Borrelia burgdorferi

Abstract: The outer surface lipoproteins of Borrelia burgdorferi, OspA and OspB, stimulate the production of nitric oxide (NO) by murine bone marrow-derived macrophages from BALB/c, C3H/HeN, and C3H/HeJ mice. Gamma interferon (IFN-gamma) caused a three- to fivefold enhancement of this production of NO, and the L-arginine analog N-guanidino-monomethyl L-arginine inhibited it. Activation of transcription of the inducible NO synthase gene in stimulated macrophages was demonstrated by reverse transcriptase rapid PCR. Although IFN-gamma increased the amount of NO produced in macrophage cultures, it did not cause transcription of the inducible NO synthase gene greater than that seen with the Borrelia proteins. OspA and OspB also induced the production of high levels (40 to 150 ng/ml) of IFN-gamma in cultures of macrophages incubated with interleukin-2 (IL-2)-elicited cells from normal (T and NK cells) and scid (NK cells) mice but not in macrophages or IL-2-elicited cells cultured individually. This suggests that OspA stimulated macrophage production of cytokines, which, in turn, stimulated the production of IFN-gamma by NK and T cells. Reverse transcriptase rapid PCR demonstrated that OspA and sonicated B. burgdorferi stimulated production of several inflammatory cytokines in macrophage cultures, including IL-1, IL-6, IL-12, IFN-beta, and tumor necrosis factor alpha. As tumor necrosis factor alpha, IFN-beta, and IL-12 are potent activators of IFN-gamma production by T and NK cells, their presence in these cocultures could be responsible for the IFN-gamma production. Lymphocytes from infected C3H mice also produced IFN-gamma when stimulated with B. burgdorferi; thus, immune cells may also modulate NO responses. The generation of NO during infection with B. burgdorferi may be important, as NO has potent antimicrobial properties. NO can also be involved in pathological inflammatory processes in which its generation is detrimental to the host. Thus, the colocalization of B. burgdorferi lipoproteins, NO-producing cells, and regulatory cytokines may determine the outcome of infection.

Abstract: The significance of various antibodies against Borrelia burgdorferi was studied by Western blot (immunoblot) by using 578 human serum samples. The proteins regularly detected by using samples from patients with Lyme borreliosis were those with bands with molecular masses of 94, 83, 75, 66, 60, 55, 46, 41, 39, 34, 31, 29, 22, and 17 kDa. The detectable frequencies of most of these proteins appeared to be significantly different between the sera from patients with Lyme borreliosis and those from normal control individuals as well as from the group with syphilis. The 39-kDa protein band recognized by polyvalent antibody was found to be the most significant marker for Lyme borreliosis. Furthermore, an anti-39-kDa immunoglobulin M response was detected in the samples from patients with early-stage Lyme borreliosis. Results from the use of monoclonal antibodies and patient sera revealed that the 39- and 41-kDa proteins may be structurally related but are immunologically distinct antigens. The significance of antibody reactivities to the 41-, 94-, 22-, 31-, and 34-kDa protein bands is also discussed.

Abstract: QWKHVXEXUEDQDQGXUEDQIRUHVWVLQWKHFLWLHVRI*GDVN6RSRWDQG*G\QLD (northern Poland), Ixodes ricinus ticks should be considered as the vector of pathogenic microorganisms that may cause significant diseases in wild and domestic animals and humans. These microorganisms include etiologic agents of Lyme disease, human anaplasmosis (HA) and babesiosis: Borrelia burgdorferi sensu lato, Anaplasma phagocytophilum and Babesia microti, respectively. DNA extracts from 701 ticks collected in 15 localities were examined by PCR for the simultaneous detection of these 3 pathogens. Overall, 14% were infected with A. phagocytophilum followed by 12.4% with B. burgdorferi s.l. and 2.3% with B. microti. In total, the percentage of infected females (32.9%) was 2.4 times higher than in males (13.7%) and 3.2 times higher than in nymphs (10.3%). Among adult ticks (n = 303), 8.3% were dually infected with A. phagocytophilum and B. burgdorferi s.l., 2.0% with the agent of human anaplasmosis and B. microti and 0.3% with borreliae and B. microti.

Abstract: Human pathogenic spirochetes causing Lyme disease belong to the Borrelia burgdorferi sensu lato complex. Borrelia burgdorferi organisms are extracellular pathogens transmitted to humans through the bite of Ixodes spp. ticks. These spirochetes are unique in that they can cause chronic infection and persist in the infected human, even though a robust humoral and cellular immune response is produced by the infected host. How this extracellular pathogen is able to evade the host immune response for such long periods of time is currently unclear. To gain a better understanding of how this organism persists in the infected human, many laboratories have focused on identifying and characterizing outer surface proteins of B. burgdorferi. As the interface between B. burgdorferi and its human host is its outer surface, proteins localized to the outer membrane must play an important role in dissemination, virulence, tissue tropism, and immune evasion. Over the last two decades, numerous outer surface proteins from B. burgdorferi have been identified, and more recent studies have begun to elucidate the functional role(s) of many borrelial outer surface proteins. This review summarizes the outer surface proteins identified in B. burgdorferi to date and provides detailed insight into the functions of many of these proteins as they relate to the unique parasitic strategy of this spirochetal pathogen.