Localization of brucella antigens that elicit a humoral immune response in Brucella abortus-infected cells

In an enzyme-linked immunosorbent assay (ELISA), purified Brucella abortus and Escherichia coli peptidoglycan-linked lipoproteins gave a strong cross-reaction with sera from rabbits hyperimmunized with the heterologous lipoprotein. When smooth E. coli cells were used as ELISA antigens, the immunological cross-reaction was not observed unless the cells were treated to remove lipopolysaccharide and other outer membrane components. In contrast, intact cells from smooth strains of B. abortus and Brucella melitensis bound anti-lipoprotein immunoglobulin G, and the controls performed by ELISA showed that this reaction was not due to antibodies to the lipopolysaccharide, group 3 outer membrane proteins, or porins. Electron microscopy of cells labeled with antilipoprotein serum and protein A-colloidal gold showed specific labeling of smooth cells from both B. abortus and B. melitensis, even though unspecific labeling by nonimmune serum was observed with rough B. abortus. These results confirm the close similarity between E. coli and Brucella peptidoglycan-linked lipoproteins and show that, in contrast to E. coli, the lipoprotein of B. abortus and B. melitensis is partially exposed on the surface of smooth cells.

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“…3C). Nonspecific binding of IgG to rough Brucella species has been observed by other investigators (30).…”

Section: Resultssupporting

confidence: 62%

Brucella outer membrane lipoprotein shares antigenic determinants with Escherichia coli Braun lipoprotein and is exposed on the cell surface

Gómez-Miguel¹,

Moriyón²,

López³

1987

Infect Immun

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“…The positively charged Br-LPS core oligosaccharide, composed of amino sugars, and the O-chain and NH homopolymers, built of nonreducing N-formyl-perosamine residues (Fig. 3A) (150,151), form a shield, masking the available negative charges on the smooth brucella surface (152). This property makes the invading bacterium "invisible" to various PRRs and resistant to the microbicidal action of cellular cationic microbicidal molecules of PMNs and other cells (102,103,148,153,154).…”

Section: Brucella Organisms Are Resistant To Bactericidal Substancesmentioning

confidence: 99%

The Role of Neutrophils in Brucellosis

Moreno

Barquero-Calvo

2020

Microbiol Mol Biol Rev

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SUMMARY Brucellosis is a bacterial disease of domestic animals and humans. The pathogenic ability of Brucella organisms relies on their stealthy strategy and their capacity to replicate within host cells and to induce long-lasting infections. Brucella organisms barely induce neutrophil activation and survive within these leukocytes by resisting microbicidal mechanisms. Very few Brucella-infected neutrophils are found in the target organs, except for the bone marrow, early in infection. Still, Brucella induces a mild reactive oxygen species formation and, through its lipopolysaccharide, promotes the premature death of neutrophils, which release chemokines and express “eat me” signals. This effect drives the phagocytosis of infected neutrophils by mononuclear cells that become thoroughly susceptible to Brucella replication and vehicles for bacterial dispersion. The premature death of the infected neutrophils proceeds without NETosis, necrosis/oncosis, or classical apoptosis morphology. In the absence of neutrophils, the Th1 response exacerbates and promotes bacterial removal, indicating that Brucella-infected neutrophils dampen adaptive immunity. This modulatory effect opens a window for bacterial dispersion in host tissues before adaptive immunity becomes fully activated. However, the hyperactivation of immunity is not without a price, since neutropenic Brucella-infected animals develop cachexia in the early phases of the disease. The delay in the immunological response seems a sine qua non requirement for the development of long-lasting brucellosis. This property may be shared with other pathogenic alphaproteobacteria closely related to Brucella. We propose a model in which Brucella-infected polymorphonuclear neutrophils (PMNs) function as “Trojan horse” vehicles for bacterial dispersal and as modulators of the Th1 adaptive immunity in infection.

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“…Normal bovine serum is known to contain IgM antibodies cross-reacting with B. abortus LPS (51). Sera from infected animals contain predominantly IgGl antibodies (3, 4, 9, 51), reacting with smooth LPS (57,58). Animals immunized with cell envelopes of rough strain 45/20 produced high levels of antibodies to porins and group 3 antigens ( Fig.…”

Section: Discussionmentioning

confidence: 99%

“…Eleven of these heifers were then vaccinated on days 107 and 246 with 5 mg of rough strain 45/20 cell envelopes in adjuvant (70). Cell envelopes from this rough vaccine strain were used to elicit antibodies against outer membrane proteins rather than primarily against smooth LPS, as is characteristic of infected animals (57,58). Each dose of vaccine contained cell envelopes (5 mg), trehalose dimycolate (5 mg), a butyryl derivative of muramyl dipeptide (5 mg), spermidine (100 ,ul), mineral oil (1.8 ml), and 0.4% Tween 80 solution (8.2 ml).…”

mentioning

confidence: 99%

Killing of Brucella abortus by bovine serum

et al. 1988

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Studies of the serum bactericidal system in bovine brucellosis were undertaken to investigate the role of the humoral immune response in protection of cattle against the facultative intracellular parasite Brucella abortus. Fresh sera from normal control cattle, infected cattle, and cattle immunized with B. abortus cell envelopes were collected before treatment and during the course of immunization or infection. Normal fresh bovine serum or fresh agammaglobulinemic serum from colostrum-deprived calves was effective in killing smooth virulent B. abortus 2308, but rough strains RB51 (a rough mutant of strain 2308) and 45/20 were much more senitive to serum. The difference in susceptibility to serum was shown to be correlated with differences in lipopolysaccharide chemotype, with the more resistant strain 2308 having 0 polysaccharide and the more susceptible strains 45/20 and RB51 lacking 0 side chains. By treatment of fresh serum with MgCl2 and EGTA [ethylene glycol-bis(IO-aminoethyl ether)-N,N,N',N'-tetraacetic acid] killing was shown to occur via the classical pathway of complement activation. When antibody to B. abortus was present, killing of strain RB51 increased but killing of smooth strain 2308 decreased. The earliest antibody response in serum from infected animals did not interfere with killing. When affinity-purified bovine immunoglobulins specific for B. abortus smooth lipopolysaccharide were added to fresh normal bovine serum, immunoglobulin Gl (IgGl) and IgG2 isotypes blocked killing but IgM and IgA isotypes did not. Thus, it appears that serum from previously unexposed animals or animals early during infection can kill smooth B. abortus, an appropriate defense mechanism before the organism becomes intracellular. At later stages of infection, blocking antibodies predominate.

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Localization of brucella antigens that elicit a humoral immune response in Brucella abortus-infected cells

Cited by 15 publications

References 14 publications

Brucella outer membrane lipoprotein shares antigenic determinants with Escherichia coli Braun lipoprotein and is exposed on the cell surface

Brucella outer membrane lipoprotein shares antigenic determinants with Escherichia coli Braun lipoprotein and is exposed on the cell surface

The Role of Neutrophils in Brucellosis

Killing of Brucella abortus by bovine serum

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