Activation of the alternative complement pathway by Naegleria fowleri

Holbrook, Thomas W.; Boackle, Robert J.; Parker, Brenda W.; Vesely, Jana

doi:10.1128/iai.30.1.58-61.1980

Cited by 36 publications

(16 citation statements)

References 9 publications

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“…The complement system, which constitutes a first line of defense against invading organisms, is activated by Naegleria trophozoites (Holbrook et al, 1980;Rowan-Kelly et al, 1980;Whiteman & Marciano-Cabral, 1987). Studies as early as 1978, using the mouse model of PAM, showed that the most susceptible mouse strain (A/HeCr) for N. fowleri infection was complement (C5) deficient (Haggerty & John, 1978).…”

Section: Complementmentioning

confidence: 99%

The immune response toNaegleria fowleriamebae and pathogenesis of infection

Marciano‐Cabral

Cabral

2007

FEMS Immunology &Amp; Medical Microbiology

150

155

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The deletion of CD4- and CD8-double-positive (DP) cells in the thymus after treatment with anti-CD3 antibodies has long been considered as a useful model for clonal deletion during T cell development, although it was reported that DP cell death was not observed in neonates where self-tolerance should be developing. We dealt with the cellular basis of this enigmatic phenomenon in this report. Due to the similar susceptibility to the antibody-treatment in vitro between neonatal and adult thymocytes, critical factors may be outside rather than within the thymus. Indeed, newborn thymus lobes transplanted into recipients of different ages showed an increased susceptibility to the thymo-toxicity as the age of the recipient increased. The thymo-toxicity seems to be based on the adrenal function of glucocorticoid (GC) synthesis, because administration of an inhibitor of GC synthesis significantly reduced the DP cell death by the antibody-treatment. Finally, adrenalectomy completely prevented DP cell death by anti-CD3 antibodies in adult mice. Therefore, the thymocyte death by anti-CD3 antibodies in vivo may not be due to the T cellreceptor mediated selection in the thymus.

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Section: Complementmentioning

confidence: 99%

The immune response toNaegleria fowleriamebae and pathogenesis of infection

Marciano‐Cabral

Cabral

2007

FEMS Immunology &Amp; Medical Microbiology

150

155

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“…During the course of amoeba host tissue invasion and multiplication in various body sites such as the olfactory mucosa and the brain, there is evidence of extensive tissue destruction. The mediators of tissue injury are believed to be of both amoebic and host origin (3, 6,8,9,12,13,16,17,21). For example, amoebae are purported to cause tissue damage by releasing cytopathogenic substances, oxygen radicals, and a number of different enzymes.…”

mentioning

confidence: 99%

Elastase in the pathogenic free-living amoebae Naegleria and Acanthamoeba spp

Fèrrante

Bates

1988

Infect Immun

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“…Neutrophils from mice immunized with N. fowleri, for example, are able to kill amoebae (10), and a macrophage inhibitory factor has been detected in response to infection with Naegleria species (8). Moreover, it is well established that N. fowleri amoebae are readily lysed by human complement (4), and complement has been implicated as an important factor in host resistance of humans (14) and mice (11,27).…”

mentioning

confidence: 99%

Host resistance of mice to Naegleria fowleri infections

Reilly¹,

White²,

Bradley³

1983

Infect Immun

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Naegleria fowleri is an etiological agent of primary amoebic meningoencephalitis in humans and laboratory animals. The determinative factors in host resistance of mice to N. fowleri infections have not been fully characterized. Male or female B6C3F1 mice stimulated by intraperitoneal administration of 10(6) amoebae of N. fowleri nN68 per mouse produced agglutinating activity and markedly elevated levels of serum and immunoglobulins M and G. Despite a marked humoral response, protective immunity was increased only marginally by active immunization. Host resistance was not impaired by prior treatment with 350 rads of 60Co radiation or 200 mg of cyclophosphamide per kg or by concurrent daily treatment with 30 mg of cyclophosphamide per kg for 14 days. Moreover, host resistance was not impaired by daily treatment with 4 mg of diethylstilbestrol per kg for 14 days, with challenge on day 2 of drug exposure or 24 h after the last drug treatment. Mice depleted of hemolytic complement by cobra venom factor were more susceptible to N. fowleri infection than were untreated mice.

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Activation of the alternative complement pathway by Naegleria fowleri

Cited by 36 publications

References 9 publications

The immune response toNaegleria fowleriamebae and pathogenesis of infection

The immune response toNaegleria fowleriamebae and pathogenesis of infection

Elastase in the pathogenic free-living amoebae Naegleria and Acanthamoeba spp

Host resistance of mice to Naegleria fowleri infections

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