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Enhanced production of IGF-I in the lungs of fibroproliferative ARDS patients.

Andonegui G, Krein PM, Mowat C, Brisebois R, Doig C, Green FH, Léger C, Winston BW - Physiol Rep (2014)

Bottom Line: Our data show that IGF-I is significantly increased in the ELF in FP-ARDS patients.A significant correlation between IGF-I and PCP-III in the ELF of FP-ARDS patients is found.Our data suggest that IGF-I found in the lungs of FP-ARDS patients results from both increased lung permeability and local production of IGF-I.

View Article: PubMed Central - PubMed

Affiliation: Department of Critical Care Medicine, Faculty of Medicine, University of Calgary Health Research Innovation Center, Calgary, Alberta, Canada Immunology Research Group, Faculty of Medicine, University of Calgary Health Research Innovation Center, Calgary, Alberta, Canada.

No MeSH data available.


Related in: MedlinePlus

IGF‐I, Collagen I and Collagen III Immunohistochemistry of Lung Biopsies. (A) Representative staining for IGF‐I immunoreactivity in lung biopsy specimen of a control individual at low magnification (100×) showing normal alveolar architecture. There is minimal IGF‐I positive immunostaining in the control lungs as evidenced by the positive immunostaining in a cluster of alveolar macrophages. High magnification inset (400×) shows the positive immunoreactivity of the alveolar macrophages as well as a minimal amount of linear staining of the alveolar type I cells (arrow). (B) Representative staining for IGF‐I in lung biopsy specimen of a FP‐ARDS patient. Low magnification (100×) shows thickening and fibrosis of the interstitium with chronic inflammatory cell infiltrates. Numerous strongly stained macrophages are seen in the alveolar lumen as well as scattered epithelial cells (arrow). Interstitial staining is also present but less strong. High power inset (400×) shows strong immunoreactivity of macrophage cells. (C) Representative collagen I immunostaining in control lung section and (D) fibroproliferative ARDS lung section. Of note, there is little collagen I staining in control lung sections but significant collagen I immunostaining in the interstitium of FP‐ARDS lung sections. (E) Representative collagen III immunostaining in control lung section and (F) FP‐ARDS lung section. Noteworthy, there is little collagen III staining in control lung sections but significant collagen III immunostaining in the interstitium in FP‐ARDS lung sections.
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fig03: IGF‐I, Collagen I and Collagen III Immunohistochemistry of Lung Biopsies. (A) Representative staining for IGF‐I immunoreactivity in lung biopsy specimen of a control individual at low magnification (100×) showing normal alveolar architecture. There is minimal IGF‐I positive immunostaining in the control lungs as evidenced by the positive immunostaining in a cluster of alveolar macrophages. High magnification inset (400×) shows the positive immunoreactivity of the alveolar macrophages as well as a minimal amount of linear staining of the alveolar type I cells (arrow). (B) Representative staining for IGF‐I in lung biopsy specimen of a FP‐ARDS patient. Low magnification (100×) shows thickening and fibrosis of the interstitium with chronic inflammatory cell infiltrates. Numerous strongly stained macrophages are seen in the alveolar lumen as well as scattered epithelial cells (arrow). Interstitial staining is also present but less strong. High power inset (400×) shows strong immunoreactivity of macrophage cells. (C) Representative collagen I immunostaining in control lung section and (D) fibroproliferative ARDS lung section. Of note, there is little collagen I staining in control lung sections but significant collagen I immunostaining in the interstitium of FP‐ARDS lung sections. (E) Representative collagen III immunostaining in control lung section and (F) FP‐ARDS lung section. Noteworthy, there is little collagen III staining in control lung sections but significant collagen III immunostaining in the interstitium in FP‐ARDS lung sections.

Mentions: The presence of IGF‐I was confirmed immunohistochemically in lung biopsy samples from two FP‐ARDS and four control individuals enrolled in this study. Control lung sections showed normal lung architecture with minimal alveolar structure distortion, little cellular infiltration, or thickening of the interstitium (Fig. 3A), whereas the lung sections from FP‐ARDS patients showed enhanced mononuclear infiltrates, loss of alveolar structure, and an increase in interstitial mass (Fig. 3B). IGF‐I immunoreactivity was seen in alveolar macrophages, epithelial cells lining the airways as well as in a variety of interstitial cells in control lungs (Fig. 3A). There was increased total staining for IGF‐I in the two FP‐ARDS biopsy samples compared to the four control biopsy specimens (Fig. 3B) as assessed by two different observers. These findings are in keeping with those previously reported Krein et al. (2003). Additionally, the lung biopsy specimens from the FP‐ARDS individuals showed enhanced collagen I (Fig. 3 C and D), and collagen III immunoreactivity (Fig. 3 E and F) compared to controls, which is in agreement with the results observed in the BALF of these patients. This confirms that the FP‐ARDS patients entered into this study with a clinical diagnosis of FP‐ARDS have clear ongoing fibroproliferation in their lungs.


