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)

In 1979 and 1980, more than 400 harbor seals (Phoca vitulina) along the New England coast of the United States died of epizootic pneumonia that was attributed to an influenza virus. Six mycoplasma isolates that were recovered from the respiratory tracts of affected seals were investigated and were found to be serologically identical and distinct from previously described species. These isolates required serum for growth, did not possess a cell wall, and did not hydrolyze urea. Arginine was hydrolyzed, glucose was not fermented, film and spots were observed on horse serum agar, phosphatase was produced, tetrazolium was not reduced, and serum and casein were not digested. The guanine-plus-cytosine content of the DNA was 27.8 mol%. We propose the name Mycoplasma phocidae for these isolates. The type strain of M. phocidae is strain 105 (= ATCC 33657).
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PMID:Mycoplasma phocidae sp. nov., isolated from harbor seals (Phoca vitulina L.). 158 Nov 81

Following intranasal infection with murine cytomegalovirus (MCMV), the levels of viral replication in the lungs of susceptible BALB/c mice were enhanced by treatment with cyclophosphamide (CY), or to a greater extent cyclosporin A (CsA) or the Nu/Nu genotype. Focal inflammation was seen 2-4 days after infection in all groups. This was followed by diffuse interstitial pneumonitis which cleared 12-20 days later in the absence of immunosuppression. Although the initial foci of inflammation were less prominent in infected mice treated with CY or CsA, the most severe interstitial pneumonitis was seen 7 days p.i. in mice given CY, whilst CsA-treatment produced focal and disseminated pneumonitis 7-14 days p.i. and Nu/Nu mice exhibited only the focal response. MCMV-infected mice maintained from weaning on a low protein (4% casein) diet also retained higher titres of virus in their lungs than did normally-fed controls, and displayed more prominent focal pneumonitis.
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PMID:Modulation of immunocompetence by cyclosporin A, cyclophosphamide or protein malnutrition potentiates murine cytomegalovirus pneumonitis. 166 28

Twenty-two patients with general variable immunodeficiency (GVI) and malabsorption syndrome (MS) were followed up for 2-12 years. III degree MS was found in 17 cases. Serum immunoglobulins concentration and T-lymphocyte count were reduced, the latter at the expense of theophylline-resistant and active E-RFC. With casein and milk albumin as the antigens, lymphokine-producing capacity of the mononuclear cells appeared elevated. MS treatment with adjuvant gamma-globulin produced a positive trend in clinical manifestations of the disease, content of T lymphocytes and relevant subpopulations. Long-term results were less favourable: partial compensation with recurrences persisted in 15 patients only. Seven patients died: two of pneumonia, five of cardiac failure and visceral dystrophy. All MS patients are recommended to undergo serum immunoglobulins diagnosis of GVI and in case of its verification to receive life-time gamma-globulin replacement therapy.
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PMID:[General variable immunologic deficiency with malabsorption syndrome]. 239 30

The course of 61 infants admitted for treatment of chronic diarrhea and malnutrition was reviewed. 30 children had (M) marasmus, 18 (K) kwashiorkor, and 13 (MK) marasmic kwashiorkor. After initial rehydration, infants were managed with a predominantly oral nutrition regimen utilizing a formula based on whole protein (casein), vegetable oil, glucose, and sucrose. Intravenous fluids were required for 38 infants (62%) for a median duration of 6 days, principally for the delivery of antibiotics, although amino acids were added in many instances. Feedings were started at 25 kcal/kg/day and were increased 35 kcal/kg/day every other day until acceptable steady weight gain ensued, provided that stool ouput did not exceed 100-50 gm/day and stool character was improving. Infants with M and MK reached a maximum intake of 151 + or - 21 kcal/dg/day after 5 weeks of treatment. Weight gain had been occurring for 2 weeks prior to this time. Infants with K were purposely not advanced past 75 kcal/kg/day until edema had cleared; a maximum intake of 135 + or - 16 kcal/kg/day was reached at 5 weeks. Mean initial serum albumin concentration in these infants with K was 1.8 + or - 0.3 gm/day and required 20 + or - 13 and 53 + or - 24 days to exceed 2.0 and 3.6 gm/dl, respectively. 14 of the 61 infants were moribund on arrival and died within the first 3 days; the remaining 8 died of overwhelming infection (6 generalized and 2 pneumonia). Data suggest that once infection is controlled, infants with chronic diarrhea and malnutrition can usually be effectively managed by enteral feeding without resorting to parenteral alimentation.
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PMID:Nutritional management of chronic diarrhea and malnutrition: primary reliance on oral feeding. 677 51

