Virulent Strains (virulent + strain)

Distribution by Scientific Domains


Selected Abstracts


Importance of EGF receptor, HER2/Neu and Erk1/2 kinase signalling for host cell elongation and scattering induced by the Helicobacter pylori CagA protein: antagonistic effects of the vacuolating cytotoxin VacA

CELLULAR MICROBIOLOGY, Issue 3 2009
Nicole Tegtmeyer
Summary Helicobacter pylori is the causative agent of gastric pathologies ranging from chronic gastritis to peptic ulcers and even cancer. Virulent strains carrying both the cag pathogenicity island (cagPAI) and the vacuolating cytotoxin VacA are key players in disease development. The cagPAI encodes a type IV secretion system (T4SS) which forms a pilus for injection of the CagA protein into gastric epithelial cells. Injected CagA undergoes tyrosine phosphorylation and induces actin-cytoskeletal rearrangements involved in host cell scattering and elongation. We show here that the CagA-induced responses can be inhibited in strains expressing highly active VacA. Further investigations revealed that VacA does not interfere with known activities of phosphorylated CagA such as inactivation of Src kinase and cortactin dephosphorylation. Instead, we demonstrate that VacA exhibits inactivating activities on the epidermal growth factor receptor EGFR and HER2/Neu, and subsequently Erk1/2 MAP kinase which are important for cell scattering and elongation. Inactivation of vacA gene, downregulation of the VacA receptor RPTP-,, addition of EGF or expression of constitutive-active MEK1 kinase restored the capability of H. pylori to induce the latter phenotypes. These data demonstrate that VacA can downregulate CagA's effects on epithelial cells, a novel molecular mechanism showing how H. pylori can avoid excessive cellular damage. [source]


Immunological basis of the development of necrotic lesions following Mycobacterium avium infection

IMMUNOLOGY, Issue 4 2002
Manuela Flórido
Summary Normal C57BL/6 mice infected with 106 colony-forming units of a highly virulent strain of Mycobacterium avium developed a progressive infection characterized by loss of T cells from the tissues and infiltration with high numbers of heavily infected macrophages. In contrast, when C57BL/6 mice were infected with 102 colony-forming units of the same strain they retained T cells and T-cell reactivity in the tissues, and granulomas evolved into large masses that, at 4 months of infection, exhibited central necrosis. The development of these necrotic lesions did not occur in nude mice, nor in mice genetically deficient in CD4, interleukin-12 (IL-12) p40, interferon-, (IFN-,) and CD40 and were reduced in mice deficient in CD54 or IL-6. They were less numerous but bigger in mice deficient in IL-10 or the inducible nitric oxide synthase, correlating with the increased resistance to mycobacterial proliferation of these strains as compared to control mice. The appearance of necrosis was not affected in mice deficient in CD8,, T-cell receptor ,, tumour necrosis factor receptor p55, and perforin, nor was it affected in mice over-expressing bcl2. The appearance of necrosis could be prevented by administering antibodies specific for CD4, IL-12p40, or IFN-, from the second month of infection when organized granulomas were already found. Our results show that the immunological mediators involved in the induction of protective immunity are also major players in the immunopathology associated with mycobacteriosis. [source]


Evidence for a perforin-mediated mechanism controlling cardiac inflammation in Trypanosoma cruzi infection

INTERNATIONAL JOURNAL OF EXPERIMENTAL PATHOLOGY, Issue 2 2002
ANDREA HENRIQUES-PONS
Summary. ,CD8+ T lymphocytes are considered an important cell population involved in the control of parasitaemia and mortality after Trypanosoma cruzi infection. However, despite recent developments in this field, the mechanism whereby this control is exerted is still not completely understood. Here we have used perforin knockout (,/,) mice infected with Y strain T. cruzi in order to evaluate specifically the participation of the perforin-based cytotoxic pathway in the destruction of cardiomyocytes, cellular inflammatory infiltration, and control of parasitaemia and mortality. We observed that although parasitaemia was equivalent in perforin (+/+) and (,/,) groups, survival rate and spontaneous physical performance were significantly lower in the perforin deficient mice. The cardiac inflammatory cell infiltration, mostly composed of CD8+ cells, was more evident in perforin (,/,) mice. Ultrastructural and immunofluorescence analysis, as well as plasma creatine kinase activity, revealed cardiomyocyte damage and necrosis, more evident in perforin (,/,) mice. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling (TUNEL) assays performed in heart samples revealed similar and modest levels of apoptosis in both perforin (+/+) and (,/,) mice. These results indicate that perforin does not play a pivotal role in the control of parasitaemia and direct lysis of cardiomyocytes, but seems to be an important molecule involved in the control of cardiac inflammation and pathology induced by a highly virulent strain of T. cruzi. [source]


