Distinct ability to accumulate eosinophils during the inflammatory cellular response to M. bovis BCG in the mouse pleural cavity

Inflammation Research

Volumn 49, Issue 5, 2000, Pages 206-213

  Werneck Barroso, E ^c   Moura, A C Novias ^a   Magalhaes Monteiro M ^c   Menezes De Lima Junior O ^c   De Nazareth Leal De Meirelles, M ^b   Das Gracas Muller O Henriques M ^c  

^a STATE UNIVERSITY OF RIO DE JANEIRO   (Brazil)

^b INSTITUTO OSWALDO CRUZ   (Brazil)

^c NONE

Author keywords

Eosinophil; Inflammation; M. bovis BCG; Neutrophil

Indexed keywords

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; CELL FUNCTION; CELL ULTRASTRUCTURE; CONTROLLED STUDY; EOSINOPHIL; GRANULOCYTE FUNCTION; HOST SUSCEPTIBILITY; INFLAMMATION; MALE; MOUSE; MYCOBACTERIOSIS; MYCOBACTERIUM BOVIS; NONHUMAN; PATHOGENESIS; PLEURISY;

ADJUVANTS, IMMUNOLOGIC; ANIMALS; BCG VACCINE; EOSINOPHILS; EXUDATES AND TRANSUDATES; LEUKOCYTE COUNT; MALE; MICE; MICE, INBRED C57BL; MICE, INBRED DBA; MICROSCOPY, ELECTRON; NEUTROPHILS; PLEURA; PLEURISY; SPECIES SPECIFICITY; TIME FACTORS;

EID: 0034044402     PISSN: 10233830     EISSN: None     Source Type: Journal    
DOI: 10.1007/s000110050581     Document Type: Article

References (30)

