Differential nitric oxide (NO) production by macrophages from mice and guinea pigs infected with virulent and avirulent <i>Legionella pneumophila</i> serogroup 1

Rajagopalan-Levasseur, Premavathy; Lecointe, Didier; Bertrand, Guylène; Fay, Michèle; Gougerot‐Pocidalo, Marie‐Anne

doi:10.1046/j.1365-2249.1996.d01-644.x

Cited by 12 publications

(11 citation statements)

References 31 publications

(50 reference statements)

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“…A critical role of NO in the bactericidal activity against Legionella pneumophila has been shown by using IFN-Q-treated murine macrophages [111 3], whereas the absence of NO production limited IFN-Qtreated human HL-60 monocytes to bacteriostasis [11]. By using a mouse model, an inverse relationship between endogenous NO production and virulence of a given L. pneumophila strain could be established [14]. In contrast, the e¡ective clearance of avirulent bacteria from the lungs of guinea pigs was mainly due to NO-independent mechanisms, since no NO activity could be detected either ex vivo or in vitro [14].…”

Section: Introductionmentioning

confidence: 99%

Induction of iNOS in human monocytes infected with different Legionella species

Neumeister

2001

FEMS Microbiology Letters

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The contribution of nitric oxide (NO) radicals to the suppression of intracellular replication of Legionella has been well established in rodents but remained questionable in humans. Considering the fact that human monocytes do not exhibit a high-output NO production, we used sensitive methods such as detection of inducible NO synthase (iNOS) mRNA by reverse transcription-PCR and demonstration of iNOS protein expression by means of flow cytometry and Western blot to compare the levels of iNOS induced by Legionella species which, in accordance to their human prevalence, show different multiplication rates within human monocytic cells. The expression of iNOS in Mono Mac 6 (MM6) cells showed an only moderate inverse correlation to the intracellular replication rate of a given Legionella species in the protein expression assays. However, stimulation of host cells with 1,25-dihydroxyvitamin D 3 to enhance NO production and inhibition of NO production by treatment of host cells with N G -methyl-L-arginine were not able to modify the intracellular multiplication of legionellae within MM6 cells. Therefore, NO production does not seem to play a crucial role for the restriction of intracellular replication of Legionella bacteria within human monocytic cells. Rodent models in investigations which are supposed to clarify the involvement of NO radicals in defense mechanisms against Legionella infections in humans are of doubtful significance. ß : S 0 3 7 8 -1 0 9 7 ( 0 1 ) 0 0 2 9 0 -7

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Section: Introductionmentioning

confidence: 99%

Induction of iNOS in human monocytes infected with different Legionella species

Neumeister

2001

FEMS Microbiology Letters

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“…When transiently produced at low levels, it serves as a critical signaling molecule (4). When produced at high levels for an extended period, nitric oxide and/or resulting reactive nitrogen intermediates are cytotoxic and can inhibit the replication of a variety of intracellular parasites in animal models of infection, including the aerosol-borne bacterial pathogens Mycobacterium tuberculosis (7) and Legionella pneumophila (31). Accumulating evidence also suggests that nitric oxide controls human infection by intracellular parasites, with the most compelling evidence coming from studies of infection by mycobacteria (24,30).…”

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Nitric Oxide InhibitsCoxiella burnetiiReplication and Parasitophorous Vacuole Maturation

et al. 2002

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Coxiella burnetii is a bacterial obligate intracellular pathogen and the etiological agent of the zoonosis Q fever. The reservoir host range of C. burnetii is extensive and includes livestock, pets, and wildlife. Infected mammals rarely show signs of disease even when shedding large numbers of organisms (25). The primary route of human infection is via inhalation of contaminated aerosols generated by domestic livestock operations.

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“…Data suggest that guinea pigs and mice may use different inflammatory effector molecules in host defense against intracellular pathogens (26) and different isolates of Chlamydia may exhibit differential sensitivity to inflammatory mediators (25). We have examined TNF production in female guinea pigs infected with the Chlamydia psittaci agent of guinea pig inclusion conjunctivitis (GPIC) and reported high levels of TNF-␣ in genital tract secretions during the first week of primary infection (11).…”

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Does Inhibition of Tumor Necrosis Factor Alpha Affect Chlamydial Genital Tract Infection in Mice and Guinea Pigs?

2000

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The role of tumor necrosis factor alpha (TNF-␣) in host defense against chlamydial infection remains unclear. In order to further evaluate the relevance of TNF-␣ to host resistance in chlamydial genital tract infection, we examined the effect of local inhibition of the TNF-␣ response in normal C57 mice and in interferon gamma gene-deficient C57 mice infected intravaginally with the mouse pneumonitis agent of Chlamydia trachomatis. Since the guinea pig model of female genital tract infection more closely approximates the human in terms of ascending infection and development of pathology, we also examined the effect of local inhibition of the TNF-␣ response in guinea pigs infected intravaginally with the guinea pig strain of Chlamydia psittaci. We successfully blocked the early TNF-␣ response in the respective animal models. This blockade had no effect on the numbers of organisms isolated from the genital tract during the time of TNF-␣ inhibition in mice or guinea pigs. Analysis of interleukin-1␤, macrophage inflammatory protein-2, and granulocyte macrophage-colony stimulating factor in the mouse model revealed that blockade of the TNF-␣ response did not alter the release of these proinflammatory proteins. Yet, in TNF-␣-depleted mice, increased numbers of neutrophils were detected in the genital tract, and, in TNF-␣-depleted guinea pigs, increased numbers of neutrophils as well as infiltrating lymphocytes were seen in the endocervix. Blockade of TNF-␣ does not affect the level of infection in mice or guinea pigs, but it may decrease TNF-␣-induced apoptosis of infiltrating inflammatory cells.

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Differential nitric oxide (NO) production by macrophages from mice and guinea pigs infected with virulent and avirulent Legionella pneumophila serogroup 1

Cited by 12 publications

References 31 publications

Induction of iNOS in human monocytes infected with different Legionella species

Induction of iNOS in human monocytes infected with different Legionella species

Nitric Oxide InhibitsCoxiella burnetiiReplication and Parasitophorous Vacuole Maturation

Does Inhibition of Tumor Necrosis Factor Alpha Affect Chlamydial Genital Tract Infection in Mice and Guinea Pigs?

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