Abstract:As previously reported (I. Yano, I. Tomiyasu, S. Kitabatake, and K. Kaneda, Acta Leprologica 2:341-349, 1984), Nocardwa rubra, one of the nonpathogenic actinomycetes, possesses three classes of mycolic acidcontaining glycolipid, i.e., glucose mycolate, trehalose dimycolate, and trehalose monomycolate. The carbon chain length of their mycolic acids is shorter (C_3&,a) than that in mycobacteria (longer than C70), and the glycolipid consists of only a-mycolic acid. One intravenous administration of 500 ,Ig of eac… Show more
“…Part of the pathological changes induced by viable bacteria might be ascribed to some factor other than glycolipid of R. equi. Granuloma-forming capacity of glycoplipid from R. equi seems to be comparable to that observed in glycolipid from Nocardia (10). Nocardia species produce various glycolipids containing mycolic acid ranging from C30 to C60, and it is shown that granuloma-forming activity is small if mycolic acid is shorter than C40.…”
By the use of various Rhodococcus equi strains differing in the length of carbon chains of glycolipid, we examined whether the glycolipid, glucose monomvcolate, was contributing to the virulence of R. equi for mice.R. equi strains with longer carbon chain mycolic acid showed a higher virulence as determined by lethality and granuloma formation in mice than those with shorter ones. When purified glycolipid was injected into mice, granuloma formation and liver damage were most prominent with the glycolipid having longer carbon chain mycolic acid. Only a representative strain with longer carbon chain mycolic acid persisted in the spleen of mice after intravenous injection, while a strain with shorter carbon chain mycolic acid was readily eliminated.These results suggested that glycolipid was at least one of the virulence factors of R. equi and that the carbon chain length of mycolic acid might be critical in the expression of virulence.
“…Part of the pathological changes induced by viable bacteria might be ascribed to some factor other than glycolipid of R. equi. Granuloma-forming capacity of glycoplipid from R. equi seems to be comparable to that observed in glycolipid from Nocardia (10). Nocardia species produce various glycolipids containing mycolic acid ranging from C30 to C60, and it is shown that granuloma-forming activity is small if mycolic acid is shorter than C40.…”
By the use of various Rhodococcus equi strains differing in the length of carbon chains of glycolipid, we examined whether the glycolipid, glucose monomvcolate, was contributing to the virulence of R. equi for mice.R. equi strains with longer carbon chain mycolic acid showed a higher virulence as determined by lethality and granuloma formation in mice than those with shorter ones. When purified glycolipid was injected into mice, granuloma formation and liver damage were most prominent with the glycolipid having longer carbon chain mycolic acid. Only a representative strain with longer carbon chain mycolic acid persisted in the spleen of mice after intravenous injection, while a strain with shorter carbon chain mycolic acid was readily eliminated.These results suggested that glycolipid was at least one of the virulence factors of R. equi and that the carbon chain length of mycolic acid might be critical in the expression of virulence.
“…Initially, cord factor was considered to be a potent virulence factor since it had been isolated from the highly virulent M. tuberculosis strain, which grows as a serpentine cord on the surface culture (4). However, it was subsequently found that cord factor and analogous glycolipids exist widely among virulent and avirulent Mycobacterium, Nocardia, Rhodococcus and Corynebacterium (1,22), and furthermore, that they possess various immunostimulatory properties including granuloma-forming activity, adjuvant activity, anti-tumor activity and non-specific infection prevention activity (1,3,16,(26)(27)(28)30). Thus, immunologically, cord factor seems to stimulate cellular immunity (Th 1 response dominant) as an adjuvant and to be non-specific as an antigen.…”
The detection of antiâcord factor (trehalose 6,6âČâdimycolate) IgG antibody in active (smearâand/or cultureâpositive) and inactive (smearâ and cultureânegative) tuberculosis patients is a useful serodiagnostic tool that can be used for early clinical diagnosis of the disease. We estimated the titers of anticord factor IgG antibody in the sera of tuberculosis patients, and compared them with those of Mycobacterium aviumâinfected patients. Most of the serum samples obtained from the tuberculosis patients were highly reactive against M. tuberculosis (MTB) cord factor isolated from M. tuberculosis H37Rv, a humanâtype mycobacterial strain, whereas they were less reactive against M. avium (MAC) cord factor. Similarly, most of the serum samples of the MACâinfected patients were highly reactive against MAC cord factor and less reactive against MTB cord factor. These results suggest that antiâcord factor IgG antibody recognizes the mycolic acid subclasses as an epitope which comprises cord factor, since MTB and MAC cord factor differ in mycolic acid subclasses and molecular species composition. To clarify the exact antigenic epitope in cord factor and to find out a more sensitive and specific diagnostic test antigen, we examined the reactivity of patients' sera to glycolipids containing trehalose (cord factor and sulfolipid) obtained from various mycobacterial species. Furthermore, the reactivity of human antisera to various mycolic acid subclasses (αâ, methoxy and keto mycolic acids) of MTB cord factor was compared. We found that antiâcord factor IgG antibody in the sera of human tuberculosis patients most strikingly recognized methoxy mycolic acid in the cord factor of M. tuberculosis, whereas it recognized αâ and keto mycolic acids weakly. Preâabsorption studies of antibody with MTB cord factor or methoxy mycolic acid methyl ester showed that antiâcord factor antibody was absorbed partially, but consistently. This is the first report describing that the specific subclass of mycolic acid from mycobacteria is antigenic in the humoral immune system of human tuberculosis infection.
“…equi produces glycolypids containing different mycolic acid structures ranging widely from C,, to C,, [28,30]. Purified glycolipids of rhodococci and Nocardia rub-a have shown various biological activ- ities, including granuloma formation and hemopoiesis [28,31,32]. Gotoh et al [28] showed that the carbon length of mycolic acid from R. equi is critical in granuloma formation in murine liver.…”
Virulence of Rhocococcus equi ATCC 33701 and its plasmid-cured derivative ATCC 33701P- was compared in BALB/c and C3H/HeJ mice in terms of bacterial growth kinetics and histological changes in the liver, spleen and lungs, and humoral immune responses. Injection with a sublethal dose of 10(6) ATCC 33701 in mice resulted in microabscess formation after rapid multiplication in the liver and spleen by day 4, and then the bacteria were gradually eliminated with the formation of granuloma and the production of specific antibodies against 15- to 17-kDa antigens of the virulent bacteria. By contrast, ATCC 33701P- was avirulent as shown by early elimination of viable bacteria and no evidence of net multiplication in the organs. Histopathological changes consisted of only slight, transient infiltration of neutrophils and macrophages in the liver. Although live ATCC 33701P- did not evoke any humoral or histological responses in the mice, a large inoculum (10(8)) of killed ATCC 33701 and ATCC 33701P- resulted in the formation of granuloma in the liver and accelerated extramedullary hemopoiesis in the spleen. These results suggest that the pathogenesis of R. equi infection involves at least two important virulence determinants, both of which play critical roles in the disease: one is the virulence plasmid, which is required for R. equi to resist and grow within host cells; and the other is the granulomagenic activity that is related to the lipids and nature of the cell wall of the species, which induces the characteristic pathological changes.
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