Structural responses of pulmonary intravascular macrophages in lentivirus-infected and/or recombinant ovine interferon-τ-treated lambs

Baljit Singh, Troy Ott, Fuller W. Bazer, Andrés De La Concha-Bermejillo

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Ovine lentivirus (OvLV), a retrovirus, infects and disseminates to various tissue organs via monocytes. The differentiation of infected monocytes into macrophages is a prerequisite for viral replication, and the presence of infected macrophages in tissue organs induces chronic immunopathology such as lymphoid interstitial pneumonia. The pulmonary intravascular macrophage (PIM) is a recently identified mononuclear phagocyte in domestic animal species, including sheep. Recombinant ovine interferon- tau (roIFN-τ), a type I IFN originally named as the ovine trophoblast protein, has potent antiviral activity against OvLV and human immunodeficiency virus and prevents the development of OvLV-associated lung pathology. We investigated and compared the structural features of PIMs in OvLV-infected and/or roIFN-τ-treated 1-month-old lambs using transmission electron microscopy. The PIMs' numerical counts were performed in toluidine blue-stained sections of Epoxy-embedded lung tissues. A reduction in the number of PIMs was observed with OvLV infection and/or roIFN-τ treatment of lambs as compared to the control group (P ≤ 0.05). The majority of the PIMs in OvLV-infected and/or roIFN-τ-treated groups were devoid of their surface coat. The PIMs of OvLV-infected lambs exhibited signs of biosynthetic activation such as expanded rough endoplasmic reticulum, prominent Golgi complexes, and accumulation of secretory vesicles. A few PIMs contained OvLV- like structures. In roIFN-τ-treated OvLV-infected lambs, the lymphocytes had ruffled plasma membranes and were in intimate contact with the PIMs, as is observed during cytotoxic cell-mediated killing of target cells. Most of the PIMs in roIFN-τ-treated OvLV-infected lambs appeared smaller in size. Ovine lentivirus and roIFN-τ, individually or in combination, alter the integrity of the surface coat of PIMs and cause their disappearance from the lungs. Ovine lentivirus infection induces morphological changes that correlate with cytotoxic cell behavior between lymphocytes and PIMs in roIFN-τ-treated or placebo-treated lambs. The loss of PIMs, probably infected with OvLV, either through direct killing by roIFN-τ or indirectly by roIFN-τ activated cytotexic T lymphocytes may represent different aspects of therapeutic actions of this cytokine.

Original languageEnglish (US)
Pages (from-to)472-485
Number of pages14
JournalAnatomical Record
Volume251
Issue number4
DOIs
StatePublished - Aug 1 1998

Fingerprint

Lentivirus
Alveolar Macrophages
interferons
Interferons
Sheep
macrophages
lambs
lungs
sheep
Ovine lentivirus
monocytes
Lentivirus Infections
Retroviridae
lymphocytes
immunopathology
toluidine blue
trophoblast
phagocytes
secretory granules
rough endoplasmic reticulum

All Science Journal Classification (ASJC) codes

  • Anatomy
  • Agricultural and Biological Sciences (miscellaneous)

Cite this

Singh, Baljit ; Ott, Troy ; Bazer, Fuller W. ; De La Concha-Bermejillo, Andrés. / Structural responses of pulmonary intravascular macrophages in lentivirus-infected and/or recombinant ovine interferon-τ-treated lambs. In: Anatomical Record. 1998 ; Vol. 251, No. 4. pp. 472-485.
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abstract = "Ovine lentivirus (OvLV), a retrovirus, infects and disseminates to various tissue organs via monocytes. The differentiation of infected monocytes into macrophages is a prerequisite for viral replication, and the presence of infected macrophages in tissue organs induces chronic immunopathology such as lymphoid interstitial pneumonia. The pulmonary intravascular macrophage (PIM) is a recently identified mononuclear phagocyte in domestic animal species, including sheep. Recombinant ovine interferon- tau (roIFN-τ), a type I IFN originally named as the ovine trophoblast protein, has potent antiviral activity against OvLV and human immunodeficiency virus and prevents the development of OvLV-associated lung pathology. We investigated and compared the structural features of PIMs in OvLV-infected and/or roIFN-τ-treated 1-month-old lambs using transmission electron microscopy. The PIMs' numerical counts were performed in toluidine blue-stained sections of Epoxy-embedded lung tissues. A reduction in the number of PIMs was observed with OvLV infection and/or roIFN-τ treatment of lambs as compared to the control group (P ≤ 0.05). The majority of the PIMs in OvLV-infected and/or roIFN-τ-treated groups were devoid of their surface coat. The PIMs of OvLV-infected lambs exhibited signs of biosynthetic activation such as expanded rough endoplasmic reticulum, prominent Golgi complexes, and accumulation of secretory vesicles. A few PIMs contained OvLV- like structures. In roIFN-τ-treated OvLV-infected lambs, the lymphocytes had ruffled plasma membranes and were in intimate contact with the PIMs, as is observed during cytotoxic cell-mediated killing of target cells. Most of the PIMs in roIFN-τ-treated OvLV-infected lambs appeared smaller in size. Ovine lentivirus and roIFN-τ, individually or in combination, alter the integrity of the surface coat of PIMs and cause their disappearance from the lungs. Ovine lentivirus infection induces morphological changes that correlate with cytotoxic cell behavior between lymphocytes and PIMs in roIFN-τ-treated or placebo-treated lambs. The loss of PIMs, probably infected with OvLV, either through direct killing by roIFN-τ or indirectly by roIFN-τ activated cytotexic T lymphocytes may represent different aspects of therapeutic actions of this cytokine.",
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Structural responses of pulmonary intravascular macrophages in lentivirus-infected and/or recombinant ovine interferon-τ-treated lambs. / Singh, Baljit; Ott, Troy; Bazer, Fuller W.; De La Concha-Bermejillo, Andrés.

