<i>Wolbachia</i> bacteria in filarial immunity and disease

Taylor, Mark J.; Cross, H. F.; Ford, Louise; Makunde, Williams H.; Prasad, Gbks; Bilo, Katja

doi:10.1046/j.1365-3024.2001.00400.x

Cited by 94 publications

(47 citation statements)

References 87 publications

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“…This down regulation, also known as the development of LPS tolerance (42,55), protects the host from developing an uncontrolled immunological response, resulting in endotoxic shock. However, it may also result in a decreased ability of the host to respond to secondary infections, thereby contributing to the development of chronic pathology in lymphatic filariasis (51). Interestingly, we did not observe a strong effect of Wolbachia on lymphatic lesion formation associated with chronic infection in the Mongolian gerbil model of human lymphatic filariasis.…”

Section: Discussioncontrasting

confidence: 66%

“…Wolbachia bacteria have now been reported to exist in many filarial nematodes, including B. malayi and Brugia pahangi (3,30,49,55). Interestingly, Wolbachia has recently been proposed to play a role in the induction of the host immune response to filariae (9,44,50,51). Some researchers suggest that lipopolysaccharide (LPS)-like molecules from filarial Wolbachia bacteria may contribute to the pathogenesis associated with lymphatic filariasis (50) and the ocular lesions associated with onchocerciasis (44).…”

mentioning

confidence: 99%

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Removal of Wolbachia from Brugia pahangi Is Closely Linked to Worm Death and Fecundity but Does Not Result in Altered Lymphatic Lesion Formation in Mongolian Gerbils ( Meriones unguiculatus )

Chirgwin¹,

Coleman²,

Porthouse³

et al. 2003

Infect Immun

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Approximately 30 years ago, researchers reported intracellular bacteria in filarial nematodes. These bacteria are relatives of the arthropod symbiont Wolbachia and occur in many filarial nematodes, including Brugia pahangi and Brugia malayi. Wolbachia bacteria have been implicated in a variety of roles, including filaria development and fecundity and the pathogenesis of lymphatic lesions associated with filarial infections. However, the role of the bacteria in worm biology or filarial disease is still not clear. The present experiments support previous data showing that tetracycline eliminates or reduces Wolbachia bacteria in B. pahangi in vivo. The elimination of Wolbachia was closely linked to a reduction in female fecundity and the viability of both sexes, suggesting that the killing of Wolbachia is detrimental to B. pahangi. The gerbils treated with tetracycline showed reduced levels of interleukin-4 (IL-4) and IL-5 mRNA in renal lymph nodes and spleens compared with the levels in B. pahangi-infected gerbils not treated with tetracycline. However, similar findings were noted in B. pahangi-infected gerbils treated with ivermectin, suggesting that the loss of circulating microfilariae, not the reduction of Wolbachia bacteria, was associated with the altered cytokine profile. Despite the change in T-cell cytokines, there was no difference in the sizes of renal lymph nodes isolated from gerbils in each treatment group. Furthermore, the numbers, sizes, or cellular compositions of granulomas examined in the lymphatics or renal lymph nodes did not differ with treatment. These data suggest that Wolbachia may not play a primary role in the formation of lymphatic lesions in gerbils chronically infected with B. pahangi.Lymphatic filariasis is caused primarily by the filarial nematodes Wuchereria bancrofti and Brugia malayi and affects more than 120 million people throughout the tropics and subtropics. The disease presents as a broad range of clinical and subclinical symptoms, including fever, acute and chronic inflammation, lymphatic edema, and elephantiasis. While much research has focused on the disease caused by infection with Brugia or Wuchereria, the mechanism(s) underlying the pathogenesis of lymphatic filariasis has not been clearly defined. In both acute and chronic infections, these mechanisms probably involve a diverse range of inflammatory reactions attributable to the parasite, host inflammatory responses, and opportunistic infections (40).Approximately 30 years ago, several researchers reported intracellular bacteria in filarial nematodes (31, 37, 54). These bacteria have since been identified as relatives of the arthropod symbiont Wolbachia (46). Wolbachia bacteria have now been reported to exist in many filarial nematodes, including B. malayi and Brugia pahangi (3,30,49,55). Interestingly, Wolbachia has recently been proposed to play a role in the induction of the host immune response to filariae (9,44,50,51). Some researchers suggest that lipopolysaccharide (LPS)-like molecules from filarial Wolbachia b...

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Section: Discussioncontrasting

confidence: 66%

mentioning

confidence: 99%

Removal of Wolbachia from Brugia pahangi Is Closely Linked to Worm Death and Fecundity but Does Not Result in Altered Lymphatic Lesion Formation in Mongolian Gerbils ( Meriones unguiculatus )

Chirgwin¹,

Coleman²,

Porthouse³

et al. 2003

Infect Immun

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“…In agreement with these data, the immunization of BALB/c mice with recombinant WSP induced the expression of iNOS and gamma interferon (IFN-␥) mRNA and the production of NO and IgG2a (Th1), which are related to macrophage-mediated proinflammatory responses (55,287). Macrophages play a role in the activation and regulation of this innate response and link the innate and adaptive responses (421). Macrophages and neutrophils are present in canine D. immitis infections (216) and in cases of human dirofilariasis, and both cell types have been described to be the most abundant cell types in pulmonary and subcutaneous nodules (328,388).…”

Section: Immunopathogenic Mechanisms In Dirofilariasissupporting

confidence: 62%

“…Macrophages and neutrophils are present in canine D. immitis infections (216) and in cases of human dirofilariasis, and both cell types have been described to be the most abundant cell types in pulmonary and subcutaneous nodules (328,388). Together with neutrophils, the key role of macrophages in the inflammation associated with onchocerciasis and lymphatic filariasis has been demonstrated (61,421). In this respect, some studies indicated that WSP induces the chemotaxis of neutrophils (37) and can inhibit their apoptosis in vitro, which could contribute to the extension of the inflammatory state (36).…”

Section: Immunopathogenic Mechanisms In Dirofilariasismentioning

confidence: 99%

Human and Animal Dirofilariasis: the Emergence of a Zoonotic Mosaic

et al. 2012

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SUMMARY Dirofilariasis represents a zoonotic mosaic, which includes two main filarial species ( Dirofilaria immitis and D. repens ) that have adapted to canine, feline, and human hosts with distinct biological and clinical implications. At the same time, both D. immitis and D. repens are themselves hosts to symbiotic bacteria of the genus Wolbachia , the study of which has resulted in a profound shift in the understanding of filarial biology, the mechanisms of the pathologies that they produce in their hosts, and issues related to dirofilariasis treatment. Moreover, because dirofilariasis is a vector-borne transmitted disease, their distribution and infection rates have undergone significant modifications influenced by global climate change. Despite advances in our knowledge of D. immitis and D. repens and the pathologies that they inflict on different hosts, there are still many unknown aspects of dirofilariasis. This review is focused on human and animal dirofilariasis, including the basic morphology, biology, protein composition, and metabolism of Dirofilaria species; the climate and human behavioral factors that influence distribution dynamics; the disease pathology; the host-parasite relationship; the mechanisms involved in parasite survival; the immune response and pathogenesis; and the clinical management of human and animal infections.

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“…Early work provided some clues as to how this could occur. For example, antibodies in the sera of schistosome-infected hosts fail to bind to the surface of the living parasites and yet bind strongly to dead parasites or parasites extracts, indicating that living parasites are able to modulate their surface structure in a way that prevents recognition (100). Recent studies have begun to provide mechanistic explanations for evasion (6,74).…”

Section: Immune Response Evasionmentioning

confidence: 99%