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Biomedical subjects

Paula J Busse

Publications and source records attributed to Paula J Busse.

7 recordsLinked to original sources
PubMed2007

Pulmonary complications of common variable immunodeficiency.

OBJECTIVES: To review pulmonary complications of common variable immunodeficiency (CVID) and summarize data available on the use of replacement antibody treatment to protect against lung changes. DATA SOURCES: Relevant articles regarding CVID and pulmonary disease identified from PubMed and reference lists of review articles. STUDY SELECTION: Key articles were selected by the authors. RESULTS: Patients with CVID often develop acute sinopulmonary infections that can lead to chronic airway inflammation, which can produce substantial morbidity and mortality. Replacement immunoglobulin treatment significantly reduces the reoccurrence of lower airway infections, but the effect on the development of chronic lung damage is not yet clear. Screening examinations, such as pulmonary function testing and high-resolution computed tomography of the chest, can be used to evaluate pulmonary status. Patients with abnormal findings may benefit from more aggressive treatment, including larger doses of immune globulin and the use of prophylactic antibiotics. CONCLUSIONS: Pulmonary complications present a significant comorbidity in CVID; monitoring may indicate which patients require more aggressive treatment.

Anti-Bacterial Agents↗
PubMed2005

Allergen sensitization evaluation and allergen avoidance education in an inner-city adult cohort with persistent asthma.

BACKGROUND: Asthma morbidity, mortality, and health services utilization are highest among inner-city populations. The National Asthma Education and Prevention Program Expert Panel recommends that all patients with moderate and severe persistent asthma be evaluated for sensitization to environmental allergens. OBJECTIVE: This study examined whether a cohort of inner-city adults hospitalized with asthma had been evaluated for allergen sensitization, received avoidance counseling, and followed through on these recommendations. METHODS: One hundred sixty-nine eligible patients who were part of a prospective cohort of all adults hospitalized in an inner-city hospital over a consecutive 12-month period completed a questionnaire to assess allergen sensitization evaluation, avoidance education, and adherence. RESULTS: Overall, 60% of patients had ever been evaluated for allergen sensitization. Among those who were evaluated, 94.0% were sensitized to at least one antigen: 91.5% to dust mites, 90.5% to outdoor allergens, 77.9% to cats, 69.5% to dogs, 68.4% to molds, and 61% to cockroaches. Approximately half of the patients sensitized to dust mite (55.1%) or mold (52.8%) were given any avoidance-abatement advice. Patient adherence to this advice was highly variable. Allergen sensitization evaluation was more likely among women (odds ratio, 3.05; CI, 1.64-8.64) and those who use oral steroids most or all of the time (odds ratio, 7.14; CI, 2.25-22.56) and less likely among smokers (odds ratio, 0.26; CI, 0.11-0.61). CONCLUSION: In this population of inner-city adults hospitalized with asthma, the quality of allergen sensitization evaluation, avoidance education, and patient adherence with these recommendations was suboptimal.

Adult↗
PubMed2005

Chronic exposure to TNF-alpha increases airway mucus gene expression in vivo.

BACKGROUND: Hypersecretion of mucus plays an important role in the pathogenesis and severity of asthma. The primary proteins in mucus are mucin glycoproteins; MUC-5AC is the primary airway mucin gene. The calcium chloride-activated channel gene hCLCA1 (gob-5 in the mouse) has been suggested to increase MUC-5AC gene expression, and both are increased in asthmatic patients and murine models. TNF-alpha increases the expression of these genes in vitro but has not been investigated in vivo. OBJECTIVE: We sought to determine whether TNF-alpha increases gene expression of gob-5 and MUC-5AC and induces mucus cell metaplasia in vivo. METHODS: Naive BALB/c mice received 50 ng of recombinant murine TNF-alpha (rmTNF-alpha) intratracheally daily for 1, 2, or 3 weeks; another group received the same dose of intratracheal rmTNF-alpha daily for 3 weeks and then alternate-day treatment for 3 additional weeks (total of 6 weeks). AKR mice received 50 ng of rmTNF-alpha intratracheally for 3 or 6 weeks daily. Naive nontreated mice were used as control animals. Airway gene products for gob-5 and MUC-5AC were determined by means of real-time PCR. Lung tissue sections were stained with periodic acid-Schiff/Alcian blue to assess mucus cell metaplasia. RESULTS: rmTNF-alpha significantly increased gene expression of airway gob-5 and MUC-5AC after 2 weeks in the BALB/c mice. There was noticeable mucus staining in all mice treated for at least 3 weeks with TNF-alpha and in 80% of the mice receiving 2 weeks of treatment. After 3 weeks of treatment, the AKR mice also showed increased gob-5 expression. CONCLUSIONS: This study demonstrates for the first time that TNF-alpha alone in vivo is sufficient to increase airway mucus gene expression in 2 murine strains.