1. [1] Smith DW, Wiegeshaus EH. What Animal Models Can Teach Us About the Pathogenesis of Tuberculosis in Humans Reviews of Infectious Diseases. 1989; II: 5385-93.
2. [2] Brown E, Atkinson JP, Fearon DT. Innate immunity. 50 ways to kill a microbe. Curr Opin Immunol 1994; 6 (1): 73-4.
3. nd ed. Charles C. Thomas, Publisher, Springfield, Illinois 1951.
4. [4] Lefford MJ. The Effect of Inoculum Size on the Immune Response to BCG Infection in Mice. Immunology 1970; 21: 369-81.
5. [5] Menezes-de-Lima-Júnior O, Werneck-Barroso E, Cordeiro RSB, Henriques MGMO. Effects of lipid inhibitors of inflammatory mediators and cytokines on eosinophil and neutrophil accumulation induced by Mycobacterium bovis bacillus Calmette-Guerin in mouse pleurisy. J Leukoc Biol 1997; 62 (6): 778-85.
6. [6] Silva PMR, Martins MA, Castro-Faria-Neto HC, Cordeiro RSB and Vargaftig BB. Generation of an eosinophilotactic activity in the pleural cavity of Platelet-activating factor injected rats. J Pharmacol Exp Ther 1991; 257: 1039-44.
7. [7] Bozza PT, Castro-Faria Neto HC, Martins MA, Larangeira AP, Perales JE, Silva PMR, et al. Pharmacological modulation of lipopolysaccharide-induced pleural eosinophilia in the rat; a role of a newly generated protein. Eur J Pharmacol 1993; 248: 41-7.
8. [8] Zlotnik A, Crowle AJ. Lymphokine-induced mycobacteriostatic activity in mouse pleural macrophages. Infect Immun 1982; 37: 786-93.
9. [9] Spector WG. The mediation of altered capillary permeability in acute inflammation. J Path Bact 1956; 72: 367-80.
10. [10] Henriques MGOM, Weg VB, Martins MA, Silva PMR, Fernandes PD, Cordeiro RSB, et al. Differential inhibition by two hetrazepine PAF antagonists of acute inflammation in the mouse. Br J Pharmacol 1990; 99: 164-8.
11. [11] Crowle AJ. The tubercle bacillus-macrophage relationship studied in vitro. In: Bendinelli M and Friedmen H (eds.) Mycobacterium tuberculosis: interactions with immune system. New York: Plenum Press, 1988: 99-135.
12. [12] Blusse van Oud Alblas A, van der Linden Schrever B, van Furth R. Origin and kinetics of pulmonary macrophages during an inflammatory reaction induced by intravenous administration of heat-killed bacillus Calmette-Guerin. J Exp Med 1981; 154: 235-52.
13. [13] Fuchs HJ, Sniezek M, Shellito JE. Cellular influx and activation increase macrophage cytotoxicity and interleukin-1 elaboration during pulmonary inflammation in rats. Am Rev Respir Dis 1988; 138: 572-7.
14. [14] Edwards D, Kirkpatrick CH. The immunology of Mycobacteria Diseases. Am Rev Respir Dis 1986; 134: 1062-71.
15. [15] Dannenberg AM Jr. Cellular hypersentivity and cellular immunity in the pathogenesis of tuberculosis: specificity, systemic and local nature, and associated macrophage enzyme. Bacteriol Rev 1968; 32: 85-102.
16. [16] Dannemberg E. Immune mechanisms in the pathogenesis of pulmonary tuberculosis. Rev Infect Dis 1989; 2: 369-77.
17. [17] Lurie MB. Resistance of tuberculosis: experimental studies in native and acquired defensive mechanisms. Cambridge, Mass: Harvard University Press 1964.
18. [18] Rook GA, al Attiyah R, Filley E. New insights into the immunopathology of tuberculosis. Pathobiology 1991; 59: 148-52.
19. [19] Savill JS, Wyllie AH, Walport MJ, Henson PM, Hasllet C. Macrophage phagocytosis of aging neutrophils in inflammation. Programmed cell death in the neutrophils lead to its recognition by macrophages. J Clin Invest 1989; 83: 865-75.
20. [20] Willians T, Hollewell P. Immunopharmacology of Neutrophils, Academic Press, Harcourt Brace and Company, 1994.
21. [21] Antony VB, Sahn AS, Antony AC, Repine JE. BCG-stimulated neutrophils release chemotaxins for monocytes in rabbits pleural spaces and in vitro. J Clin Invest 1985; 76: 1514-21.
22. [22] Mariano M. The experimental granuloma. A hypothesis to explain the persistence of the lesion. Rev Inst Med Trop São Paulo 1995; 37: 161-76.
23. [23] Moura ACN, Leonardo PS, Henriques MGMO, Cordeiro RSB. Opposite effects of M. leprae or M. bovis BCG delipidation on cellular accumulation into mouse pleural cavity. Distinct accomplishment of mycobacterial lipids in vivo. Inflamm Res 1999; 48: 308-13.
24. + T cells are required for antigen-specific recruitment of neutrophils by BCG-immune spleen cells. Immunol 1992; 75: 414-9.
25. [25] Bozza PT, Castro-Faria Neto HC, Penido C, Larangeira AP, Silva PMR, Martins MA, Cordeiro RSB. IL-5 accounts for the mouse pleural eosinophil accumulation triggered by antigen but not by LPS. Immunopharmacology 1994; 27: 131-6.
26. [26] Cooper AM, Dalton DK, Stewart AT, Griffin JP, Russel DG, Orme IM. Disseminated tuberculosis in interferon γ gene-disrupted mice. J Exp Med 1993; 178: 2243-7.
27. [27] Nadeau JH, Arbuckle LD, Skamene E. Genetic dissection of inflammatory responses. J Inflamm 1995; 45: 27-48.
28. [28] Castro AG, Esaguy N, Macedo PM, Aguas AP, Silva MT. Live but not heat-killed mycobacteria cause rapid chemotaxis of large numbers of eosinophils in vivo and are ingested by the attracted granulocytes. Infect Immun 1991; 59 (9): 3009-14.
29. [29] Forget A, Skamene E, Gros P, Miailhe AC, Turcotte R. Differences in response among inbred mouse strains to infection with small doses of Mycobacterium bovis BCG. Infect Immun 1981; 32: 42-7.
30. [30] Gros P, Skamene E, Forget A. Cellular mechanisms of genetically controlled host resistance to Mycobacterium bovis (BCG). J Immunol 1983; 131: 1966-72.