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PubMed1988

Alteration of non-specific resistance to infection with Listeria monocytogenes.

The experimental infection of murine hosts with Listeria monocytogenes is often used as a model for cell-mediated immunity. However, the natural immunity or non-specific resistance to listeriosis can be influenced by the parasite itself and also by a wide array of endogenous and exogenous host factors. The most important host factor in inbred mouse strains is their genetically determined susceptibility or resistance to Listeria monocytogenes. Secondly, the age of the mice is crucial for the outcome of infection. Resistance is only slowly developed by newborn mice, while aged mice possess an increased non-specific resistance as compared to young adult animals. Resistance is further influenced by the nutritional status, by pregnancy or by a simultaneous second antigenic stimulation. Regarding exogenous factors, macrophage blocking agents can totally abolish the resistance to listeriosis, while a lot of immunomodulating agents, such as BCG, killed Bordetella pertussis or Propionibacterium acnes organisms, lipopolysaccharides, suramin etc., can either increase or decrease the resistance. The mononuclear phagocyte system seems to be the main target of all these immunomodifiers. The timing between listeria infection and application of the immunomodulator determines the effect on non-specific resistance. A simultaneous injection of parasite and immunomodulator results in a decrease of resistance, while the application of immunoadjuvants several days before infection can dramatically increase the resistance to listeriosis. The delicate equilibrium of the mononuclear phagocyte system must therefore be taken into account, when infection with Listeria monocytogenes is used to test for immune-modifying agents, which are intended for use in humans or animals.

Adjuvants, Immunologic↗

PubMed2006

Differential expansion, activation and effector functions of conventional and plasmacytoid dendritic cells in mouse tissues transiently infected with Listeria monocytogenes.

Dendritic cells (DC) are crucial in generating immunity to infection. Here we characterize changes in DC in terms of number, activation and effector functions, focusing on conventional DC (cDC) and plasmacytoid DC (pDC), in Listeria-infected mice. Kinetic studies showed a subset- and tissue-specific expansion of cDC and upregulation of CD80 and CD86 on splenic and mesenteric lymph node (MLN) cDC after intragastric infection. Expansion of pDC was more prolonged than cDC, and pDC upregulated CD86 and MHC-II, but not CD80, in both the spleen and MLN. cDC were an important source of IL-12 but not TNF-alpha during infection, while pDC made neither of these cytokines. Instead other CD11c(int) cells produced these cytokines. Using five-colour flow cytometry and double intracellular cytokine staining, we detected phenotypically similar CD11c(int)CD11b(+)Gr1(+) cells with distinct capacities to produce TNF-alpha/IL-12 or TNF-alpha/iNOS (inducible nitric oxide synthase) in Listeria-infected tissues. IL-12p70 was also produced by sorted CD11c(hi) and CD11c(int)CD11b(+)Gr1(+) cells. Furthermore, production of TNF-alpha, iNOS and IL-12 was differentially dependent on cellular localization of the bacteria. Cytosol-restricted bacteria induced TNF-alpha and iNOS-producing cells, albeit at lower frequency than wild-type bacteria. In contrast, IL-12 was induced only with wild-type bacteria. These data provide new insight into the relative abundance and function of distinct CD11c-expressing populations during the early stage of Listeria infection.

Animals↗

PubMed1989

Administration of purified anti-L3T4 monoclonal antibody impairs the resistance of mice to Listeria monocytogenes infection.

Anti-L3T4 monoclonal antibody (GK1.5) treatment significantly impaired the antilisteria resistance of mice as manifested by increased recovery of listeriae from the spleens and livers of anti-L3T4-treated mice and by greater severity of damage to the liver and other organs. Anti-L3T4-treated mice demonstrated a profound decrease in their T cell-mediated responses to Listeria monocytogenes and its products; they failed to develop delayed type hypersensitivity to soluble listeria antigens in vivo, and their spleen cells proliferated poorly in response to stimulation by either mitogens or listeria antigens in vitro. Spleen cells from control listeria-infected mice produced significant amounts of gamma interferon when stimulated with listeria antigens in vitro, whereas under the same conditions spleen cells from anti-L3T4-treated listeria-infected mice failed to produce detectable gamma interferon. Anti-L3T4 treatment resulted in a slight increase in serum colony-stimulating activity as compared with control listeria-infected mice, probably as a result of the increased bacterial burden in these animals. Despite the dramatic decrease in T-cell activities, anti-L3T4-treated mice succeeded in clearing L. monocytogenes from the spleen and liver in a manner that was only slightly delayed as compared with control listeria-infected mice. In addition, anti-L3T4-treated listeria-immunized mice exhibited a moderate degree of enhanced resistance to rechallenge with L. monocytogenes, and their spleen cells were able to transfer a limited degree of antilisteria resistance to naive recipient mice. Both of these responses, however, were diminished as compared with those of control listeria-immunized mice in the same experiments. Although these observations establish a critical role for L3T4+ cells in the development of maximal resistance to listeriosis, they also suggest that compensatory mechanisms may allow mice to develop considerable antilisteria resistance even when L3T4+ cell activities are substantially reduced.