Soil survival of Escherichia coli O157:H7 acquired by a child from garden soil recently fertilized with cattle manure

JOURNAL OF APPLIED MICROBIOLOGY, Issue 2 2006
A. Mukherjee
Abstract Aims:, This investigation was conducted to determine the survival of a naturally occurring Escherichia coli O157:H7 in garden soil linked to a sporadic case of E. coli O157 infection in Minnesota. Methods and Results:, The presence and viability of E. coli O157:H7 was monitored in manure-contaminated garden soil for several weeks. Bacterial isolates were characterized using PCR and pulsed-field gel electrophoresis (PFGE). Isolates obtained from the patient and the garden plots during this investigation had indistinguishable PFGE patterns and had the same virulence factors (stx1, stx2, eaeA, ehxA). The E. coli O157:H7 levels obtained from the garden plots declined gradually for a period of 2 months, and on day 69 only one garden plot of four had detectable levels of pathogen. All plots were negative on day 92. The rate of decline in the soil samples stored at 4°C was faster compared with soil samples that remained in ambient conditions, and in refrigerated storage E. coli O157:H7 could not be detected after 10 days. Conclusions:,E. coli O157:H7 strains can survive on manure-amended soil for more than 2 months, and this survival could be reduced by low temperature. Significance and Impact of the Study:, This is one of the few reports that have investigated the survival of a proven virulent strain in naturally contaminated soil samples. This case stresses the importance of avoiding the use of raw cattle manure to amend soil for cultivation of foods, including soils in residential garden plots. [source]


Identification of the genes associated with a virulent strain of Porphyromonas gingivalis using the subtractive hybridization technique

MOLECULAR ORAL MICROBIOLOGY, Issue 1 2008
M. Tachibana-Ono
Background/aims:,Porphyromonas gingivalis, a major etiological organism implicated in periodontal disease, can be classified into virulent and avirulent strains. Our aim was to identify a gene for the virulence of P. gingivalis. Methods:, The subtractive hybridization technique was employed to identify the genes specific to P. gingivalis W83, a virulent strain. In this study, P. gingivalis W83 was used as the tester strain, and P. gingivalis ATCC 33277 was the driver strain. The prevalence of W83-specific genes was determined by Southern blot analysis of several P. gingivalis strains. Results:, We obtained 575 colonies using the subtractive hybridization technique. From among these, 26 DNA fragments were subjected to a homology search using the BLAST program. Compared with strain ATCC 33277, strain W83 contained 12 unique clones. The specificities of the isolated DNA fragments were analyzed among four P. gingivalis strains by Southern blot analysis. Five genes showed specificity for strain W83 compared with strain ATCC 33277. All five genes were also identified in strain W50. Conclusions:, The subtractive hybridization technique was effective in screening the two strains for specific DNA sequences, some of which might be responsible for determining virulence. The results suggested that several genes specific to strain W83 were associated with its virulence. Further analysis of these DNA fragments will provide important information on the pathogenesis of virulent P. gingivalis strains. [source]


Potential for recombinant Babesia bovis antigens to protect against a highly virulent isolate

PARASITE IMMUNOLOGY, Issue 12 2005
M. HOPE
SUMMARY Two antigens from Babesia bovis,12D3 and 11C5, were expressed and purified as recombinant proteins in Escherichia coli and used to vaccinate groups of six Babesia -susceptible cattle. These were subsequently challenged with a highly virulent strain of B. bovis. All cattle showed symptoms of disease and most required treatment. Cattle vaccination groups receiving either 12D3 or 11C5 or a combination of both, reduced parasitaemia by approximately fourfold and a number of individual animals appeared to control the parasite infection. Control of parasites correlated with high monocyte numbers late in infection. The results thus confirm the potential usefulness of both antigens but also demonstrate the limitations of current formulations. [source]


