Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0242706 (
hyperoxia
)
5,219
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Surfactant protein D
(
SP-D
), which has structural homology to C-type lectin binding regions, may play a role in host defense and has no known surfactant function. Because other surfactant proteins have been shown to be increased after prolonged periods of
hyperoxia
, we sought to evaluate the early effects of
hyperoxia
(95% O2) on expression of
SP-D
in the adult male rat lung. Animals were exposed to air or to 12, 36, or 60 h of 95% O2. Northern blot analysis of total lung RNA revealed marked
SP-D
mRNA increases at 12 h 95% O2 compared with air-exposed controls, with decreasing expression to near that of air-exposed animals by 60 h. Semiquantitative in situ RNA hybridization demonstrated parallel results, with increased numbers of labeled alveolar epithelial (AE) and bronchiolar epithelial (BE) cells at 12 h and increased intensity of labeled alveolar cells, compared with air-exposed controls. After 60 h of exposure to 95% O2, mRNA label intensity in AE and BE was decreased to levels near those seen in air-exposed animals. In contrast, Western blotting showed a decline in total lung
SP-D
with 95% O2 exposure, beginning at 12 h and continuing at 36 and 60 h, respectively. Semiquantitative immunohistochemistry demonstrated a decline in AE labeling parallel to the total lung Western blot results, but labeled total BE cell numbers increased (P = 0.10).
Hyperoxia
had differential effects on
SP-D
abundance in AE and BE cells, and therefore may influence the availability of
SP-D
to bind microbial pathogens in the airways depending on cell type and location.
...
PMID:Brief exposure to 95% oxygen alters surfactant protein D and mRNA in adult rat alveolar and bronchiolar epithelium. 992 12
Surfactant protein D
(
SP-D
), a member of the collectin superfamily, modulates pulmonary inflammatory responses and innate immunity. Disruption of the
SP-D
gene in mice induces peribronchiolar inflammation, accumulation of large, foamy macrophages, increased bronchoalveolar lavage (BAL) phospholipid, and pulmonary emphysema. We hypothesized that absence of
SP-D
aggravates
hyperoxia
-induced injury. To test this,
SP-D
-deficient (
SP-D
-/-) and wild-type (SP-D+/+) mice were exposed to 80% or 21% oxygen. Paradoxically, during 14 days of
hyperoxia
,
SP-D
-/- mice had 100% survival vs. 30% in SP-D+/+. The survival advantage in
SP-D
-/- mice was accompanied by lower histopathological injury scores at days 5 and 14, although total BAL cells (8.2 +/- 1.4 x 10(5) in
SP-D
-/- vs. 4.04 +/- 0.25 x 10(5) in SP-D+/+ mice) and neutrophils (1.2 +/- 0.4 x 10(5) vs. 0.03 +/- 0.02 x 10(5) in
SP-D
-/- and SP-D+/+, respectively) were increased. In addition, BAL protein and lung-to-body weight ratios were similarly elevated in both groups after 3, 5, and 14 days of continuous exposure. Biochemically, in contrast to SP-D+/+,
SP-D
-/- mice had higher levels of surfactant phospholipid and SP-B at baseline and 5 days after
hyperoxia
accompanied by a preservation of surfactant biophysical activity. From a multiplex assay of nine cytokines, we found elevated levels of IL-13 in BAL fluid of normoxic
SP-D
-/- mice compared with SP-D+/+. We conclude that the resistance of
SP-D
-deficient mice to
hyperoxia
reflects homeostatic changes in the
SP-D
-/- phenotype involving both phospholipid and SP-B-mediated induced resistance of surfactant to inactivation as well as changes in the immunomodulatory BAL cytokine profile.
...
PMID:SP-D-deficient mice are resistant to hyperoxia. 1715 97
