Editorial
Volume 4 Issue 5 - 2020
HDFx and Transferal of Plasma from Animals that Survive Lethal Hemorrhage, Bowel Ischemic Shock, Endotoxins, Centripetal Forces or Body Trauma to Naïve Animals Induces Cross-Resistance to these Various Experimental Forms of Injury and Trauma: Importance of Macrophages, NK Cells and Relevance to Design of Molecules to Treat/Ameliorate Effects of Corona Viral Diseases
Burton M Altura1-6*, Asefa Gebrewold1,5 and Anthony Carella1,5
1Department of Physiology and Pharmacology, The State University of New York Downstate Medical Center, Brooklyn, New York, USA
2Department of Medicine, The State University of New York Downstate Medical Center, Brooklyn, New York, USA
3The Center for Cardiovascular and Muscle Research, The State University of New York Downstate Medical Center, Brooklyn, New York, USA
4The School for Graduate Studies in Molecular and Cellular Science, The State University of New York Downstate Medical Center, Brooklyn, New York, USA
5Bio-Defense Systems, Inc, Rockville Centre, New York, USA
6Orient Biomedica, Estero, Florida, USA
*Corresponding Author: Burton M Altura, Professor, Department of Physiology and Pharmacology, The State University of New York Downstate Medical Center, Brooklyn, New York, USA.
Received: March 31, 2020; Published: April 11, 2020




Abstract

Introduction

Various, new viral diseases have been emerging on our planet for more than 100 years. Three of these, termed coronal viral diseases started to emerge in 2003 with SARS, followed a few years later by MERS and most recently by COVID-19 from Wuhan, China. Although the former two are known to have emerged in bats, the host for COVID-19 has yet to be identified, although it is thought also to have arisen from bats. This will be very difficult to track-down as there are more than 1,400 species of bats.

Discovery of HDFx and its protective properties including regenerative attributes

In 1957, Zweifach and Thomas reported that rats adapted to endotoxin shock became cross-tolerant to hemorrhagic and traumatic shock [1].

Working with anesthetized mice, rats and guinea-pigs more than 50 years ago, our laboratories showed that treatment of these diverse rodents with various colloids, lipids and peptides made these animals tolerant to sublethal hemorrhage, sublethal bowel ischemic shock, sublethal whole body trauma, sublethal centripetal forces, and endotoxins [2-24]. In many cases, using these diverse reticuloendothelial cell (REC) stimulants, we found that the plasma taken from the surviving animals often made naïve rodent animals cross-tolerant to these sublethal forms of systemic stresses [4,12,16-18,23,24]. Further, extensive investigations, on thousands of animals, revealed that macrophages and natural killer cells (NK cells) of the innate immune system, harvested from the survivors, produced quantities of a 35 - 50 KD protein [25] we termed “host defense factor x (i.e. HDFx) [22-25]); the greater the initial degree of stress, the greater the harvested amount of HDFx in the surviving animals. Surprisingly, CD4 and CD8 T-lymphocytes which were found to release massive amounts of cytokines, in the naive -traumatized and shocked animals, showed markedly reduced -released amounts of the cytokines (i.e., reduced levels of TNF-alpha, interleukins) [24-27].

