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Home / Equine Research Bank / Vet Res / Depletion of pulmonary intravascular macrophages partially i...
Veterinary research2005; 36(4); 557-569; doi: 10.1051/vetres:2005016

Depletion of pulmonary intravascular macrophages partially inhibits lipopolysaccharide-induced lung inflammation in horses.

Abstract: Horses are unique in their extreme sensitivity to endotoxin-induced cardio-pulmonary shock and mortality. The mechanisms behind increased sensitivity of the horse to endotoxin remain unknown. Pulmonary intravascular macrophages (PIMs) are pro-inflammatory cells occurring in horses. Because the functions of equine PIMs in endotoxemia remain unknown, we studied the role played by equine PIMs in endotoxin-induced pulmonary pathophysiology. We achieved this by using a recently developed protocol to deplete PIMs in order to compare lipopolysaccharide (LPS)-induced pulmonary responses in horses with or without PIMs. Horses treated with gadolinium chloride (GC; 10 mg/kg intravenous) to deplete PIMs or endotoxin-free saline (n = 4) were injected with Escherichia coli LPS (E. coli LPS; 50 ng/kg intravenously) 48 h after GC or saline. Control horses (n = 5) received two injections of endotoxin-free saline at 48 h intervals. All the horses were euthanized 2 h after LPS or saline challenge. Immunohistology for the PIMs showed their reduced numbers in GC-treated horses. The LPS treatment of normal and GC-treated horses increased diastolic and systolic pulmonary arterial pressures at 30 min compared to the saline-treated horses (P < 0.05). However, horses pre-treated with GC did not have an LPS-induced increase in mean pulmonary arterial pressure compared to the LPS-treated horses (P < 0.05). Light and electron microscopic immunocytochemistry detected extensive labeling for LPS in PIMs of LPS-treated horses. Both the LPS-treated groups had more alveolar septal cells positive for TNF-alpha and IL-1beta compared to control horses, which did not receive LPS (P < 0.05). However, GC-treated horses challenged with the LPS showed less IL-1beta-positive cells (P < 0.05). Immuno-electron microscopy localized TNF-alpha and IL-1beta in PIMs. These new data show that PIMs endocytose LPS and contain TNF-alpha and IL-1beta and their depletion partially inhibits LPS-induced pulmonary inflammatory responses.
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Publication Date: 2005-06-16 PubMed ID: 15955281DOI: 10.1051/vetres:2005016Google Scholar: Lookup
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  • Journal Article
  • Research Support
  • Non-U.S. Gov't

Summary

This research summary has been generated with artificial intelligence and may contain errors and omissions. Refer to the original study to confirm details provided. Submit correction.

This study investigates the role of pulmonary intravascular macrophages, inflammatory cells found in horses, during lung inflammation caused by lipopolysaccharide, a toxin linked to bacterial infection. Results suggest that depleting these cells partially inhibited the inflammatory response caused by the toxin.

Objective and Methodology

  • The research aimed to understand the role of Pulmonary IntraVascular Macrophages (PIMs) in horses during inflammation caused by a bacteria-produced toxin, Lipopolysaccharide (LPS).
  • A novel protocol was employed to deplete the PIMs in horses, which then allowed the researchers to compare the LPS-induced inflammation in horse lungs with and without PIMs.
  • The treatment was applied using gadolinium chloride to deplete PIMs and Escherichia coli LPS was injected to induce an inflammatory response.
  • This setup was compared with a control group of horses who received saline injections instead of the antagonistic agents.
  • All horses were put to sleep 2 hours after the inflammatory challenge, and immunohistology was then conducted on the PIMs in the horse.

Key Findings

  • There was a notable reduction in the number of PIMs in horses treated with gadolinium chloride.
  • Both normal and treated horses demonstrated an increase in diastolic and systolic pulmonary arterial pressures 30 minutes after receiving the LPS.
  • However, horses pre-treated with gadolinium chloride (PIMs depleted) did not show an increase in the mean pulmonary arterial pressure post-LPS challenge.
  • A visible interaction between LPS and PIMs was observed, with PIMs found to ‘swallow’ (endocytose) the LPS and contain inflammatory markers TNF-alpha and IL-1beta.
  • Importantly, horses pre-treated with gadolinium chloride that were subsequently exposed to LPS demonstrated fewer IL-1beta-positive cells, suggesting a lower inflammatory response.

Conclusion

  • The study demonstrated the active interaction between PIMs and LPS, with PIMs responsible for generating an inflammatory response in horse lungs when interacting with LPS.
  • Importantly, the research showed that the depletion of these PIMs could partially inhibit the LPS-induced inflammatory response, suggesting a potential therapeutic direction for managing bacterial infection in horses.

