PubMed Health⌕ Search

Biomedical subjects

Kate Ackerman

Publications and source records attributed to Kate Ackerman.

8 recordsLinked to original sources
PubMed2003

Lipoxins and aspirin-triggered lipoxins in airway responses.

Here, we have demonstrated potent inhibition of allergen-mediated pulmonary inflammation and airway hyper-responsiveness by a novel dual-pronged action of LX's. Moreover, these results indicate that LX's play pivotal and previously unappreciated roles in regulating allergy and pulmonary inflammation.

Animals↗
PubMed2002

Multi-pronged inhibition of airway hyper-responsiveness and inflammation by lipoxin A(4).

The prevalence of asthma continues to increase and its optimal treatment remains a challenge. Here, we investigated the actions of lipoxin A(4) (LXA(4)) and its leukocyte receptor in pulmonary inflammation using a murine model of asthma. Allergen challenge initiated airway biosynthesis of LXA(4) and increased expression of its receptor. Administration of a stable analog of LXA(4) blocked both airway hyper-responsiveness and pulmonary inflammation, as shown by decreased leukocytes and mediators, including interleukin-5, interleukin-13, eotaxin, prostanoids and cysteinyl leukotrienes. Moreover, transgenic expression of human LXA(4) receptors in murine leukocytes led to significant inhibition of pulmonary inflammation and eicosanoid-initiated eosinophil tissue infiltration. Inhibition of airway hyper-responsiveness and allergic airway inflammation with a stable LXA(4) analog highlights a unique counter-regulatory profile for the LXA(4) system and its leukocyte receptor in airway responses. Moreover, our findings suggest that lipoxin and related pathways offer novel multi-pronged therapeutic approaches for human asthma.

Animals↗
PubMed2002

Development of spontaneous airway changes consistent with human asthma in mice lacking T-bet.

Human asthma is associated with airway infiltration by T helper 2 (TH2) lymphocytes. We observed reduced expression of the TH1 transcription factor, T-bet, in T cells from airways of patients with asthma compared with that in T cells from airways of nonasthmatic patients, suggesting that loss of T-bet might be associated with asthma. Mice with a targeted deletion of the T-bet gene and severe combined immunodeficient mice receiving CD4+ cells from T-bet knockout mice spontaneously demonstrated multiple physiological and inflammatory features characteristic of asthma. Thus, T-bet deficiency, in the absence of allergen exposure, induces a murine phenotype reminiscent of both acute and chronic human asthma.

Adoptive Transfer↗