Inactivation of Virulent Burkholderia pseudomallei by Sunlight

PHOTOCHEMISTRY & PHOTOBIOLOGY, Issue 4 2009
Jose-Luis Sagripanti
The goal of this study was to determine the sensitivity of virulent Burkholderia pseudomallei to natural sunlight. We describe solar dosimetry calibrated to integrate radiation between 295 and 305 nm and an exposure system that minimizes thermal effects on bacterial cells. Burkholderia pseudomallei cells were either exposed to sunlight in UV transparent dishes or maintained in the dark covered by opaque foil. The cells maintained in the dark remained at constant levels for the duration of all experiments. The exposed cells nearby were killed with a kinetic studied through 5 Log10 inactivation. We found that cells in stationary phase of growth were nearly two-fold more resistant to sunlight than cells in lag or exponential growth. A virulent strain of B. pseudomallei that produced mucoid colonies showed sensitivity to sunlight similar to both a virulent strain that produced nonmucoid colonies and a strain of B. thailandensis. The inactivation of B. pseudomallei by sunlight in different types of water of environmental relevance or inside amoebae was investigated. The sensitivity of virulent B. pseudomallei was calculated and its comparison with previous studies employing monochromatic germicidal light (254 nm) is discussed. This may be the first report in the open literature of the inactivation of a virulent biological threat agent by natural sunlight. These data should assist in estimating the risk for contracting melioidosis and in predicting the time period during which B. pseudomallei remains infectious after an accidental or intentional release in the environment. [source]


Arabidopsis WRKY33 transcription factor is required for resistance to necrotrophic fungal pathogens

THE PLANT JOURNAL, Issue 4 2006
Zuyu Zheng
Summary Plant WRKY transcription factors are key regulatory components of plant responses to microbial infection. In addition to regulating the expression of defense-related genes, WRKY transcription factors have also been shown to regulate cross-talk between jasmonate- and salicylate-regulated disease response pathways. The two pathways mediate resistance against different types of microbial pathogens, and there are numerous reports of antagonistic interactions between them. Here we show that mutations of the Arabidopsis WRKY33 gene encoding a WRKY transcription factor cause enhanced susceptibility to the necrotrophic fungal pathogens Botrytis cinerea and Alternaria brassicicola concomitant with reduced expression of the jasmonate-regulated plant defensin PDF1.2 gene. Ectopic over-expression of WRKY33, on the other hand, increases resistance to the two necrotrophic fungal pathogens. The wrky33 mutants do not show altered responses to a virulent strain of the bacterial pathogen Pseudomonas syringae, although the ectopic expression of WRKY33 results in enhanced susceptibility to this pathogen. The susceptibility of WRKY33 -over-expressing plants to P. syringae is associated with reduced expression of the salicylate-regulated PR-1 gene. The WRKY33 transcript is induced in response to pathogen infection, or treatment with salicylate or the paraquat herbicide that generates activated oxygen species in exposed cells. WRKY33 is localized to the nucleus of plant cells and recognizes DNA molecules containing the TTGACC W-box sequence. Together, these results indicate that pathogen-induced WRKY33 is an important transcription factor that regulates the antagonistic relationship between defense pathways mediating responses to P. syringae and necrotrophic pathogens. [source]


VIRULENCE AND COMPETITIVENESS: TESTING THE RELATIONSHIP DURING INTER- AND INTRASPECIFIC MIXED INFECTIONS

EVOLUTION, Issue 9 2010
Peter A. Staves
Understanding the reasons why different parasites cause different degrees of harm to their hosts is an important objective in evolutionary biology. One group of models predicts that if hosts are infected with more than one strain or species of parasite, then competition between the parasites will select for higher virulence. While this idea makes intuitive sense, empirical data to support it are rare and equivocal. We investigated the relationship between fitness and virulence during both inter- and intraspecific competition for a fungal parasite of insects, Metarhizium anisopliae. Contrary to theoretical expectations, competition favored parasite strains with either a lower or a higher virulence depending on the competitor: when in interspecific competition with an entomopathogenic nematode, Steinernema feltiae, less virulent strains of the fungus were more successful, but when competing against conspecific fungi, more virulent strains were better competitors. We suggest that the nature of competition (direct via toxin production when competing against the nematode, indirect via exploitation of the host when competing against conspecific fungal strains) determines the relationship between virulence and competitive ability. [source]