Animals↗

PubMed1991

Factors involved in the depression of hepatic mixed function oxidase during infections with Listeria monocytogenes.

A number of infections are capable of depressing the capacity of the liver to metabolize drugs. We have studied a number of factors which could be involved in the depression of cytochrome P-450 and related drug biotransformation enzymes during infections with Listeria monocytogenes. During the course of the infection, drug metabolism and heme content of hepatic microsomes were depressed but heme oxygenase was elevated. A free radical scavenger alpha-tocopherol did not prevent the loss and xanthine oxidase activities did not correlate with the time course of the loss. Infections in susceptible (balb/c) mice produced a larger loss in drug metabolism than in resistant (C57BL/6) mice, and an avirulent strain of the bacteria was without effect. A preparation of hemolysin isolated from Listeria monocytogenes produced a dose-dependent loss of cytochrome P-450 in isolated hepatocytes. These experiments indicate that the loss of drug metabolism during Listeria infections is most likely due to hemolysin released by the bacteria.

Animals↗

PubMed1988

Effects of Staphylococcus epidermidis on cellular immunity to infection with Listeria monocytogenes.

With the present study, the effects of intravenous applications of Staphylococcus epidermidis (SE) on the course of experimental infections of mice with Listeria monocytogenes were evaluated. SE treatment 24 h prior to Listeria infection led to a reduced growth of Listeria organisms in both livers and spleens and to an increased resistance of infected animals against a lethal Listeria challenge. SE treatment 24 h after Listeria infection resulted in an enhanced growth of and retarded elimination of Listeria organisms from animal organs as well as in a reduction of delayed-type hypersensitivity to soluble Listeria antigen. Adoptive immunotherapy accomplished by transferring immune peritoneal exudate T-lymphocyte-enriched cells (PETLEs) to Listeria-infected recipients 24 h before SE treatment did not prevent the delay in clearance of Listeria organisms. When Listeria-infected recipients compromised in their immune response by SE treatment were infused with immune PETLEs either immediately or 24 h after the application of SE, the immunosuppression induced by SE proved to be reversible. It is concluded that, in analogy to other bacterial immunomodulators, Staphylococcus epidermidis is able to either nonspecifically activate macrophages or interfere with T-lymphocyte functions.

Animals↗

PubMed1994

Specific cellular and humoral reactions as markers of Listeria monocytogenes infections.

The purpose of the study was to test in experimental mouse model if some immunological parameters could be helpful in recognizing Listeria infections. Delayed type hypersensitivity (DTH) and ELISA tests carried out with soluble fractions of L. innocua (serotype 6a) or L. monocytogenes (serotype 4b) seem to be useful in detecting listeriosis at an early stage. Although crude antigen fractions were used in this study, very weak only nonspecific DTH reactions were observed in unifected animals and they could be easily distinguished from the DTH reactions developed by the animals infected with Listeria. However, genetic factors influenced specific anti-listerial reactivity and it was especially observed when DTH test was used as an indicator of Listeria infection. In contrast to DTH and ELISA tests, determination of antibodies active in agglutination or passive haemagglutination assay seem useless in detecting listeriosis at an early stage of infection.

Agglutination Tests↗

PubMed2004

Delayed presentation of prosthetic joint infection due to Listeria monocytogenes.

