Palma-Ramos A, Castrillón-Rivera LE, Castañeda-Sánchez JI, Muñoz DAR, Mendoza PF, Padilla DC

Language: Spanish
References: 25
Page: 85-91
PDF size: 276.06 Kb.

ABSTRACT

Introduction: The mycetoma cause for Actinomadura madurae, is a chronic granulomatous infectious process characterized by volume increase and «killed»-like stony consistency, during the infection few drining filamentous exudate fistulas could be observed, the exudate contains grains whose size varies from 1 to 5 mm. Within the grains there are components of the host immune response, including keratinocytes, neutrophils, mast cells, eosinophils and macrophages which can engulf and destroy pathogens. Objective: To study the host-pathogen interaction in murine peritoneal macrophages when these are infected whit Actinomadura madurae in order to know if this pathogen is able to activate the murine peritoneal macrophages in vitro this interaction was observed by transmission electron microscopy technique. Material and methods: Inoculum, Actinomadura madurae strain ATCC 19425, was grown in broth Yeme at 37 ^oC for 15 days a 300 x 106 CFU/mL solution was used to infect macrophages. The phagocytosis assays were performed using 0.1 mL of the solution work to infect muerine peritoneal macrophages, cells were icubated at 37 ^oC in a CO₂ atmosphere at 5%, after different times (15, 30, 45 and 60 min), aliquots were taken and fixed with 2.5% glutaraldehyde solution in 0.1 M cacodilatos buffer cells were included in resin to finally observe them by the electron microscope Jeol EX 2000. To test the cellular activation we used the phosphatase acid tecnique and observed in the electron microscope. Results: During hos-pthogen interaction different stages of phagocytosis and macrophage activation were observed as well as the destruction of A. madurae. Conclusion: Actinomadura madurae is engulfed and destroyed by murine peritoneal macrophages in vitro.

REFERENCES

1. López-Martínez R, Méndez-Tovar LJ, Lavalle P, Welsh O, Saúl A, Macotela-Ruíz E. Epidemiology of mycetoma in Mexico: study of 2105 cases. Gac Med Mex. 1992; 128: 477-481.

2. Lavalle-Aguilar P, Padilla-Desgarennes MC, Pérez-Gutiérrez J, Rivera I, Reynoso-Rangel S. Micetomas por Actinomadura madurae en México. Rev Cent Dermatol Pascua. 2000; 9: 19-24.

3. Jerez R, Schafer F, Fich F, García P, León P, González S. Micetoma actinomicótico por Actinomadura madurae. Rev Chil Infectol. 2012; 29: 459-463.

4. Padilla DC, Guardado DV. Micetoma por Actinomadura madurae en un paciente con tuberculosis pulmonar. Comunicación de un caso. Dermatología Rev Mex. 2009; 53:145-149.

5. Palma RA, Castrillón RL, Padilla DC, Rosas HLL, Márquez C. Purificación y determinación de la estructura de los polisacáridos que forman el cemento de unión en granos de actinomicetomas ocasionados por Actinomadura madurae y Nocardia brasiliensis. Dermatología Rev Mex. 2006; 50: 165-173.

6. Bonifaz A, González-Silva A, Albrandt-Salmerón A, Padilla Mdel C, Saúl A, Ponce RM. Utility of helical computed tomography to evaluate the invasion of actinomycetoma; a report of 21 cases. Br J Dermatol. 2008; 158: 698-704.

7. El Hassan AM, Fahal AH, Veress B. Cell phenotypes, immunoglobulins and complement in lesions of eumycetoma caused by Madurella mycetomatis. J Sudanese Dermatology. 2006; 4: 2-5.

8. Fahal AH, el Toum EA, el Hassan AM, Mahgoub ES, Gumaa SA. The host tissue reaction to Madurella mycetomatis: new classification. J Med Vet Mycol. 1995; 33: 15-17.

9. Janeway CA Jr, Medzhitov R. Innate immune recognition. Annu Rev Immunol. 2002; 20: 197-216.

10. Ochoa-Carrillo FJ, Bravo-Cuellar A. Los macrófagos, ángeles o demonios. GAMO. 2013; 12: 1-3.

11. Biswas SK, Sica A, Lewis CE. Plasticity of macrophage function during tumor progression: regulation by distinct molecular mechanisms. J Immunol. 2008; 180: 2011-2017.

12. Hao NB, Lü MH, Fan YH, Cao YL, Zhang ZR, Yang SM. Macrophages in tumor microenvironments and the progression of tumors. Clin Dev Immunol. 2012; 2012: 948098.

13. Santana A, Lemes A, Bolaños B, Parra A, Martín M, Molero T. Citoquímica de la fosfatasa ácida: Consideraciones metodológicas. Rev Diagn Biol. 2001; 50: 89-92.

14. Guija E, Soberón M, Haak-Mares H. Mecanismo de acción de las fosfatasas ácidas de bajo peso molecular. An Fac Med. 2007; 68: 356-362.

15. Cimasoni G. Crevicular fluid updated. New York: S. Karger; 1983. p. 111.

16. English D, Martin M, Harvey KA, Akard LP, Allen R, Widlanski TS et al. Characterization and purification of neutrophil ecto-phosphatidic acid phosphohydrolase. Biochem J. 1997; 324: 941-950.

17. De Duve C, Wattiaux R. Functions of lysosomes. Annu Rev Physiol. 1966; 28: 435-492.

18. Olea MT, Nagata T. Simultaneous localization of 3H-thymidine incorporation and acid phosphatase activity in mouse spleen: EM radioautography and cytochemistry. Cell Mol Biol. 1992; 38: 115-122.

19. Itoiz ME, Carranza Jr. FA, Cabrini RL. Histotopographic distribution of alkaline and acid phosphatases in periodontal tissues of laboratory animals. J Periodontol. 1964; 35: 470-475.

20. Cabrini RL, Carranza FA Jr. Histochemical distribution of acid phosphatase in human gingiva. J Periodontol. 1958; 29: 34-37.

21. Perry DK, Stevens VL, Widlanski TS, Lambeth JD. A novel ecto-phosphatidic acid phosphohydrolase activity mediates activation of neutrophil superoxide generation by exogenous phosphatidic acid. J Biol Chem. 1993; 268: 25302-25310.

22. Krane SM, Potts JT Jr. Skeletal remodeling and factors influencing bone and bone metabolism. In: Harrison’s principles of internal medicine. 9th ed. 1980.

23. Larmas L. A comparative enzyme histochemical study of hydantoin induced hyperplastic and normal human gingiva. Proc Finn Dent Soc. 1977; 73 Suppl 1: 1-27.

24. Yajima T. Acid phosphatase activity and intracellular collagen degradation by fibroblasts in vitro. Cell Tissue Res. 1986; 245: 253-260.

25. Lewis PR, Knight DP. Cytochemical staining methods for electron microscopy. The Netherlands: Elsevier Sc. Pub.; 1992. pp. 107-109.