References

  1. Zweifach BW and Thomas l. “The relationship between the vascular manifestations of shock produced by endotoxin, trauma, and hemorrhage”. Journal of Experimental Medicine 3 (1957): 385-401.
  2. Hershey SG and Altura BM. “Effects of pretreatment with aggregate human albumin on the reticuloendothelial system activity and after experimental shock”. The Society for Experimental Biology and Medicine 122 (1966): 1195-1199.
  3. Altura BM and Hershey SG. “Use of reticuloendothelial phagocytic function as an index in shock therapy”. The bulletin of the New York Academy of Medicine 43 (1967): 259-266.
  4. Altura BM and Hershey SG. “RES phagocytic function in trauma and adaptation to experimental shock”. American Journal of Physiology 215 (1968): 1414-1419.
  5. Altura BM and Hershey SG. “Influence of vasopressor drugs on reticuloendothelial phagocytic function in experimental shock”. In: Intermedes Proceedings 1968: Combined Injuries and Shock”. Almqvist and Wiksel, Stockholm (1968): 185-1993.
  6. Hershey SG and Altura BM. “Influence of RES stimulating material compatible for man on phagocytosis after experimental shock”. In: Intermedes Proceedings 1968: Combined Injuries and Shock. Almqvist and Wiksel, Stockholm (1968): 195-203.
  7. Altura BM and Hershey SG. “Patterns of RES phagocytic function in trauma and experimental adaptation to shock”. In: Intermedes Proceedings 1968: Combined Injuries and Shock”. Almqvist and Wiksel, Stockholm (1968): 205-213.
  8. Hershey SG and Altura BM. “Function of the reticuloendothelial system in experimental shock and combined injury”. Anesthesiology 30 (1969): 138-143.
  9. Hershey SG and Altura BM. “The effects of vasoactive drugs on reticuloendothelial function in experimental shock and combined injury”. Anesthesiology 30 (1969): 144-149.
  10. Altura BM and Hershey SG. “Effects of glyceryl trioleate on the reticuloendothelial system and survival after experimental shock”. Journal of Pharmacology and Experimental Therapeutics 175 (1970): 555-564.
  11. Altura BM and Hershey SG. “Sequential changes in reticuloendothelial system function after acute hemorrhage”. Proceedings Society Experimental Biology Medicine 139 (1972): 935-939.
  12. Altura BM and Hershey SG. “Reticuloendothelial function in experimental injury and tolerance to shock”. In: Advances in Experimental Medicine and Biology, Neurohumoral and Metabolic Aspects of Injury, Kovach AGB, ed. Plenum Press, New York 33 (1973): 549-569.
  13. Altura BM. “DPAVP: A vasopressin analog with selective microvascular and RES actions for the treatment of circulatory shock in rats”. European Journal of Pharmacology 37 (1976): 155-168.
  14. Altura BM. “Microcirculatory approach to the treatment of circulatory shock using a new analog of vasopressin, [2-phenylalanine, 8-ornithine]- vasopressin”. Journal of Pharmacology and Experimental Therapeutics 198 (1976): 187-196.
  15. Altura BM. “Sex and estrogens in protection against circulatory stress reactions”. American Journal of Physiology 231 (1976): 842-847.
  16. Altura BM. “Reticuloendothelial and neuro-endocrine stimulation in shock therapy”. Advances in Shock Research 3 (1980): 3-25.
  17. Altura BM. “Recent progress in patho-physiology of shock: Reticuloendothelial and neuro-endocrine stimulation”. The Journal of Clinical Anesthesia 4 (1980): 745-758.
  18. Altura BM. “Reticulo-endothelial cells and host defense”. Adv in Microcirculation 11 (1980): 77-113.
  19. Altura BM and Saba TM. “Pathophysiology of the Reticuloendothelial System”. Raven Press, New York (1981): 233.
  20. Altura BM. “Reticuloendothelial system function and histamine release in shock and trauma”. Klinische Wochenschrift 60 (1982): 282-290.
  21. Halevy S., et al. “Pathophysiological basis for the use of steroids in the treatment of shock and trauma”. Klinische Wochenschrift 60 (1982): 1021-1030.
  22. Altura BM. “Role of reticuloendothelial and endothelial cells in response to shock and trauma”. In: Pathophysiology of Combined Injuries and Trauma, Conklin JT, edition. Univ Park Press, Baltimore (1985).
  23. Altura BM. “Microcirculatory regulation and dysfunction: Relation to RES function and tolerance to shock and trauma”. In: The Reticuloendothelial System, vol 7B, Reichard SM, Filkins JP, eds. Plenum Press, New York (1985): 355-395.
  24. Altura BM. “Endothelial and reticuloendothelial cell function: roles in injury and low-flow states”. In: The Scientific Basis for the Care of the Critically Ill, Little RA, Frayn KN, eds. Manchester Univ. Press, Manchester, The UK (1986): 259-274.
  25. Altura BM., et al. “A novel biologic immunomodulator, HDFx, protects against lethal hemorrhage, endotoxins, and traumatic injury”. International Journal of Clinical and Experimental Medicine 2 (2009): 266-279.
  26. Altura BM., et al. “HDFx: a novel biologic immunomodulator is therapeutically-effective in hemorrhagic and intestinal ischemic shock: importance of microcirculatory-immunological interactions and their potential implications for the warfighter and disaster victims”. International Journal of Clinical and Experimental Medicine 4 (2011): 331-340.
  27. Altura BM., et al. “HDFx, A naturally-occurring host-defense biologic protects against fungal toxins and is anti-inflammatory”. Submitted (2020).
  28. Altura BM. “HDFx: A novel immunomodulator and potential fighter against cytokine storms in viral flu infections”. Sci Fed Journal of Flu Science 1 (2017): 1-4.
  29. Altura BM., et al. “HDFx: A novel immunomodulator and potential fighter against cytokine storms in inflammatory and septic conditions in dogs and farm animals”. International Journal of Veterinary Health Science and Research 2 (2017): 1-3.
  30. Altura BM., et al. “A novel biologic immunomodulator accelerates wound healing and is suggestive of unique regenerative properties: Potential implications for the warfighter and disaster victims”. International Journal of Clinical and Experimental Medicine 5 (2012): 289-295.
  31. Altura BM., et al. “HDFx: A potential new treatment and prophylactic against nonalcoholic steatohepatitis (NASH) and subsequent hepatocarcinomas: Is hypomagnesemia a complication of the disease”. Journal of Alcoholism and Drug Dependence 4 (2016): 1000e133.
  32. Altura BM., et al. “HDFx: Identification of transcriptional and epigenetic pathways of activated-macrophages”. Submitted (2020).
  33. Casadevall A and Pirofski L-a. “The convalescent sera option for containing COVID-19”. Journal of Clinical Investigation (2020).
Citation: Burton M Altura., et al. “HDFx and Transferal of Plasma from Animals that Survive Lethal Hemorrhage, Bowel Ischemic Shock, Endotoxins, Centripetal Forces or Body Trauma to Naïve Animals Induces Cross-Resistance to these Various Experimental Forms of Injury and Trauma: Importance of Macrophages, NK Cells and Relevance to Design of Molecules to Treat/Ameliorate Effects of Corona Viral Diseases”. EC Emergency Medicine and Critical Care 4.5 (2020): 01-04.

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