Animals↗
PubMed2002

Primary leptomeningeal lymphoma in a patient with concomitant CD4+ lymphocytopenia.

BACKGROUND: Idiopathic CD4+ lymphocytopenia (ICL) is a rare disorder in which patients have mild and/or severe opportunistic infections or maybe without symptoms. The etiology is currently unknown. Diagnosis is made by excluding retroviral infections (human immunodeficiency virus-1 or -2, human T cell lymphotropic virus-1 or -2) or other known causes of immunosuppression. OBJECTIVE: To provide a case report of a patient with possible ICL who presented with a rare form of primary non-Hodgkin lymphoma (NHL) of the central nervous system (CNS). Review of the literature has identified only five other patients with NHL and ICL; however, none of these had a CNS lymphoma. RESULTS: We describe a patient with possible ICL, and address links between lymphopenia and lymphoproliferative disorders. CONCLUSIONS: Although not uncommon for patients infected with human immunodeficiency virus to develop CNS NHL, this is the first case of a possible ICL patient with such a lymphoma. This case revisits an important relationship between lymphopenia and lymphoproliferative disorders.

Adult↗
PubMed2002

B-cell epitopes as a screening instrument for persistent cow's milk allergy.

BACKGROUND: Cow's milk is one of the most common causes of food allergy in the first years of life. We recently defined IgE-binding epitopes of all 6 major cow's milk proteins (alpha(s1)-, alpha(s2)-, beta-, and kappa-casein; alpha-lactalbumin; and beta-lactoglobulin) and had some evidence suggesting that IgE antibodies from patients with persistent cow's milk allergy (CMA) recognize different epitopes on cow's milk proteins than do those from patients who were likely to outgrow their allergy. OBJECTIVE: In this study we sought to assess whether recognition of IgE antibodies of certain epitopes of cow's milk proteins would clearly separate the patients with life-long CMA from those who will become clinically tolerant to cow's milk. METHODS: According to the known IgE-binding regions of cow's milk proteins, 25 decapeptides of alpha(s1)-casein, alpha(s2)-casein, kappa-casein, alpha-lactalbumin, and beta-lactoglobulin, comprising the core epitopes, were synthesized on a cellulose-derivatized membrane. Sera from 10 patients with persistent CMA and 10 patients who subsequently outgrew their milk allergy were used to investigate the differences in epitope recognition. RESULTS: Five IgE-binding epitopes (2 on alpha(s1)-casein, 1 on alpha(s2)-casein, and 2 on kappa-casein) were not recognized by any of the patients with transient CMA but showed binding by the majority of the patients with persistent allergy. The presence of IgE antibodies against at least 1 of 3 epitopes (amino acid [AA] 123-132 on alpha(s1)-casein, AA 171-180 on alpha(s2)-casein, and AA 155-164 on kappa-casein) identified all patients with persistent CMA. CONCLUSIONS: The presence of IgE antibodies to distinct allergenic epitopes of cow's milk proteins can be used as a marker of persistent CMA. Prospective studies are needed to investigate the usefulness of these informative epitopes in predicting life-long CMA in young children.

Adolescent↗
PubMed2002

Identification of sequential IgE-binding epitopes on bovine alpha(s2)-casein in cow's milk allergic patients.

BACKGROUND: Caseins are the major allergens responsible for cow's milk allergy (CMA). We have previously identified the IgE-binding epitopes of the major cow's milk (CM) proteins except for alpha(s2)-casein. METHODS: Overlapping decapeptides representing the entire length of alpha(s2)-casein were synthesized on a cellulose-derivatized membrane. Sera from 13 CM-allergic children, 4-15 years of age, with a median level of CM-specific IgE >100 kU/l (range 33.7 to > 100 kU/l) were used to identify IgE-binding epitopes. RESULTS: Four major and six minor sequential IgE-binding regions were identified on alpha(s2)-casein. The first major region is located in the middle of the protein at amino acids (AA) 83-100, and the other three major regions are located in the carboxy terminal portion of the protein at AA 143-158, 157-172 and 165-188. The minor IgE-binding regions were identified at AA 31-44, 43-56, 93-106, 105-114, 117-128, and 191-200. CONCLUSION: We identified 10 sequential IgE-binding regions on alpha(s2)-casein and performed the first crucial step in the development of immunotherapeutic interventions for CMA.

Adolescent↗