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Characterization of pulmonary cellular influx differentials to known toxic agents between species

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In this study, we have shown that chickens, frogs, and toads are resistant to acute pulmonary injury by a variety of toxic agents, (O2, hyperbaric O2, paraquat, and silica), that cause extensive acute injury in mammals. Acute pulmonary injury is defined as a massive influx of inflammatory cells, both interstitially and into the alveolar spaces, pulmonary edema, hemorrhage, and the presence of H2O2 and O 2 in the lavaged supernatant, occurring within 48 h. In some cases, chronic effects of the toxins were observed after 90 h., i.e., hemorrhage, fibrosis, and an accumulation of interstitial inflammatory cells. In all three nonmammal systems, isolated inflammatory cells failed to respond chemotactically in vitro to known mammalian chemotaxins. Pulmonary lavage of the exposed chickens, frogs, and toads also failed to produce inflammatory cells. Pulmonary edema was not detected in any of the animals by comparison of lung weight to total body weight. Intratracheal injections of silica for 2 weeks did produce chronic effects in chickens and frogs. Morphologically, the lungs showed signs of fibrosis and accumulation of interstitial inflammatory cells, but no intraalveolar cells. After 90 h of hyperbaric O2, frogs exhibited a massive infiltration of interstitial inflammatory cells and hemorrhage. Elevated O2 levels (100%) for 2 weeks under normal atmospheric conditions produced no changes in frog lungs or in the amount of inflammatory cells in the lungs. Intravenous injections of paraquat for up to 208 h failed to initiate an accumulation of pulmonary inflammatory cells or the development of pulmonary edema in chickens. There was also no detectable H2O2 or O2 in the lavaged supernatant. It was not determined whether paraquat had a longer or more chronic effect on chickens. We suggest that the lack of an acute pulmonary inflammatory mechanism in chickens, frogs, and toads is in part responsible for the resistance of these animals to acute pulmonary injury by oxidizing mammalian toxins.

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  1. 1.

    Somayajulu, R. S. N., S. P. Mukherjee, W. S. Lynn, andP. B. Bennett. 1978. Pulmonary oxygen toxicity in chickens and rabbits.Undersea Biomed. J. 5(1): 1–8.

  2. 2.

    Somayajulu, R. S. N., andW. S. Lynn. 1978. The effect of oxygen, Freund's adjuvant and cortisone on the lung of rabbit and chickens as studied by histochemical methods.Folia Histochem. Cytochem. 16(1):3–12.

  3. 3.

    Shasby, D. M., R. B. Fox, R. N. Harada, andJ. E. Repine. 1980. Mechanisms of pulmonary oxygen toxicity: Neutropenia protects against acute lung injury from hyperoxia.Am. Rev. Resp. Dis. 121(4, pt. 2):258.

  4. 4.

    Lynn, W. S., R. S. N. Somayajulu, S. Sahu, andJ. Selph. 1978. Characterization of chemotactic agents produced in experimental pleural inflammation.In Leukocyte Chemotaxis: Methods, Physiology and Clinical Implications. J. I. Quinn and P. G. Quie, editors. Raven Press, New York. 299–306.

  5. 5.

    Merchant, D., R. Kahn, andW. H., Murphy. 1964. Handbook of Cell and Organ Culture. Burgess, Minneapolis, Minnesota. 181.

  6. 6.

    Pickett, J. P. 1967. Manual of Histopathological and Histochemical Procedures. Pathology Department, Duke Medical Center, Durham, North Carolina. 15–16.

  7. 7.

    Lynn, W. S., andC. Mukherjee. 1978. Motility of human polymorphonuclear leukocytes: Roles of hydroxy fatty acids, other lipids and cations.Am. J. Pathol. 91:581–593.

  8. 8.

    Lynn, W. S., andN. Mohapatra. 1980. Control of leukocyte functions: Role of internal H+ concentration and a membrane-bound esterase.Inflammation 4:329–341.

  9. 9.

    Sorokin, S. P. 1977. Phagocytes in the lungs. Incidence, general behavior, and phylogeny.In Respiratory Defense Mechanisms. J. D. Brain, D. F. Proctor, and L. M. Reid, editors. Marcel Dekker, New York.5(2):711–848.

  10. 10.

    Sloan, B., W. R. Abrams, D. R. Heranze, P. Kimbel, andG. Weinbaum. 1981. Emphysema induced in vitro and in vivo in dogs by a purified elastase from homologous leukocytes.Am. Rev. Respir. Dis. 124:295–301.

  11. 11.

    Johnson, K. J., J. C. Fontane III, J. Kaplan, andP. A. Ward. 1981. In vivo damage of rat lungs by oxygen metabolites.J. Clin. Invest. 67:983–993.

  12. 12.

    Weiss, S. J., J. Young, A. F. LoBuglio, A. Shivka, andN. F. Nimeh. 1981. Role of hydrogen peroxide on neutrophil-mediated destruction of cultured endothelial cells.J. Clin. Invest. 68:714–721.

  13. 13.

    Giri, S. N., M. A. Hollinger, andM. J. Schiedt. 1981. The effects of paraquat and superoxide dismutase on pulmonary vascular permeability and edema in mice.Arch. Environ. Health 36:149–154.

  14. 14.

    Martin, W. J., J. E. Cradek, G. W. Hunninghake, andR. G. Crystal. 1981. Oxidant injury of lung parenchymal cells.J. Clin. Invest. 68:1277–1288.

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Brown, C.F., Pratt, P.C. & Lynn, W.S. Characterization of pulmonary cellular influx differentials to known toxic agents between species. Inflammation 6, 327–341 (1982). https://doi.org/10.1007/BF00917305

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  • Pulmonary Edema
  • Paraquat
  • Chronic Effect
  • Total Body Weight
  • Toxic Agent