Cite This Article

APA
Parbhakar OP, Duke T, Townsend HG, Singh B. (2005). Depletion of pulmonary intravascular macrophages partially inhibits lipopolysaccharide-induced lung inflammation in horses. Vet Res, 36(4), 557-569. https://doi.org/10.1051/vetres:2005016

Publication

Veterinary research
ISSN: 0928-4249
NlmUniqueID: 9309551
Country: England
Language: English
Volume: 36
Issue: 4
Pages: 557-569

Researcher Affiliations

Parbhakar, Om P
  • Department of Veterinary Biomedical Sciences, University of Saskatchewan, 52 Campus Drive, Saskatoon, Saskatchewan S7N 5B4, Canada.
Duke, Tanya
    Townsend, Hugh G G
      Singh, Baljit

        MeSH Terms

        • Animals
        • Horse Diseases / chemically induced
        • Horse Diseases / immunology
        • Horse Diseases / pathology
        • Horses
        • Interleukin-1 / metabolism
        • Lipopolysaccharides
        • Lung / pathology
        • Macrophages, Alveolar / physiology
        • Pneumonia / immunology
        • Pneumonia / pathology
        • Pneumonia / veterinary
        • Time Factors
        • Tumor Necrosis Factor-alpha / metabolism

        Citations

        This article has been cited 12 times.
        1. Townsend M, Fowler B, Aulakh GK, Singh B. Expression of pentraxin 3 in equine lungs and neutrophils.. Can J Vet Res 2023 Jan;87(1):9-16.
          pubmed: 36606044
        2. Simões J, Batista M, Tilley P. The Immune Mechanisms of Severe Equine Asthma-Current Understanding and What Is Missing.. Animals (Basel) 2022 Mar 16;12(6).
          doi: 10.3390/ani12060744pubmed: 35327141google scholar: lookup
        3. Bocking T, Singh B. Light and electron-microscopic localization of CD9 and surfactant protein A and D in normal lungs of the horse.. Can J Vet Res 2021 Jul;85(3):170-176.
          pubmed: 34248260
        4. Bocking T, Johnson L, Singh A, Desai A, Aulakh GK, Singh B. Research article expression of surfactant protein-A and D, and CD9 in lungs of 1 and 30 day old foals.. BMC Vet Res 2021 Jul 5;17(1):236.
          doi: 10.1186/s12917-021-02943-5pubmed: 34225699google scholar: lookup
        5. Le NPK, Gerdts V, Singh B. Integrin alpha-v/beta3 expression in equine lungs and jejunum.. Can J Vet Res 2020 Oct;84(4):245-251.
          pubmed: 33012972
        6. Bordet E, Maisonnasse P, Renson P, Bouguyon E, Crisci E, Tiret M, Descamps D, Bernelin-Cottet C, Urien C, Lefèvre F, Jouneau L, Bourry O, Leplat JJ, Schwartz-Cornil I, Bertho N. Porcine Alveolar Macrophage-like cells are pro-inflammatory Pulmonary Intravascular Macrophages that produce large titers of Porcine Reproductive and Respiratory Syndrome Virus.. Sci Rep 2018 Jul 5;8(1):10172.
          doi: 10.1038/s41598-018-28234-ypubmed: 29977043google scholar: lookup
        7. Harrison JM, Quanstrom LM, Robinson AR, Wobeser B, Anderson SL, Singh B. Expression of von Willebrand factor, pulmonary intravascular macrophages, and Toll-like receptors in lungs of septic foals.. J Vet Sci 2017 Mar 30;18(1):17-23.
          doi: 10.4142/jvs.2017.18.1.17pubmed: 27297419google scholar: lookup
        8. de Prost N, Tucci MR, Melo MF. Assessment of lung inflammation with 18F-FDG PET during acute lung injury.. AJR Am J Roentgenol 2010 Aug;195(2):292-300.
          doi: 10.2214/AJR.10.4499pubmed: 20651183google scholar: lookup
        9. Aharonson-Raz K, Singh B. Pulmonary intravascular macrophages and endotoxin-induced pulmonary pathophysiology in horses.. Can J Vet Res 2010 Jan;74(1):45-9.
          pubmed: 20357958
        10. O'Dea KP, Wilson MR, Dokpesi JO, Wakabayashi K, Tatton L, van Rooijen N, Takata M. Mobilization and margination of bone marrow Gr-1high monocytes during subclinical endotoxemia predisposes the lungs toward acute injury.. J Immunol 2009 Jan 15;182(2):1155-66.
          doi: 10.4049/jimmunol.182.2.1155pubmed: 19124759google scholar: lookup
        11. Gill SS, Suri SS, Janardhan KS, Caldwell S, Duke T, Singh B. Role of pulmonary intravascular macrophages in endotoxin-induced lung inflammation and mortality in a rat model.. Respir Res 2008 Oct 24;9(1):69.
          doi: 10.1186/1465-9921-9-69pubmed: 18950499google scholar: lookup
        12. Gamage LN, Charavaryamath C, Swift TL, Singh B. Lung inflammation following a single exposure to swine barn air.. J Occup Med Toxicol 2007 Dec 18;2:18.
          doi: 10.1186/1745-6673-2-18pubmed: 18088427google scholar: lookup
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