In: Anatomical Record, Vol. 251, No. 4, 01.08.1998, p. 472-485.

Research output: Contribution to journalArticle

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T1 - Structural responses of pulmonary intravascular macrophages in lentivirus-infected and/or recombinant ovine interferon-τ-treated lambs

AU - Singh, Baljit

AU - Ott, Troy

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N2 - Ovine lentivirus (OvLV), a retrovirus, infects and disseminates to various tissue organs via monocytes. The differentiation of infected monocytes into macrophages is a prerequisite for viral replication, and the presence of infected macrophages in tissue organs induces chronic immunopathology such as lymphoid interstitial pneumonia. The pulmonary intravascular macrophage (PIM) is a recently identified mononuclear phagocyte in domestic animal species, including sheep. Recombinant ovine interferon- tau (roIFN-τ), a type I IFN originally named as the ovine trophoblast protein, has potent antiviral activity against OvLV and human immunodeficiency virus and prevents the development of OvLV-associated lung pathology. We investigated and compared the structural features of PIMs in OvLV-infected and/or roIFN-τ-treated 1-month-old lambs using transmission electron microscopy. The PIMs' numerical counts were performed in toluidine blue-stained sections of Epoxy-embedded lung tissues. A reduction in the number of PIMs was observed with OvLV infection and/or roIFN-τ treatment of lambs as compared to the control group (P ≤ 0.05). The majority of the PIMs in OvLV-infected and/or roIFN-τ-treated groups were devoid of their surface coat. The PIMs of OvLV-infected lambs exhibited signs of biosynthetic activation such as expanded rough endoplasmic reticulum, prominent Golgi complexes, and accumulation of secretory vesicles. A few PIMs contained OvLV- like structures. In roIFN-τ-treated OvLV-infected lambs, the lymphocytes had ruffled plasma membranes and were in intimate contact with the PIMs, as is observed during cytotoxic cell-mediated killing of target cells. Most of the PIMs in roIFN-τ-treated OvLV-infected lambs appeared smaller in size. Ovine lentivirus and roIFN-τ, individually or in combination, alter the integrity of the surface coat of PIMs and cause their disappearance from the lungs. Ovine lentivirus infection induces morphological changes that correlate with cytotoxic cell behavior between lymphocytes and PIMs in roIFN-τ-treated or placebo-treated lambs. The loss of PIMs, probably infected with OvLV, either through direct killing by roIFN-τ or indirectly by roIFN-τ activated cytotexic T lymphocytes may represent different aspects of therapeutic actions of this cytokine.

AB - Ovine lentivirus (OvLV), a retrovirus, infects and disseminates to various tissue organs via monocytes. The differentiation of infected monocytes into macrophages is a prerequisite for viral replication, and the presence of infected macrophages in tissue organs induces chronic immunopathology such as lymphoid interstitial pneumonia. The pulmonary intravascular macrophage (PIM) is a recently identified mononuclear phagocyte in domestic animal species, including sheep. Recombinant ovine interferon- tau (roIFN-τ), a type I IFN originally named as the ovine trophoblast protein, has potent antiviral activity against OvLV and human immunodeficiency virus and prevents the development of OvLV-associated lung pathology. We investigated and compared the structural features of PIMs in OvLV-infected and/or roIFN-τ-treated 1-month-old lambs using transmission electron microscopy. The PIMs' numerical counts were performed in toluidine blue-stained sections of Epoxy-embedded lung tissues. A reduction in the number of PIMs was observed with OvLV infection and/or roIFN-τ treatment of lambs as compared to the control group (P ≤ 0.05). The majority of the PIMs in OvLV-infected and/or roIFN-τ-treated groups were devoid of their surface coat. The PIMs of OvLV-infected lambs exhibited signs of biosynthetic activation such as expanded rough endoplasmic reticulum, prominent Golgi complexes, and accumulation of secretory vesicles. A few PIMs contained OvLV- like structures. In roIFN-τ-treated OvLV-infected lambs, the lymphocytes had ruffled plasma membranes and were in intimate contact with the PIMs, as is observed during cytotoxic cell-mediated killing of target cells. Most of the PIMs in roIFN-τ-treated OvLV-infected lambs appeared smaller in size. Ovine lentivirus and roIFN-τ, individually or in combination, alter the integrity of the surface coat of PIMs and cause their disappearance from the lungs. Ovine lentivirus infection induces morphological changes that correlate with cytotoxic cell behavior between lymphocytes and PIMs in roIFN-τ-treated or placebo-treated lambs. The loss of PIMs, probably infected with OvLV, either through direct killing by roIFN-τ or indirectly by roIFN-τ activated cytotexic T lymphocytes may represent different aspects of therapeutic actions of this cytokine.

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