The novel chemokine mob-1: Involvement in adult respiratory distress syndrome

Fizan Abdullah, Phillip Ovadia, Giora Feuerstein, Louis F. Neville, Richard Morrison, Geunther Mathiak, Mark Whiteford, Reuven Rabinovici

Research output: Contribution to journalArticle

Abstract

Background. Using differential display reverse transcriptase-polymerase chain reaction we have recently identified mob-1, the novel rat homologue of the human α-chemokine IP-10, as a highly inducible gene in adult respiratory distress syndrome (ARDS) lungs. The present study aimed to further implicate mob-1 in the pathogenesis of ARDS. Methods. Pulmonary mob-1 mRNA upregulation was confirmed by Northern blot analysis in three different rat models of ARDS-like lung injury and localized to pulmonary macrophages by using in situ hybridization. Also, Escherichia coli-derived recombinant mob-1 (rmob-1) was tested for its properties in relationship to lung injury. Results. In vivo, intratracheal injection of rmob-1 (50 μg/rat) induced pulmonary leuko- sequestration (myeloperoxidase +93 % ± 8 % versus control, p <0.05) with preferential accumulation of neutrophils in bronchoalveolar lavage fluid (36. 0 % ± 1.0% versus 0. 1 % ± 0.1% in controls, p <0. 01). vitro, transwell migration studies demonstrated chemotactic activity of rmob-1 (50 to 100 ng/ml) toward human monocytes (+151% ± 34 % versus rmob-1 vehicle, p <0. 01) and only weak chemotaxis for human neutrophils (+15% ± 0 % versus rmob- 1 vehicle, p <0. 01). Utilizing a rat aortic ring model ex vivo, rmob-1 at 100 ng/ml exerted a very potent inhibitory effect on angiogenesis (-78.7% ± 6.3% versus rmob-1 vehicle, p <0.01), a major component of the resolution phase of ARDS. Conclusions. Taken together, these data support the involvement of mob-1 in the pathogenic mechanisms of ARDS possibly through chemotactic actions on inflammatory cells and modulation of angiogenesis in the recovery phase of the disease.

Original languageEnglish (US)
Pages (from-to)303-312
Number of pages10
JournalSurgery
Volume122
Issue number2
DOIs
StatePublished - Aug 1997
Externally publishedYes

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Adult Respiratory Distress Syndrome
Chemokines
Lung Injury
Neutrophils
Bronchopulmonary Sequestration
Lung
Bronchoalveolar Lavage Fluid
Alveolar Macrophages
Chemotaxis
Reverse Transcriptase Polymerase Chain Reaction
Northern Blotting
Peroxidase
In Situ Hybridization
Monocytes
Up-Regulation
Escherichia coli
Messenger RNA
Injections
Genes

ASJC Scopus subject areas

  • Surgery

Cite this

Abdullah, F., Ovadia, P., Feuerstein, G., Neville, L. F., Morrison, R., Mathiak, G., ... Rabinovici, R. (1997). The novel chemokine mob-1: Involvement in adult respiratory distress syndrome. Surgery, 122(2), 303-312. https://doi.org/10.1016/S0039-6060(97)90022-2

The novel chemokine mob-1 : Involvement in adult respiratory distress syndrome. / Abdullah, Fizan; Ovadia, Phillip; Feuerstein, Giora; Neville, Louis F.; Morrison, Richard; Mathiak, Geunther; Whiteford, Mark; Rabinovici, Reuven.

In: Surgery, Vol. 122, No. 2, 08.1997, p. 303-312.

Research output: Contribution to journalArticle

Abdullah, F, Ovadia, P, Feuerstein, G, Neville, LF, Morrison, R, Mathiak, G, Whiteford, M & Rabinovici, R 1997, 'The novel chemokine mob-1: Involvement in adult respiratory distress syndrome', Surgery, vol. 122, no. 2, pp. 303-312. https://doi.org/10.1016/S0039-6060(97)90022-2
Abdullah F, Ovadia P, Feuerstein G, Neville LF, Morrison R, Mathiak G et al. The novel chemokine mob-1: Involvement in adult respiratory distress syndrome. Surgery. 1997 Aug;122(2):303-312. https://doi.org/10.1016/S0039-6060(97)90022-2
Abdullah, Fizan ; Ovadia, Phillip ; Feuerstein, Giora ; Neville, Louis F. ; Morrison, Richard ; Mathiak, Geunther ; Whiteford, Mark ; Rabinovici, Reuven. / The novel chemokine mob-1 : Involvement in adult respiratory distress syndrome. In: Surgery. 1997 ; Vol. 122, No. 2. pp. 303-312.
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abstract = "Background. Using differential display reverse transcriptase-polymerase chain reaction we have recently identified mob-1, the novel rat homologue of the human α-chemokine IP-10, as a highly inducible gene in adult respiratory distress syndrome (ARDS) lungs. The present study aimed to further implicate mob-1 in the pathogenesis of ARDS. Methods. Pulmonary mob-1 mRNA upregulation was confirmed by Northern blot analysis in three different rat models of ARDS-like lung injury and localized to pulmonary macrophages by using in situ hybridization. Also, Escherichia coli-derived recombinant mob-1 (rmob-1) was tested for its properties in relationship to lung injury. Results. In vivo, intratracheal injection of rmob-1 (50 μg/rat) induced pulmonary leuko- sequestration (myeloperoxidase +93 {\%} ± 8 {\%} versus control, p <0.05) with preferential accumulation of neutrophils in bronchoalveolar lavage fluid (36. 0 {\%} ± 1.0{\%} versus 0. 1 {\%} ± 0.1{\%} in controls, p <0. 01). vitro, transwell migration studies demonstrated chemotactic activity of rmob-1 (50 to 100 ng/ml) toward human monocytes (+151{\%} ± 34 {\%} versus rmob-1 vehicle, p <0. 01) and only weak chemotaxis for human neutrophils (+15{\%} ± 0 {\%} versus rmob- 1 vehicle, p <0. 01). Utilizing a rat aortic ring model ex vivo, rmob-1 at 100 ng/ml exerted a very potent inhibitory effect on angiogenesis (-78.7{\%} ± 6.3{\%} versus rmob-1 vehicle, p <0.01), a major component of the resolution phase of ARDS. Conclusions. Taken together, these data support the involvement of mob-1 in the pathogenic mechanisms of ARDS possibly through chemotactic actions on inflammatory cells and modulation of angiogenesis in the recovery phase of the disease.",
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AU - Abdullah, Fizan