VACCINATION, WITHIN-HOST DYNAMICS, AND VIRULENCE EVOLUTION

EVOLUTION, Issue 1 2006
Jean-Baptiste André
Abstract We explore the potential consequences of vaccination on parasite epidemiology and evolution. Our model combines a microscopic (within-host dynamics) and a macroscopic (epidemiological dynamics) description of the interaction between the parasite and its host. This approach allows relevant epidemiological traits such as parasite transmission, parasite virulence, and host recovery to emerge from a mechanistic model of acute infection describing the interaction between the parasite and the host immune system. We model the effect of a vaccine as an activator of immunity enhancing the replication rate of lymphocytes, their initial density at infection's initiation, their efficacy to kill the parasite, or their activation delay after infection. We analyze the evolution of the replication rate of parasites and show that vaccination may promote the evolution of faster replicating and, consequently, more virulent strains. We also show that intermediate vaccination coverage may lead to the coexistence of two different parasite strategies (a low-virulence strain adapted to naive hosts, and a high-virulence strain, more generalist, adapted to both naive and vaccinated hosts). We discuss the consequences of various vaccination strategies under different epidemiological situations using several distinct measures to evaluate the cost induced by the parasite on individuals and entire host populations. [source]


Vascular endothelium: the battlefield of dengue viruses

FEMS IMMUNOLOGY & MEDICAL MICROBIOLOGY, Issue 3 2008
Atanu Basu
Abstract Increased vascular permeability without morphological damage to the capillary endothelium is the cardinal feature of dengue haemorrhagic fever (DHF)/dengue shock syndrome (DSS). Extensive plasma leakage in various tissue spaces and serous cavities of the body, including the pleural, pericardial and peritoneal cavities in patients with DHF, may result in profound shock. Among various mechanisms that have been considered include immune complex disease, T-cell-mediated, antibodies cross-reacting with vascular endothelium, enhancing antibodies, complement and its products, various soluble mediators including cytokines, selection of virulent strains and virus virulence, but the most favoured are enhancing antibodies and memory T cells in a secondary infection resulting in cytokine tsunami. Whatever the mechanism, it ultimately targets vascular endothelium (making it a battlefield) leading to severe dengue disease. Extensive recent work has been done in vitro on endothelial cell monolayer models to understand the pathophysiology of vascular endothelium during dengue virus (DV) infection that may be translated to help understand the pathogenesis of DHF/DSS. The present review provides a broad overview of the effects of DV infection and the associated host responses contributing towards alterations in vascular endothelial cell physiology and damage that may be responsible for the DHF/DSS. [source]


In vitro markers for virulence in Yersinia ruckeri

JOURNAL OF FISH DISEASES, Issue 3 2010
E Tobback
Abstract In this study, different traits that have been associated with bacterial virulence were studied in Yersinia ruckeri. Two isolates that had been shown to cause disease and mortality in experimentally infected rainbow trout were compared with five avirulent isolates. Both virulent isolates showed high adhesion to gill and intestinal mucus of rainbow trout, whereas the majority of non-virulent strains demonstrated significantly lower adhesion. A decrease in adherence capability following bacterial treatment with sodium metaperiodate and proteolytic enzymes suggested the involvement of carbohydrates and proteins. All strains were able to adhere to and invade chinook salmon embryo cell line (CHSE-214), fathead minnow epithelial cell line (FHM) and rainbow trout liver cell line (R1). One non-virulent strain was highly adhesive and invasive in the three cell lines, whereas the virulent strains showed moderate adhesive and invasive capacity. The internalization of several isolates was inhibited by colchicine and cytochalasin-D, suggesting that microtubules and microfilaments play a role. For all strains, intracellular survival assays showed a decrease of viable bacteria in the cells 6 h after inoculation, suggesting that Y. ruckeri is not able to multiply or survive inside cultured cells. Analysis of the susceptibility to the bactericidal effect of rainbow trout serum demonstrated that virulent Y. ruckeri strains were serum resistant, whereas non-virulent strains were generally serum sensitive. [source]


Investigation of seven Vibrio virulence genes among Vibrio alginolyticus and Vibrio parahaemolyticus strains from the coastal mariculture systems in Guangdong, China

