ...
PMID:Sporadic Legionnaires' disease. A pathologic study of 23 fatal cases. 689 76

Tissues from corticosteroid-treated gerbils hyperinfected with Strongyloides stercoralis were compared grossly and microscopically to similar tissues from animals with uncomplicated strongyloidiasis. Gerbils with hyperinfection developed severe pulmonary alveolar haemorrhage with a variable degree of subacute eosinophilic interstitial pneumonia associated with numerous alveolar, vascular and interstitial larvae. Hyperinfection induced by corticosteroids, given either before inoculation of S. stercoralis larvae or after a chronic Strongyloides infection was established, produced similar lesions. In contrast, lungs from gerbils with uncomplicated Strongyloides infection had severe eosinophilic perivasculitis and vasculitis with very little haemorrhage, no pneumonia and no larvae. Sections of adult worms were present in the proximal part of the intestinal tract, lodged in spaces between mucosal epithelial cells. Adult worms were not associated with inflammation and were more common in the corticosteroid-treated gerbils. In corticosteroid-treated gerbils only, there were numerous larvae in the distal intestinal tract, throughout the intestinal wall and adjacent mesentery, within interstitial tissues and in lymphatic vessels. Significant inflammation with associated larvae was only present in the caecum and mesenteric lymph nodes, suggesting that the caecum was the main site for initiation of parenteral migration with subsequent invasion of the lymphatic system and lungs. The lesions in these gerbils were similar to those found in humans. Infection of gerbils with S. stercoralis is the best rodent model of human strongyloidiasis.
 ...
PMID:Strongyloides stercoralis: histopathology of uncomplicated and hyperinfective strongyloidiasis in the Mongolian gerbil, a rodent model for human strongyloidiasis [corrected]. 763 16

In lung or heart-lung transplant recipients, complications as a result of pulmonary infections continue to be the most frequent causes of morbidity and mortality. This study was undertaken to identify the contributions of (1) thoracotomy, (2) interruption of lymphatic vessels and bronchial arteries, (3) transplant procedure, (4) drug-induced immunosuppression, and (5) graft allogenicity to the increased risk of pneumonia in lung transplantation. Lewis rats were inoculated with 10(5) colony-forming units of Legionella pneumophila serogroup 1 by direct instillation into the trachea after one of the following: a general anesthetic with no operation; a left thoracotomy; a left thoracotomy with pulmonary hilar stripping; an isogeneic orthotopic left lung transplant with or without immunosuppression; or an allogeneic transplant with immunosuppression with Brown-Norway rats as donors. Immunosuppression was induced with an intramuscular injection of cyclosporine (25 mg/kg of body weight) from the inoculation day to day 3. All rats were killed on day 6, and severity of infection was determined by quantitative culture of Legionella organisms in the lungs and spleen, titer of Legionella urinary antigen, differential cell count in bronchoalveolar lavage fluid, body weight loss, and gross inspection of the lung. Significant increases in lung Legionella concentration occurred as a result of the addition of pulmonary hilar stripping (from 10(5.13 +/- 0.34) in the thoracotomy group to 10(5.66 +/- 0.25) in the thoracotomy with hilar stripping group, p = 0.013) and the addition of immunosuppression (from 10(5.47 +/- 0.47) in the isogeneic transplant group to 10(6.94 +/- 0.52) in the isogeneic transplant with immunosuppression group, p = 0.00016). Thoracotomy, transplant procedures, and allogenicity itself resulted in no significant increases. The results for all other indicators paralleled those for lung culture. We conclude that the combination of drug-induced immunosuppression with lung denervation and interruption of lymphatic vessels and bronchial arteries results in the early development and increased severity of pneumonia in lung transplantation.
 ...
PMID:Aspects of lung transplantation that contribute to increased severity of pneumonia. An experimental study. 836 Nov 86

A 67-year-old female was admitted to our hospital because of pneumonia-like shadow on chest roentgenogram with persistent cough and sputum of 4 months duration. Diagnosis as lung cancer was delayed more than 4 months. She showed fever and inflammatory reactions. Antibiotics were effective to inflammatory reactions, but not effective to pneumonia-like shadow. Transbronchial lung biopsy was useful for the diagnosis. Right lower lobectomy was performed. In this case, tumor extents were limited within one lobe. Tumor cells did not invade blood and lymphatic vessels, and extrathoracic metastases were not detected. The prognosis of bronchiolo-alveolar cell carcinoma was determined by intra-pulmonary tumor extent. Based on a comparison with the outcome of unresected cases, bronchiolo-alveolar cell carcinoma limited within one lobe should be surgically resected.
 ...
PMID:[A resected case of a bronchiolo-alveolar cell carcinoma of the lung accompanying pneumonia-like shadow on chest roentgenogram]. 975 49

Diffuse alveolar damage represents the pathologic basis of most cases of the acute respiratory distress syndrome. Diffuse alveolar damage reflects injury to the pulmonary alveolar wall and microvasculature, leading to the exudation of water and plasma proteins that can overwhelm the local lymphatic drainage. Organizing pneumonia is a prominent histopathologic feature in some cases of diffuse alveolar damage. We examined whether diffuse alveolar damage-organizing pneumonia and changes in lymphatic architecture might be indicators of clinical outcome in acute respiratory distress syndrome. Formalin-fixed lung sections (n = 26) from thoracoscopic lung biopsies of patients with diffuse alveolar damage in the fibroproliferative phase, with or without organizing pneumonia, were immunostained with anti-CD31 and anti-D240, markers of vascular and lymphatic endothelium, respectively, and examined by morphometric analysis. Positively staining vessels were enumerated and maximal luminal diameters recorded in randomly selected low-power fields. Patients with diffuse alveolar damage-organizing pneumonia showed greater survival than those with diffuse alveolar damage (67% versus 33%, P = .03). The maximal luminal diameter of D240+ lymphatic vessels was larger for diffuse alveolar damage-organizing pneumonia than diffuse alveolar damage (28 +/- 4 versus 59 +/- 16 microm, P = .02). In addition, larger lymphatic luminal diameters (28 +/- 4 versus 47 +/- 11 microm) were associated with increased survival (P = .12). We conclude that lung biopsy histopathology and pulmonary lymphatic morphology may predict survival in acute respiratory distress syndrome.
 ...
PMID:Organizing pneumonia and pulmonary lymphatic architecture in diffuse alveolar damage. 1860 71

