Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0206061 (interstitial pneumonia)
 6,105 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of in vivo treatment with anti-CD11b (MAC-1) antibody (Ab) was examined in an inflammatory disease model, the viable moth-eaten (mev) mutant mouse. The autosomal recessive mev gene occurred spontaneously as a point mutation of the hematopoietic cell protein tyrosine phosphatase in C57BL/6 mice. Homozygotes (mev/mev) develop a chronic myelomonocytic inflammation, involving accumulation of myelomonocytic cells in lungs and skin, resulting in interstitial pneumonitis and severe edema in the paws. These mice also exhibit abnormalities in lymphoid development, thymic atrophy, with T cell and NK cell dysfunction. These inflammatory changes are transferrable by bone marrow cells of mev/mev mice, indicating that mev mutation is due to a stem cell defect in the myelomonocytic pathway. An anti-CD-11b (5C6) Ab inhibited the immunopathologic changes in the bone marrow chimeras, when the Ab treatment was initiated on day -1 or day 0 of the bone marrow transplant. The lungs, paws, and thymus all remained normal after treatment. Furthermore, the Ab also delayed the onset of the mev syndromes when the Ab was given 10 days after the bone marrow transfer. Therefore anti-CD11b Ab inhibited inflammation both prophylactically and therapeutically, and restored normal function of T and NK cells in this disease model. These results support the contention that CD11b molecules expressed in the myelomonocytic cells play a critical role in this naturally occurring inflammatory disease.
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PMID:Anti-CD11b antibody prevents immunopathologic changes in viable moth-eaten bone marrow chimeric mice. 825 88

The clinical, radiological and pathological findings in 12 dogs with canine leucocyte adhesion deficiency (CLAD) from six litters are described. All the dogs were younger than 15 weeks at admission, all had been febrile and 11 had been treated with antibiotics. Seven had been treated for omphalophlebitis. At admission, all had gingivitis, lymph node enlargement and profound neutrophilia. Ten dogs were radiographed and showed various skeletal lesions compatible with metaphyseal osteopathy, craniomandibular osteopathy and osteomyelitis. Four dogs had clinical signs of respiratory distress and seven exhibited a mild interstitial pneumonia at necropsy. Six dogs had skin wounds, with strikingly few neutrophils seen on stained sections. All dogs were euthanased before six months of age due to severe and incurable infections. The clinical signs, radiological features and haematology were strongly suggestive of CLAD. The diagnosis was confirmed by granulocyte function tests and flow cytometry, which revealed impaired adhesion, impaired C3b-mediated phagocytosis and absence of adhesion proteins CD11b/CD18.
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PMID:Clinical, radiological and pathological features of 12 Irish setters with canine leucocyte adhesion deficiency. 1090 23

Idiopathic interstitial pneumonias are a group of idiopathic interstitial lung diseases of which idiopathic pulmonary fibrosis (IPF) is the lesion of usual interstitial pneumonia. Although the pathogenic mechanisms remain incompletely understood, disease-specific changes in blood, a readily accessible biospecimen, have not been fully characterized. To identify biomarkers from blood and sera, the immune status of IPF patients and control subjects without structural lung disease was quantified by measuring cell surface markers, mRNA levels, and serum proteins. Statistically significant differences in cellular and molecular markers were observed between the 2 groups. The cytokine receptor IL-17RB was significantly higher in CD14+ peripheral blood mononuclear cells (PBMCs) from IPF patients, whereas expression of the chemokine receptor CXCR4 was lower. Gene expression analyses identified 18 differentially expressed genes out of 195 selected. Of these, EMR1, CCR3, UPAR, FCGR2A, OPN, CEACAM3, CD16a, CD18, CD11b, LTF, and LCN2 were up-regulated, whereas IL-17RB, IL-10, PDGFA, CD301/Clec10a, CD25/IL-2RA, IL-23p19, and IL-15 were down-regulated in IPF. Differentially regulated genes were in the functional areas of inflammation and cell signaling. Serum levels of UPAR and OPN were higher in IPF. These observations reveal significant differences in cell and molecular markers involved in monocyte/macrophage activation and migration, and suggest a role for IL-17RB in IPF.
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PMID:Differential expression of monocyte/macrophage- selective markers in human idiopathic pulmonary fibrosis. 2130 37