LETTERS IN APPLIED MICROBIOLOGY, Issue 2 2005
Z.-Y. Xie
Abstract Aims:, To investigate the distribution of the virulence of two Vibrio species among different strains obtained from the mariculture systems on the coast of Guangdong in China and the correlation between the virulence strains and the virulence genes among Vibrio alginolyticus. Methods:, Besides three strains, 72 V. alginolyticus strains and seven Vibrio parahaemolyticus strains were examined by PCR or semi-nested PCR for the virulence genes (tlh, trh, tdh, toxR, toxRS, ctxA, VPI). Additionally, the virulence of 18 V. alginolyticus strains was tested. Significance and Impact of the Study:, Virulence genes homologous to those in the V. parahaemolyticus and Vibrio cholerae are widely distributed among V. alginolyticus and V. parahaemolyticus in the coastal mariculture systems in Guangdong, China. Some of the V. alginolyticus strains are pathogenic to aquatic animals, and might have derived their virulence genes from V. parahaemolyticus or V. cholerae, representing a possible reservoir of these genes. However, there is no correlation between presence and absence of the virulence genes used to investigate V. alginolyticus and its virulent strains. In this report, we also show that tlh is distributed among V. alginolyticus. [source]


Overexpression of CRK13, an Arabidopsis cysteine-rich receptor-like kinase, results in enhanced resistance to Pseudomonas syringae

THE PLANT JOURNAL, Issue 3 2007
Biswa R. Acharya
Summary Protein kinases play important roles in relaying information from perception of a signal to the effector genes in all organisms. Cysteine-rich receptor-like kinases (CRKs) constitute a sub-family of plant receptor-like kinases (RLKs) with more than 40 members that contain the novel C-X8-C-X2-C motif (DUF26) in the extracellular domains. Here we report molecular characterization of one member of this gene family, CRK13. Expression of this gene is induced more quickly and strongly in response to the avirulent compared with the virulent strains of Pseudomonas syringae, and peaks within 4 h after pathogen infection. In response to dexamethasone (DEX) treatment, plants expressing the CRK13 gene from a DEX-inducible promoter exhibited all tested features of pathogen defense activation, including rapid tissue collapse, accumulation of high levels of several defense-related gene transcripts including PR1, PR5 and ICS1, and accumulation of salicylic acid (SA). In addition, these plants suppressed growth of virulent pathogens by about 20-fold compared with the wild-type Col-0. CRK13 -conferred pathogen resistance is salicylic acid-dependent. Gene expression analysis using custom cDNA microarrays revealed a remarkable overlap between the expression profiles of the plants overexpressing CRK13 and the plants treated with Pst DC3000 (avrRpm1). Our studies suggest that upregulation of CRK13 leads to hypersensitive response-associated cell death, and induces defense against pathogens by causing increased accumulation of salicylic acid. [source]


The Arabidopsis thaliana TIR-NB-LRR R-protein, RPP1A; protein localization and constitutive activation of defence by truncated alleles in tobacco and Arabidopsis

THE PLANT JOURNAL, Issue 6 2006
L. Michael Weaver
Summary Specific recognition of Hyaloperonospora parasitica isolate Cala2 by Arabidopsis thaliana Ws-0 is mediated by the resistance gene RPP1A. Transient expression of different truncations of RPP1A in tobacco leaves revealed that its TIR-NB-ARC portion is sufficient to induce an elicitor-independent cell death. In stable transgenic lines of Arabidopsis, overexpression of the RPP1A TIR-NB-ARC domains (E12) using the 35S promoter leads to broad-spectrum resistance to virulent strains of H. parasitica and Pseudomonas syringae DC3000. The TIR-NB-ARC-mediated constitutive immunity is due to activation of the salicylic acid-dependent resistance pathway and is relieved by either a mutation in EDS1 or the presence of the salicylate hydroxylase gene, NahG. Growth of 35S::E12 plants is reduced, a phenotype observed in many constitutively resistant mutants. RPP1A carries a hydrophobic peptide at its N-terminus that directs the RPP1A protein into membranes, though it may not be the sole determinant mediating membrane association of RPP1A. Two-phase partitioning and sucrose density gradient sedimentation established that RPP1A resides in the endoplasmic reticulum and/or Golgi apparatus. [source]


The BOS loci of Arabidopsis are required for resistance to Botrytis cinerea infection