Infection with Listeria monocytogenes is rare and has been described in prosthetic valves, stent grafts and prosthetic joints. The route of infection appears to be haematogenous. The choice between conservative treatment with antibiotics or surgical treatment with debridement and revision of the components remains controversial. The best antibiotic treatment is not known with ampicillin being the first choice in most cases. Prosthetic infections with Listeria monocytogenes usually occur in patients with malignancy, diabetes mellitus, chronic renal disease, liver disease, elderly patients and patients receiving immunosuppressive therapy. The hip is the commonest prosthetic joint affected followed by the knee. We report the seventh case of Listeria monocytogenes infection in a non-immunocompromised patient involving a prosthetic joint.

Aged↗

PubMed2001

Administration of superantigens protects mice from lethal Listeria monocytogenes infection by enhancing cytotoxic T cells.

Superantigens stimulate T-cell-receptor Vbeta-selective T-cell proliferation accompanying the release of cytokines, which may eventually protect the host from microbial infections. We investigated here whether superantigens can rescue the host from lethal bacterial infection. Mice were pretreated with Staphylococcus aureus enterotoxin B (SEB) 1 and 2 days before bacterial infection, and the mortality of infected mice was assessed. SEB pretreatment protected mice from lethal infection with Listeria monocytogenes but not from lethal infection with Streptococcus pyogenes. This enhanced protection was also observed upon pretreatment with recombinant streptococcal pyrogenic exotoxin A. Furthermore, L. monocytogenes-specific delayed-type hypersensitivity (DTH) due to type 1 helper T (Th1) cells and the cytotoxicity of CD8(+) T cells were significantly enhanced after SEB administration and bacterial infection. Depletion of either CD4(+) T cells or CD8(+) T cells in SEB-pretreated mice completely abolished this protection. This phenomenon was ascribed to the elimination of L. monocytogenes-specific CD8(+) cytotoxic T lymphocytes (CTL). It was found that CD4(+) T cells contributed to the induction of the CTL populations. Furthermore, SEB pretreatment of heat-killed L. monocytogenes-immunized mice enhanced the protection from challenge of L. monocytogenes. Taken together, these results indicated that administrations of superantigens protected mice from infection with L. monocytogenes, which was dependent on the enhanced L. monocytogenes-specific CTL activity in the presence of CD4(+) T cells, and superantigens exhibited adjuvant activity in the immunization against intracellular pathogens.

Animals↗

PubMed1987

Role of local immunosuppression in murine fetoplacental listeriosis.

Recent evidence suggests that local immunoregulation may prevent rejection of the placenta by the mother. This local immunoregulation may also compromise the response to placental infection. Listeria monocytogenes infection in 121 pregnant mice and 1,050 fetoplacental units was examined and the kinetics of bacterial growth in various maternal and fetal tissues were determined. A subset of pregnant mice developed overwhelming placental listeria infections. Pregnancy did not impair the maternal immune response in the liver and spleen. Pregnant mice without placental infection had numbers of listeria equivalent to nonpregnant controls and mice immunized during pregnancy had significantly less listeria than nonimmunized controls. The secondary response in immunized pregnant mice had no effect on the development of placental infection and the histologic features of placental infection were distinct from those in other organs. Our data suggest that an ineffective local immune response may contribute to the pathogenicity of listeria for the placenta.

Animals↗

PubMed1994

Treatment with anti-interleukin-10 monoclonal antibody enhances early resistance to but impairs complete clearance of Listeria monocytogenes infection in mice.

Mice that received an anti-interleukin-10 (anti-IL-10) neutralizing monoclonal antibody (MAb) (SXC-1) prior to infection with Listeria monocytogenes initially demonstrated resistance to the infection, as indicated by reduced recovery of L. monocytogenes from their spleens and livers during the first 5 days after challenge. Anti-IL-10 MAb-treated mice then demonstrated reduced resistance during the later stage of infection, as indicated by persistent infection with L. monocytogenes in their livers 11 days after challenge. Aspartate aminotransferase (AST) levels (a measure of liver damage) in the sera of control mice increased between 1 and 5 days after challenge, while anti-IL-10 MAb-treated mice maintained lower AST levels. At 7 days after challenge, AST levels in the sera of control mice decreased as the numbers of organisms declined. In contrast, AST levels increased as the infections persisted in anti-IL-10 MAb-treated mice. The AST levels in serum reflected liver histopathology as anti-IL-10 MAb-treated mice exhibited fewer granulomatous lesions and less necrosis of liver tissue than the control mice during the first 5 days after challenge. Anti-IL-10 MAb treatment altered the expression of inflammatory cytokine mRNAs during L. monocytogenes infection. Control MAb-treated mice exhibited increased expression of tumor necrosis factor alpha and granulocyte-macrophage colony-stimulating factor mRNA in their lives during L. monocytogenes infection, but this increase did not occur in anti-IL-10 MAb-treated mice. Gamma interferon mRNA expression in the livers of the control MAb-treated mice was increased between 1 and 5 days after L. monocytogenes challenge and then decreased at 7 days after challenge. In contrast, gamma interferon mRNA expression in the livers of anti-IL-10 MAb-treated mice was not decreased until 7 days after challenge. These results indicate that endogenous IL-10 has both beneficial and detrimental effects on the host response to L. monocytogenes infection in mice.

