Disease relevance of Pulmonary Eosinophilia

• In a murine model of respiratory syncytial virus disease, prior sensitization to the attachment glycoprotein (G) leads to pulmonary eosinophilia and enhanced illness [1].
• Dose-for-dose, infected mice receiving G-specific cells suffered the most severe (sometimes fatal) illness, characterized by lung hemorrhage, pulmonary neutrophil recruitment (shock lung) and intense pulmonary eosinophilia [2].
• MBP may also mediate altered lung function in various inflammatory lung diseases associated with pulmonary eosinophilia [3].
• Eosinophilic pneumonia and respiratory failure associated with a trazodone overdose [4].
• It is concluded that drug hypersensitivity to sulfadoxine was the cause of the eosinophilic pneumonia in this patient [5].

High impact information on Pulmonary Eosinophilia

• Clofibrate and eosinophilic pneumonia [6].
• Lowering adenosine and 2'-deoxyadenosine levels using ADA enzyme therapy decreased the pulmonary eosinophilia and resolved many of the lung histopathologies [7].
• Therefore, we have identified an association between peptide 184- 198 of natural G protein and the CD4(+) T cell-mediated induction of pulmonary eosinophilia after live RSV challenge [8].
• In contrast, mice immunized with a peptide (208-222) conjugate associated with induction of IFN-gamma secreting spleen cells did not exhibit pulmonary eosinophilia after challenge [8].
• This reduction in pulmonary eosinophilia correlated with the suppression of Th2 type cytokine production [9].

Chemical compound and disease context of Pulmonary Eosinophilia

• Pulmonary eosinophilia associated with dapsone [10].
• The specificity of the response was established by immunizing with HDE and challenging with purified cockroach allergen, which induced pulmonary eosinophilia and airway hyperreactivity [11].
• Steroid-refractory neonatal eosinophilic pneumonia responsive to cyclosporin A [12].
• 5-Oxo-ETE and CC chemokines may combine to induce pulmonary eosinophilia in asthma [13].
• Spirometric and lung volume measurements were carried out before and after treatment with diethylcarbamazine in 19 patients with tropical eosinophilia [14].

Biological context of Pulmonary Eosinophilia

• Distinct kinetics between urinary EDN/EPX and eosinophil counts differentiated the recurrence of chronic eosinophilic pneumonia from an asthma attack in one patient [15].
• Immune responses to the nonglycosylated ectodomain of respiratory syncytial virus attachment glycoprotein mediate pulmonary eosinophilia in inbred strains of mice with different MHC haplotypes [16].
• Acute eosinophilic pneumonia associated with intramuscular administration of progesterone as luteal phase support after IVF: case report [17].
• Genetic polymorphisms of eosinophil-derived neurotoxin and eosinophil cationic protein in tropical pulmonary eosinophilia [18].
• As demonstrated by IL-5-dependent pulmonary eosinophilia after challenge and serum anti-G protein IgG1 to IgG2 ratios, highly purified native G protein sensitized all strains for a Type 2 T cell phenotype [16].

Anatomical context of Pulmonary Eosinophilia

• OX40 ligation on activated T cells enhances the control of Cryptococcus neoformans and reduces pulmonary eosinophilia [19].
• After OVA pulsing and adoptive transfer, lung macrophages selectively promoted a Th1 response in Ag-sensitized recipients and did not induce pulmonary eosinophilia [20].
• In vivo expression of CD69 on lung eosinophils in eosinophilic pneumonia: CD69 as a possible activation marker for eosinophils [21].
• Our results, in concordance with previous studies, demonstrate the potential activity of TARC for recruiting Th2 cells to the lungs and suggest a significant role for TARC in the pathogenesis of eosinophilic pneumonia [22].
• Sulfadoxine specific lymphocyte transformation in a patient with eosinophilic pneumonia induced by sulfadoxine-pyrimethamine (Fansidar) [5].

Gene context of Pulmonary Eosinophilia

• Administration of IL-12 (1 microgram/d x 5 d) at the time of a single antigen challenge abolished the airway hyperresponsiveness and pulmonary eosinophilia and promoted an increase in interferon (IFN) gamma and decreases in IL-4 and IL-5 expression [23].
• In support of this, mice genetically deficient for VCAM-1 and intercellular adhesion molecule-1 failed to develop pulmonary eosinophilia [24].
• Pulmonary eosinophilia was absent in both IL-4 KO and IL-10 KO mice compared with WT mice [25].
• Second, in order to address the specific role of eotaxin-2 in IL-13-induced pulmonary eosinophilia, we generated eotaxin-2 gene-deficient mice by homologous recombination [26].
• Using two different protocols of allergen challenge, we demonstrate that absence of CCR8 does not affect the development of pulmonary eosinophilia and Th2 cytokine responses [27].

Analytical, diagnostic and therapeutic context of Pulmonary Eosinophilia

• Mucosal peptide vaccination reduced pulmonary eosinophilia in mice subsequently immunized with G and challenged with RSV [28].
• A sensitive MAb (CA101)-based ELISA for measuring circulating parasite antigen was capable of detecting antigen in the sera of 93% of patients with microfilaremia, 46% of those with lymphatic obstruction, and 56% of patients with tropical pulmonary eosinophilia syndrome [29].
• Elevated chemokine levels in bronchoalveolar lavage fluid of patients with eosinophilic pneumonia [30].
• The pulmonary eosinophilia was similar to that induced by a facsimile of a formalin-inactivated vaccine used in previous clinical trials and was prevented by prior in vivo treatment with anti-IL-5 but not with control immunoglobulin G or anti-IFN-gamma neutralizing monoclonal antibodies [31].
• Allergen-induced pulmonary eosinophilia in Brown Norway rats was used subsequently to determine anti-inflammatory activity in an animal model [32].

References