THE PLANT JOURNAL, Issue 4 2004
Paola Veronese
Summary Three Botrytis -susceptible mutants bos2, bos3, and bos4 which define independent and novel genetic loci required for Arabidopsis resistance to Botrytis cinerea were isolated. The bos2 mutant is susceptible to B. cinerea but retains wild-type levels of resistance to other pathogens tested, indicative of a defect in a response pathway more specific to B. cinerea. The bos3 and bos4 mutants also show increased susceptibility to Alternaria brassicicola, another necrotrophic pathogen, suggesting a broader role for these loci in resistance. bos4 shows the broadest range of effects on resistance, being more susceptible to avirulent strain of Pseudomonas syringae pv. tomato. Interestingly, bos3 is more resistant than wild-type plants to virulent strains of the biotrophic pathogen Peronospora parasitica and the bacterial pathogen P. syringae pv. tomato. The Pathogenesis Related gene 1 (PR-1), a molecular marker of the salicylic acid (SA)-dependent resistance pathway, shows a wild-type pattern of expression in bos2, while in bos3 this gene was expressed at elevated levels, both constitutively and in response to pathogen challenge. In bos4 plants, PR-1 expression was reduced compared with wild type in response to B. cinerea and SA. In bos3, the mutant most susceptible to B. cinerea and with the highest expression of PR-1, removal of SA resulted in reduced PR-1 expression but no change to the B. cinerea response. Expression of the plant defensin gene PDF1-2 was generally lower in bos mutants compared with wild-type plants, with a particularly strong reduction in bos3. Production of the phytoalexin camalexin is another well-characterized plant defense response. The bos2 and bos4 mutants accumulate reduced levels of camalexin whereas bos3 accumulates significantly higher levels of camalexin than wild-type plants in response to B. cinerea. The BOS2, BOS3, and BOS4 loci may affect camalexin levels and responsiveness to ethylene and jasmonate. The three new mutants appear to mediate disease responses through mechanisms independent of the previously described BOS1 gene. Based on the differences in the phenotypes of the bos mutants, it appears that they affect different points in defense response pathways. [source]


A novel multiplex PCR method for detecting virulent strains of Vibrio alginolyticus

AQUACULTURE RESEARCH, Issue 1 2009
Shuang-Hu Cai
Abstract The bacterial strains obtained from various origins were tested with the novel primers targeting the collagenase gene, ompK gene and toxR gene to establish a multiplex polymerase chain reaction (PCR) method. These primers successfully recognized all virulent strains of Vibrio alginolyticus, but the avirulent strains were not recognized by the multiplex PCR because of lack of the collagenase and toxR genes. In a 50 ,L multiplex PCR mixture, the lowest detection limit is 8.8 × 102 cells of virulent strains of V. alginolyticus. The multiplex PCR method was successfully developed to identify virulent strains of V. alginolyticus, and provides a rapid, sensitive, specific and reliable technology for diagnosing virulent strains of V. alginolyticus. Therefore, the novel multiplex PCR in the present paper can be useful for any laboratory working with vibriosis detection of aquatic animals. [source]


Growth of Brucella abortus in macrophages from resistant and susceptible mouse strains

CLINICAL & EXPERIMENTAL IMMUNOLOGY, Issue 2 2000
J. Sathiyaseelan
C57Bl/10 mice have a superior ability to control chronic infections with virulent strains of the intracellular bacteria Brucella abortus compared with BALB/c mice. While a number of differences in the cytokines produced by lymphocytes following infection of these two strains of mice have been shown, macrophages have not been evaluated for their role in conveying relative resistance. The importance of macrophages in control of brucella infections is demonstrated by the observations that intracellular survival of various strains of B. abortus directly correlates with their virulence in vivo, and the ability of macrophages to control brucellae in vitro has been shown to correlate with a brucella-resistant phenotype in ruminants. While both BALB/c and C57Bl are Nramp -susceptible mouse strains, additional differences in macrophage function outside of the Nramp1 gene effects could influence susceptibility to brucellosis. The studies conducted here comparing the ability of macrophages from C57Bl/10 and BALB/c mice indicate that the macrophages from resistant mice did not control intracellular growth of B. abortus strain 2308 more efficiently than those from the susceptible mice, either in the absence of, or following, interferon-gamma activation or iron supplementation. A number of different conditions for culturing macrophages were evaluated to rule out the influence of antibiotics on the conclusions drawn from the results. [source]