One hundred twenty male Sprague-Dawley rats (3 weeks old) were given biotin-deficient diets containing ovalbumin as the protein source. Ten control rats of the same origin were fed a commercially available purified diet that used casein as a protein source. Eosinophils and histiocytes were observed at a higher frequency in lungs of rats fed the purified diets containing ovalbumin than in the controls. Foam cells were confined to subpleural and peribronchial regions, reacting positively to anti-lysozyme antibody. The incidence of pulmonary histiocytosis was 76/120 rats (63.3%) in the groups fed the ovalbumin-containing diets as compared with 1/10 (10.0%) in the controls. The accumulation of eosinophils in lung was highest (6/24 rats, 25%) at 3 months. This lesion was not seen in the controls. Eosinophils were first observed in the perivascular and peribronchiolar regions. In advanced lesions, macrophages and mast cells also appeared in the lesions, which at this stage resembled so-called idiopathic chronic eosinophilic pneumonia of human beings. Neither foam cells nor eosinophils were present in any of the other organs. Because there was no difference in the composition of the diets with the exception of the protein source, these lung lesions may be due to biotin deficiency resulting from the use of ovalbumin as the protein source.
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PMID:Eosinophil and foam cell accumulation in lungs of Sprague-Dawley rats fed purified, biotin-deficient diets. 857 40

Members of the choline binding protein (Cbp) family are noncovalently bound to phosphorylcholine residues on the surface of Streptococcus pneumoniae. It has been suggested that CbpG plays a role in adherence and increase virulence both at the mucosal surface and in the bloodstream, but the function of this protein has been unclear. A new sequence analysis indicated that CbpG is a possible member of the S1 family of multifunctional surface-associated serine proteases. Clinical isolates contained two alleles of cbpG, and one-third of the strains expressed a truncated protein lacking the C-terminal, cell wall-anchoring choline binding domain. CbpG on the surface of pneumococci (full length) or released into the supernatant (truncated) showed proteolytic activity for fibronectin and casein, as did CbpG expressed on lactobacilli or as a purified full-length or truncated recombinant protein. Recombinant CbpG (rCbpG)-coated beads adhered to eukaryotic cells, and TIGR4 mutants lacking CbpG or having a truncated CbpG protein showed decreased adherence in vitro and attenuation of disease in mouse challenge models of colonization, pneumonia, and bacteremia. Immunization with rCbpG was protective in an animal model of colonization and sepsis. We propose that CbpG is a multifunctional surface protein that in the cell-attached or secreted form cleaves host extracellular matrix and in the cell-attached form participates in bacterial adherence. This is the first example of distinct functions in virulence that are dependent on natural variation in expression of a choline binding domain.
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PMID:Multifunctional role of choline binding protein G in pneumococcal pathogenesis. 1642 24

