Linked Life Data

11345807

Source:http://linkedlifedata.com/resource/pubmed/id/11345807

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
13-14
pubmed:dateCreated
2001-5-10
pubmed:abstractText
A number of immunomodulating mechanisms are necessary to prevent uncontrolled inflammation in the lower respiratory tract. Proliferative responses of immune cells are tightly controlled in both bronchi and alveoli in the healthy lung. In diseases such as bronchial asthma, there is not only a partial failure of these mechanisms, but also an immune-deviation with a propensity towards a Th2-cell involvement. The role of alveolar macrophages (AM) controlling T- and B-cell activation in the lower respiratory tract is discussed by considering mainly published results. This review focuses on immunomodulating mechanisms exerted via cytokines, such as Interleukin-10 (IL-10), transforming growth factor-beta (TGF-beta), and Interleukin-1 receptor-antagonist (IL-1ra), prostaglandins, such as prostaglandin E2 (PGE2), and especially nitric oxide (NO). The Th1 and Th2 concept in asthma is introduced, being the best-described mechanism of immune-deviation in the lung. The possibility of re-inducing T-cell unresponsiveness is of particular interest. The physiological immunomodulating mechanisms used by AM are explained in detail, as they offer many possibilities for therapeutic immunomodulation. Special emphasis is put on the cGMP/phosphatase dependent, reversible mechanism of NO-mediated immunomodulation and differences in the activation of NO synthases between murine and human alveolar macrophages are mentioned.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1424-7860
pubmed:author
pubmed:issnType
Print
pubmed:day
7
pubmed:volume
131
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
171-9
pubmed:dateRevised
2011-2-15
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
Immunomodulating mechanisms in the lower respiratory tract: nitric oxide mediated interactions between alveolar macrophages, epithelial cells, and T-cells.
pubmed:affiliation
Departement Innere Medizin, Medizinische Universitätsklinik A, Kantonsspital Basel, Switzerland. rolandbingisser@hotmail.com
pubmed:publicationType
Journal Article, Review