Enhanced production of IGF-I in the lungs of fibroproliferative ARDS patients.

Andonegui G, Krein PM, Mowat C, Brisebois R, Doig C, Green FH, Léger C, Winston BW - Physiol Rep (2014)

IGF‐I, Collagen I and Collagen III Immunohistochemistry of Lung Biopsies. (A) Representative staining for IGF‐I immunoreactivity in lung biopsy specimen of a control individual at low magnification (100×) showing normal alveolar architecture. There is minimal IGF‐I positive immunostaining in the control lungs as evidenced by the positive immunostaining in a cluster of alveolar macrophages. High magnification inset (400×) shows the positive immunoreactivity of the alveolar macrophages as well as a minimal amount of linear staining of the alveolar type I cells (arrow). (B) Representative staining for IGF‐I in lung biopsy specimen of a FP‐ARDS patient. Low magnification (100×) shows thickening and fibrosis of the interstitium with chronic inflammatory cell infiltrates. Numerous strongly stained macrophages are seen in the alveolar lumen as well as scattered epithelial cells (arrow). Interstitial staining is also present but less strong. High power inset (400×) shows strong immunoreactivity of macrophage cells. (C) Representative collagen I immunostaining in control lung section and (D) fibroproliferative ARDS lung section. Of note, there is little collagen I staining in control lung sections but significant collagen I immunostaining in the interstitium of FP‐ARDS lung sections. (E) Representative collagen III immunostaining in control lung section and (F) FP‐ARDS lung section. Noteworthy, there is little collagen III staining in control lung sections but significant collagen III immunostaining in the interstitium in FP‐ARDS lung sections.
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Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4255805&req=5

fig03: IGF‐I, Collagen I and Collagen III Immunohistochemistry of Lung Biopsies. (A) Representative staining for IGF‐I immunoreactivity in lung biopsy specimen of a control individual at low magnification (100×) showing normal alveolar architecture. There is minimal IGF‐I positive immunostaining in the control lungs as evidenced by the positive immunostaining in a cluster of alveolar macrophages. High magnification inset (400×) shows the positive immunoreactivity of the alveolar macrophages as well as a minimal amount of linear staining of the alveolar type I cells (arrow). (B) Representative staining for IGF‐I in lung biopsy specimen of a FP‐ARDS patient. Low magnification (100×) shows thickening and fibrosis of the interstitium with chronic inflammatory cell infiltrates. Numerous strongly stained macrophages are seen in the alveolar lumen as well as scattered epithelial cells (arrow). Interstitial staining is also present but less strong. High power inset (400×) shows strong immunoreactivity of macrophage cells. (C) Representative collagen I immunostaining in control lung section and (D) fibroproliferative ARDS lung section. Of note, there is little collagen I staining in control lung sections but significant collagen I immunostaining in the interstitium of FP‐ARDS lung sections. (E) Representative collagen III immunostaining in control lung section and (F) FP‐ARDS lung section. Noteworthy, there is little collagen III staining in control lung sections but significant collagen III immunostaining in the interstitium in FP‐ARDS lung sections.
Mentions: The presence of IGF‐I was confirmed immunohistochemically in lung biopsy samples from two FP‐ARDS and four control individuals enrolled in this study. Control lung sections showed normal lung architecture with minimal alveolar structure distortion, little cellular infiltration, or thickening of the interstitium (Fig. 3A), whereas the lung sections from FP‐ARDS patients showed enhanced mononuclear infiltrates, loss of alveolar structure, and an increase in interstitial mass (Fig. 3B). IGF‐I immunoreactivity was seen in alveolar macrophages, epithelial cells lining the airways as well as in a variety of interstitial cells in control lungs (Fig. 3A). There was increased total staining for IGF‐I in the two FP‐ARDS biopsy samples compared to the four control biopsy specimens (Fig. 3B) as assessed by two different observers. These findings are in keeping with those previously reported Krein et al. (2003). Additionally, the lung biopsy specimens from the FP‐ARDS individuals showed enhanced collagen I (Fig. 3 C and D), and collagen III immunoreactivity (Fig. 3 E and F) compared to controls, which is in agreement with the results observed in the BALF of these patients. This confirms that the FP‐ARDS patients entered into this study with a clinical diagnosis of FP‐ARDS have clear ongoing fibroproliferation in their lungs.

Bottom Line: Our data show that IGF-I is significantly increased in the ELF in FP-ARDS patients.A significant correlation between IGF-I and PCP-III in the ELF of FP-ARDS patients is found.Our data suggest that IGF-I found in the lungs of FP-ARDS patients results from both increased lung permeability and local production of IGF-I.

View Article: PubMed Central - PubMed

Affiliation: Department of Critical Care Medicine, Faculty of Medicine, University of Calgary Health Research Innovation Center, Calgary, Alberta, Canada Immunology Research Group, Faculty of Medicine, University of Calgary Health Research Innovation Center, Calgary, Alberta, Canada.

No MeSH data available.


Related in: MedlinePlus