Mycoplasma pneumoniae accounts for 20 to 30% of all community-acquired pneumonia and has been associated with other airway pathologies, including asthma, and a range of extrapulmonary manifestations. Although the entire genomic sequence of M. pneumoniae has been completed, the functions of many of these genes in mycoplasma physiology are unknown. In this study, we focused on clpB, a well-known heat shock gene in other bacteria, to examine its role in mycoplasma growth. Transcriptional and translational analyses of heat shock in M. pneumoniae indicated that clpB is significantly upregulated, reinforcing its status as a critical responder to heat stress. Interestingly, M. pneumoniae ClpB does not use dual translational start points for ClpB synthesis, like other ClpB-characterized bacteria. Biochemical characterization of purified M. pneumoniae recombinant ClpB revealed casein- and lysine-independent ATPase activity and DnaK-DnaJ-GrpE-dependent chaperone activity. An M. pneumoniae mini-Tn4001-integrated, clpB-null mutant was impaired in its ability to replicate under permissive growth conditions, demonstrating the growth-promoting status of ClpB.
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PMID:Characterization of a unique ClpB protein of Mycoplasma pneumoniae and its impact on growth. 1877 36

Pneumocystis species are opportunistic fungal pathogens that cause severe pneumonia in immunocompromised hosts. Recent evidence has suggested that unidentified proteases are involved in Pneumocystis life cycle regulation. Proteolytically active ADAM (named for "a disintegrin and metalloprotease") family molecules have been identified in some fungal organisms, such as Aspergillus fumigatus and Schizosaccharomyces pombe, and some have been shown to participate in life cycle regulation. Accordingly, we sought to characterize ADAM-like molecules in the fungal opportunistic pathogen, Pneumocystis carinii (PcADAM). After an in silico search of the P. carinii genomic sequencing project identified a 329-bp partial sequence with homology to known ADAM proteins, the full-length PcADAM sequence was obtained by PCR extension cloning, yielding a final coding sequence of 1,650 bp. Sequence analysis detected the presence of a typical ADAM catalytic active site (HEXXHXXGXXHD). Expression of PcADAM over the Pneumocystis life cycle was analyzed by Northern blot. Southern and contour-clamped homogenous electronic field blot analysis demonstrated its presence in the P. carinii genome. Expression of PcADAM was observed to be increased in Pneumocystis cysts compared to trophic forms. The full-length gene was subsequently cloned and heterologously expressed in Saccharomyces cerevisiae. Purified PcADAMp protein was proteolytically active in casein zymography, requiring divalent zinc. Furthermore, native PcADAMp extracted directly from freshly isolated Pneumocystis organisms also exhibited protease activity. This is the first report of protease activity attributable to a specific, characterized protein in the clinically important opportunistic fungal pathogen Pneumocystis.
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PMID:Characterization of a novel ADAM protease expressed by Pneumocystis carinii. 1945 Dec 39

It has been speculated that the addition of antioxidants to diet could act as either radioprotectors or as mitigators of radiation injury. In preparation for studies of the mitigation efficacy of antioxidants, rats were placed on a modified version of AIN-76A, the diet typically used in such studies. This AIN-76A diet is refined and has no synthetic antioxidants or isoflavones. Compared to the natural-ingredient Teklad 8904 diet used in previous studies, use of the AIN-76A diet from 1-18 wk after irradiation significantly reduced injury in a radiation nephropathy model. A confirmation study included an additional arm in which the AIN-76A diet was started 2 wk prior to irradiation; again, the switch to AIN-76A postirradiation mitigated radiation nephropathy (p < 0.001), but switching to the AIN-76A diet preirradiation had no effect (p > 0.2). The two diets do not differ in salt content, but the AIN-76A diet is somewhat lower in protein (18% vs. 24%). The protein source (primarily soy in Teklad 8904 vs. casein in AIN-76A) might explain the effects. However, replacing the casein in AIN-76A with soy did not change the mitigation efficacy of the diet (p > 0.2 for comparison of the different AIN-76A diets). A similar study in a rat radiation pneumonitis model also suggested mitigation by postirradiation use of AIN-76A, although the effect was not statistically significant (p = 0.07). In conclusion, base diet alone can have biologically significant effects on organ radiosensitivity, but the mechanistic basis for the effect and its dependence of timing relative to irradiation are unclear.
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PMID:Effects of Diet on Late Radiation Injuries in Rats. 3062 56