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

The mucosubstances of the bronchial epithelial goblet cells in non-pneumonic calves were almost exclusively sulphomucin; neutral mucin, sialomucin and sulphomucin were produced by the submucosal glands. Calves with lesions of cuffing pneumonia from which M. dispar was frequently cultured had increased numbers of epithelial goblet cells extending into the peripheral airways as far as the bronchioles. These pneumonic animals had epithelial goblet cells, some of which contained sialomucin, while in the gland a switch from neutral to acid mucosubstance in the form of increased sulphomucins and sialomucins was detected.
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PMID:A histochemical study of mucosubstances in the bovine respiratory tract with special reference to cuffing pneumonia. 59 Aug 84

The glycoproteins in the normal pig bronchial gland are identified by the combined Alcian Blue (AB)-periodic acid Schiff (PAS) technique, with the use of sialidase digestion and AB staining either at pH 2-6 or at pH 1-0. In enzootic pneumonia (produced experimentally by infection with Mycoplasma hyorhinis) the bronchial gland hypertrophies, mucous and serous cells both increase, in number and size; hence the total glycoprotein content of the gland increases. The distribution of glycoproteins in the hypertrophied gland differs from that in the normal. Quantitative analysis of the mucous cells shows that in the hypertrophied gland the acid glycoprotein is increased relative to the neutral. There is also a relative change in the amounts of sialidase-sensitive sialomucin and sulphomucin; both are significantly increased at the expense of the sialidase-resistant sialomucin. Qualitative analysis of the serous cells shows that in the normal gland most of the glycoprotein is neutral and that the small amount of acid glycoprotein is sialidase-resistant sialomucin. In the hypertrophied gland there is relatively more acid glycoprotein which is either sialidase-resistant sialomucin or sulphomucin; in addition, in pigs with enzootic pneumonia there is an increase in the height of the bronchial epithelium and a depletion in both goblet cell number and glycoprotein content, which latter has more neutral glycoprotein and less acid glycoprotein.
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PMID:Histochemical identification of glycoproteins in pig bronchial epithelium: (a) normal and (b) hypertrophied from enzootic pneumonia. 115 72

Mycoplasma hyopneumoniae causes pneumonia in pigs. The effect of infection by this organism on histochemical characteristics of airway mucin within epithelial cells was studied. Seven- to 10-week-old pigs were inoculated intratracheally with M hyopneumoniae or culture broth, and lung tissues were collected from inoculated and control pigs at 2, 4, and 6 weeks after inoculation. Tissue sections were stained with periodic acid-Schiff/Alcian blue, pH 2.5 or high iron diamine/Alcian blue. Histologic features of randomly selected bronchi, bronchioles, and submucosal glands were compared in sections stained with periodic acid-Schiff/Alcian blue. Bronchial goblet cell sulfomucin and sialomucin were quantitated by image analysis of sections stained with high iron diamine/Alcian blue. Bronchi and bronchioles of infected pigs contained proportionately fewer goblet cells with mucin at all stages of infection than age-matched control pigs. Goblet cells in bronchi of infected pigs contained significantly less total mucin and sialomucin, and significantly more sulfomucin than goblet cells of control pigs. Increased sulfated mucin in bronchial goblet cells may reflect altered glycoprotein production or secretion in response to infection with M hyopneumoniae.
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PMID:Histochemical and morphologic changes of porcine airway epithelial cells in response to infection with Mycoplasma hyopneumoniae. 141 80

The D2-40 antigen is a glycosylated sialomucin that is strongly expressed by lymphatic endothelial cells. Recently we observed the expression of D2-40 on the luminal surface of pulmonary airspaces in lung sections. The aim of the study was to assess the expression of D2-40 antigen in normal lung development and in various pathologic conditions in which abnormal alveolar infiltrates were present. Formalin-fixed lung tissue was selected from 42 fetal/neonatal autopsy cases ranging in gestational age from 12 to 41 weeks and from 10 adult lungs. In the fetal/neonatal group, 22 cases were histologically normal, whereas 20 were abnormal (including cases of pneumonia, alveolar hemorrhage, meconium aspiration, pulmonary hypoplasia, and pulmonary interstitial emphysema). In the adult group, 5 cases were histologically normal and 5 had pneumonia. Immunohistochemical staining was performed on all cases using antibody to D2-40. All cases of normal fetal/neonatal lung and normal adult lung showed diffuse strong expression of D2-40 on the luminal surface of the alveolar lining cells. D2-40 expression was also noted on the bronchiolar lining cells of normal fetal/neonatal lung. In all cases in which there was an abnormal infiltrate or foreign material within the airspaces, expression of D2-40 was lost in the alveolar lining. The production of the D2-40 antigen in the alveolar lining occurs as early as 12 weeks gestation and continues to be present throughout all other stages of lung development, as well as in adult lung. These results suggest that D2-40 may have a cell membrane protective function.
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PMID:D2-40 is expressed on the luminal surface of pulmonary airspaces in normal developing and adult lung but is lost in conditions associated with intra-alveolar infiltrates. 2215 May 77