Adjuvant treatment increases the resistance to Mycobacterium avium infection of Mycobacteria‐susceptible BALB/c mice

• Published in: Clinical and experimental immunology Vol. 92; no. 3; pp. 466 - 472
• Main Authors: CASTRO, A. P., ÁGUAS, A. P., SILVA, M. T.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01-06-1993; Blackwell
• Subjects: Animals; Antigens, Bacterial - immunology; Bacterial diseases; Biological and medical sciences; Disease Models, Animal; Experimental bacterial diseases and models; Female; Freund's Adjuvant - immunology; granulocytes; Granulocytes - immunology; Immunity, Innate; infection; Infectious diseases; inflammation; Leukocyte Count; Medical sciences; Mice; Mice, Inbred BALB C; Mice, Inbred C3H; Mice, Nude; mycobacteria; Mycobacterium avium; Mycobacterium avium - immunology; neutrophils; Tuberculosis - immunology; Animal model; Host parasite relation; Intraperitoneal administration; Rodentia; Mycobacterium avium; Inflammation; Injection; Infection; Resistance; Vertebrata; Experimental disease; Mammalia; Incomplete Freund's adjuvant; Mouse; Mycobacteriales; Mycobacteriaceae; Bacteriosis; Bacteria; Actinomycetes
• ISSN: 0009-9104; 1365-2249
• DOI: 10.1111/j.1365-2249.1993.tb03422.x

SUMMARY
We have investigated thc effect of inflammation on host resistance against infection by Mycobacterium avium. an atypical mycobactcria species that is responsible for life‐threatening opportunistic infections in AIDS patients. Inflammation was induced in BALB/c mice by two intraperitoneal injections of mineral oil (Freund's incomplete adjuvant, FIA). The BALB/c strain was chosen because it is naturally susceptible to Myco. avium infection. One week after the second FIA injection, the BALB c mice were infected intravenously with 26 ± 106Myco. avium bacilli: at this time, the mice showed systemic granulocytosis because of the FIA injections. The kinetics of the murine infection was determined during 3 months by quantification of Myco. avium loads in the major target organs (liver and spleen) of the mycobacteria. The FIA treatment resulted in a significant decrease in the growth of Myco. avium in the infected BALBx mice. This enhancement in host resistance to Myco. avium infection lasted for 2 3 months. In contrast with BALB/c animals. C3B mice (naturally resistant to Myco. avium infection) did not show an increased anti‐Myco. avium action in association with the FIA treatment. The anlimycobaeterial effect of the FIA injections in BALBx mice was compared with that produced by the injection of mycobacterial antigens (heat‐killed Myco. tuberculosis) added to the mineral oil (i.e. Freund's complete adjuvant, FCA). The FCA treatment resulted in strong and sustained enhancements in the microbicidal capacities of BALB/c. and also of C3H mice. Data obtained with mutant athymic BALB/c mice revealed that the anti‐Myco. avium effect of the FCA treatment was T cell‐dependent. Our results indicate that: (i) non‐immune inflammatory stimulation (FIA) of Myco. avium‐susceptible hosts is able to cause a significant, albeit transient, increase in the resistance to Myco. avium infection; (ii) this protective effect is enhanced if heat‐killed mycobacteria arc added to the phlogistic agent (FCA). i.e. if a T cell‐dependent response is induced: and (iii) systemic increase in the number of circulating granulocytes may help host defence against Myco. avium infection.