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AU - Morrison, Richard

AU - Mathiak, Geunther

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N2 - Background. Using differential display reverse transcriptase-polymerase chain reaction we have recently identified mob-1, the novel rat homologue of the human α-chemokine IP-10, as a highly inducible gene in adult respiratory distress syndrome (ARDS) lungs. The present study aimed to further implicate mob-1 in the pathogenesis of ARDS. Methods. Pulmonary mob-1 mRNA upregulation was confirmed by Northern blot analysis in three different rat models of ARDS-like lung injury and localized to pulmonary macrophages by using in situ hybridization. Also, Escherichia coli-derived recombinant mob-1 (rmob-1) was tested for its properties in relationship to lung injury. Results. In vivo, intratracheal injection of rmob-1 (50 μg/rat) induced pulmonary leuko- sequestration (myeloperoxidase +93 % ± 8 % versus control, p <0.05) with preferential accumulation of neutrophils in bronchoalveolar lavage fluid (36. 0 % ± 1.0% versus 0. 1 % ± 0.1% in controls, p <0. 01). vitro, transwell migration studies demonstrated chemotactic activity of rmob-1 (50 to 100 ng/ml) toward human monocytes (+151% ± 34 % versus rmob-1 vehicle, p <0. 01) and only weak chemotaxis for human neutrophils (+15% ± 0 % versus rmob- 1 vehicle, p <0. 01). Utilizing a rat aortic ring model ex vivo, rmob-1 at 100 ng/ml exerted a very potent inhibitory effect on angiogenesis (-78.7% ± 6.3% versus rmob-1 vehicle, p <0.01), a major component of the resolution phase of ARDS. Conclusions. Taken together, these data support the involvement of mob-1 in the pathogenic mechanisms of ARDS possibly through chemotactic actions on inflammatory cells and modulation of angiogenesis in the recovery phase of the disease.

AB - Background. Using differential display reverse transcriptase-polymerase chain reaction we have recently identified mob-1, the novel rat homologue of the human α-chemokine IP-10, as a highly inducible gene in adult respiratory distress syndrome (ARDS) lungs. The present study aimed to further implicate mob-1 in the pathogenesis of ARDS. Methods. Pulmonary mob-1 mRNA upregulation was confirmed by Northern blot analysis in three different rat models of ARDS-like lung injury and localized to pulmonary macrophages by using in situ hybridization. Also, Escherichia coli-derived recombinant mob-1 (rmob-1) was tested for its properties in relationship to lung injury. Results. In vivo, intratracheal injection of rmob-1 (50 μg/rat) induced pulmonary leuko- sequestration (myeloperoxidase +93 % ± 8 % versus control, p <0.05) with preferential accumulation of neutrophils in bronchoalveolar lavage fluid (36. 0 % ± 1.0% versus 0. 1 % ± 0.1% in controls, p <0. 01). vitro, transwell migration studies demonstrated chemotactic activity of rmob-1 (50 to 100 ng/ml) toward human monocytes (+151% ± 34 % versus rmob-1 vehicle, p <0. 01) and only weak chemotaxis for human neutrophils (+15% ± 0 % versus rmob- 1 vehicle, p <0. 01). Utilizing a rat aortic ring model ex vivo, rmob-1 at 100 ng/ml exerted a very potent inhibitory effect on angiogenesis (-78.7% ± 6.3% versus rmob-1 vehicle, p <0.01), a major component of the resolution phase of ARDS. Conclusions. Taken together, these data support the involvement of mob-1 in the pathogenic mechanisms of ARDS possibly through chemotactic actions on inflammatory cells and modulation of angiogenesis in the recovery phase of the disease.

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