Animals↗

PubMed2005

Multistate outbreak of Listeria monocytogenes infection linked to delicatessen turkey meat.

BACKGROUND: Despite a decreasing incidence of listeriosis in the United States, molecular subtyping has increased the number of recognized outbreaks. In September 2000, the New York City Department of Health identified a cluster of infections caused by Listeria monocytogenes isolates with identical molecular subtypes by pulsed-field gel electrophoresis (PFGE) and ribotyping. METHODS: To determine the magnitude of the outbreak and identify risk factors for infection, we notified state health departments and conducted a case-control study. A case was defined as a patient or mother-infant pair infected with Listeria monocytogenes whose isolate yielded the outbreak PFGE pattern. Controls were patients infected with Listeria monocytogenes whose isolate yielded a different PFGE pattern. Patients were asked about food and drink consumed during the 30 days before the onset of illness. RESULTS: Between May and December 2000, there were 30 clinical isolates of Listeria monocytogenes with identical PFGE patterns identified in 11 US states. Cases of infection caused by these isolates were associated with 4 deaths and 3 miscarriages. A case-control study implicated sliced processed turkey from a delicatessen (Mantel-Haenszel odds ratio, 8.0; 95% confidence interval, 1.2-43.3). A traceback investigation identified a single processing plant as the likely source of the outbreak, and the company voluntarily recalled 16 million pounds of processed meat. The same plant had been identified in a Listeria contamination event that had occurred more than a decade previously. CONCLUSIONS: Prevention of persistent L. monocytogenes contamination in food processing plants presents a critical challenge to food safety professionals.

Adult↗

PubMed2001

Memory phenotype CD8(+) T cells in IL-15 transgenic mice are involved in early protection against a primary infection with Listeria monocytogenes.

We recently constructed IL-15 transgenic (Tg) mice using cDNA encoding a secretable isoform of the IL-15 precursor protein under the control of an MHC class I promoter. The IL-15 Tg mice exhibited resistance against a primary infection with Listeria monocytogenes. The numbers of memory CD8(+) T cells were markedly increased in the IL-15 Tg mice following Listeria infection accompanied by sustained IL-15 production. The increased CD44(+)CD8(+) T cells in the infected IL-15 Tg mice were not specialized to recognize Listeria-specific antigen but produced a large amount of IFN-gamma in response to bystander stimulation exogenous IL-15 in combination with IL-12. Furthermore, Listeria-specific Th1 response by CD4(+) T cells was significantly augmented in the IL-15 Tg mice compared with control mice following Listeria infection. In vivo depletion of the CD8(+) T cells by anti-CD8 monoclonal antibody and adoptive transfer of the T cells from naive IL-15 Tg mice indicated that the CD8(+) T cells functioned not only to eliminate bacteria at the early stage of infection but also to promote Th1 response to L. monocytogenes. Overexpression of IL-15 shed light on a novel role of memory CD8(+) T cells in early protection and promotion of Th1 response against a primary infection with L. monocytogenes.

Adoptive Transfer↗

PubMed1995

Listeria monocytogenes infection and serotype distribution among HIV-infected persons in Los Angeles County, 1985-1992.