Fungi of the genus Pneumocystis are opportunistic pathogens which cause lethal pneumonia in immunocompromised hosts. Those fungi may also invade other visceral organs where they induce lesions, although, the pathways or mechanisms of the in vivo infection are still unknown. The corticosteroid-treated rat model was used to evaluate the course of extrapulmonary pneumocystosis. Liver, kidney, spleen, and mesenteric lymph nodes of 16 rats were examined for the presence of mtLSU gene fragments of P. carinii and P. wakefieldiae using the nested PCR method. Pneumocystis DNA was detected in 26 organ samples of which 17 contained both species (P. carinii and P. wakefieldiae) and 9 contained only P. carinii. Positive samples were received from 10 rats examined after 6-9 weeks of immunosuppression. The highest percentage of positive samples (62.5%) was obtained among examined visceral lymph nodes. Pneumocystis DNA was detected in the blood serum of two rats with no traces of the DNA in their internal organs. Conversely, Pneumocystis DNA was found in the internal organs of two other rats, although their serum samples were negative. The average number of Pneumocystis cysts in the lungs of animals in which extrapulmonary infection was detected was 3.4 per one microscopic view field. In the case of animals where the infection was limited to the lung tissue this number was almost two times lower (1.8 cysts per one microscopic view field). An analysis of the results of the presently reported experiment showed that massive Pneumocystis infection in the lungs makes it more likely that Pneumocystis will spread to other internal organs. This spread probably takes place via the lymphatic vessels. The extrapulmonary foci may contain either P. carinii alone, or both pathogens: P. carinii and P. wakefieldiae.
 ...
PMID:[Presence of Pneumocystis carinii and Pneumocystis wakefieldiae DNA in the extrapulmonary tissues of immunocompromised laboratory rats]. 1967 May 32

Granulomatous lung diseases include a large number of conditions among granulomas are the pathological hallmark. Some of these conditions are frequently encountered in clinical practice. Differentiating infectious from noninfectious forms is a priority for the different specialists approaching these diseases, given the different implications for management and treatment. However, differential diagnosis is not always straightforward and the diagnosis of granulomatous disease, considering separately the clinical, radiological and pathological aspects, is at times incomplete or uncertain and requires multidisciplinary assessment. In this paper, we propose a combined HRCT-pathological approach to assess both the topographical and morphological features of the lesions. Based on topography, we can distinguish between granulomatous lesions distributed along the lymphatic vessels, with random distribution or centred on the airways. The prototype of the disease with lymphatic granulomas is sarcoidosis. In contrast, diseases exhibiting a random distribution of granulomas are those with haematogenous spread, the most typical of which is miliary tuberculosis (TB). Many diseases have distribution along the airways including hypersensitivity pneumonia and granulomatous bronchiolitis (including infections with bronchial spread, especially mycobacteriosis). The anatomical approach is completed by the assessment of the morphological aspects of the lesions and associated signs, reflecting both the possible mechanisms of spread and the different types of pathological and/or reparative tissue related to the disease.
...
PMID:Diffuse granulomatous lung disease: combined pathological-HRCT approach. 2448 91

CLCA1 is a member of the CLCA (calcium-activated chloride channel regulator) family and plays an essential role in goblet cell mucus production from the respiratory tract epithelium. CLCA1 also regulates Ca2+-dependent Cl- transport that involves the channel protein transmembrane protein 16A (TMEM16A) and its accessary molecules. CLCA1 modulates epithelial cell chloride current and participates in the pathogenesis of mucus hypersecretory-associated respiratory and gastrointestinal diseases, including asthma, chronic obstructive pulmonary disease, cystic fibrosis, pneumonia, colon colitis, cystic fibrosis intestinal mucous disease, ulcerative colitis, and gastrointestinal parasitic infection. Most studies have been focused on the expression regulation of CLCA1 in human specimens. Limited studies used the CLCA1-deficient mice and CLCA1 blocking agents and yielded inconsistent conclusions regarding its role in these diseases. CLCA1 not only regulates mucin expression, but also participates in innate immune responses by binding to yet unidentified molecules on inflammatory cells for cytokine and chemokine production. CLCA1 also targets lymphatic endothelial cells and cancer cells by regulating lymphatic cell proliferation and lymphatic sinus growth in the lymphatic organs and controlling cancer cell differentiation, proliferation, and apoptosis, all which depend on the location of the lymphatic vessels, the type of cancers, the presence of Th2 cytokines, and possibly the availability and type of CLCA1-binding proteins. Here we summarize available studies related to these different activities of CLCA1 to assist our understanding of how this secreted modifier of calcium-activated chloride channels (CaCCs) affects mucus production and innate immunity during the pathogenesis of respiratory, gastrointestinal, and malignant diseases.
 ...
PMID:Calcium-activated chloride channel regulator 1 (CLCA1): More than a regulator of chloride transport and mucus production. 3187 32


1