Persons infected with human immunodeficiency virus (HIV) are at greater risk of infection with Listeria monocytogenes (LM) than the general population. We quantify the risk of listeriosis in persons with acquired immune deficiency syndrome (AIDS) and HIV infection in Los Angeles County (LAC) and report the LM serotype distribution among HIV-infected patients with listeriosis. Active surveillance for listeriosis was performed in LAC during most of the period from 1985 through 1992. Thirty-four (10%) of 351 nonperinatal cases of listeriosis reported in LAC from 1985 through 1992 were in HIV-infected persons, 25 of whom met the 1987 AIDS case definition. The incidence of listeriosis was 95.8 and 8.8 cases per 100,000 person-years among persons with AIDS and all HIV-infected persons, respectively, but only 1.0 case per 100,000 person-years in the total population. Excluding cases from a 1985 listeriosis epidemic associated with consumption of contaminated Mexican-style cheese, 11 (65%) of 17 HIV-infected persons with available isolates were infected with LM serotype 1/2b, whereas only 64 (31%) of 208 other persons with listeriosis and available isolates were infected with LM serotype 1/2b (odds ratio = 4.1; 95% confidence interval = 1.3-14.1). LM serogroup 1/2b may have been more common among HIV-infected persons in LAC than among other persons with listeriosis because of differences in diet or sexual practices, or to chance alone. Persons with HIV-infection, especially those with AIDS, should be educated in avoiding foods at high risk of listerial contamination, such as soft cheeses, foods sold from delicatessen counters, and undercooked chicken.

Adolescent↗

PubMed1994

A comparison of aerosol and intragastric routes of infection with Listeria spp.

Aerosol infection (AI) of Porton outbred mice with Listeria species, exhibiting varying degrees of virulence, was compared with gastric intubation (GI) on the basis of numbers of deaths, 50% lethal dose (LD50) and pattern of listerial infection. The AI route appeared to be more sensitive, efficient and consistent than GI in that it required 10(5) fewer micro-organisms to obtain infection and death then ensued within 4 days, with GI deaths usually occurring on day 7. All the virulent strains tested caused 100% mortality by AI, while virulent and avirulent strains were indistinguishable by GI. Bacterial counts in the livers and spleens of infected mice were consistent with the relative virulence of the infectious agent using AI but not in GI mice. There were higher numbers of micro-organisms and more widespread lesions in the organs of AI mice than in GI. Results indicate that AI is an accurate in vivo indicator of virulence in listeria and using AI, bacterial counts in the liver and spleen could replace LD50 tests, thereby reducing the number of animals required for in vivo virulence testing.

Aerosols↗

PubMed2002

Comparison of host resistance to primary and secondary Listeria monocytogenes infections in mice by intranasal and intravenous routes.

There have been no studies on the susceptibility and host immune responses to an intranasal infection with Listeria monocytogenes. In this study, we compared the susceptibilities and cytokine responses between intranasal and intravenous infections with L. monocytogenes in mice. Moreover, we compared efficiency of acquisition of host resistance to L. monocytogenes infection between intranasally and intravenously immunized mice because an intranasal immunization of vaccines is reportedly available for induction of adaptive immunity against various infectious pathogens. The susceptibility to an intranasal infection with L. monocytogenes was markedly lower than that to the intravenous infection. The bacterial growth in the lungs, spleens, and livers was substantially similar between intranasally and intravenously infected mice. Titers of endogenous gamma interferon (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha) in the spleens, livers, and lungs were parallel to bacterial numbers in each organ of mice during intranasal infection and intravenous infection. IFN-gamma-deficient mice and TNF-alpha-deficient mice were highly susceptible to intranasal infection as well as intravenous infection. Susceptibilities to intranasal and intravenous L. monocytogenes infection were the same in these cytokine-deficient mice. These results suggest that both IFN-gamma and TNF-alpha play critical roles in host resistance to intranasal L. monocytogenes infection as well as the intravenous infection. Acquisition of host resistance to intravenous and intranasal L. monocytogenes infection was induced in intranasally immunized mice as well as intravenously immunized mice, suggesting that intranasal immunization is effective for prevention of a systemic infection with L. monocytogenes.

Administration, Intranasal↗

PubMed1992

Augmentation of host resistance to Listeria monocytogenes infection by a traditional Chinese medicine, ren-shen-yang-rong-tang (Japanese name: ninjin-youei-to).

Ren-shen-yang-rong-tang (Japanese name: Ninjin-youei-to, NIN), a traditional Chinese medicine, is a drug made of spray-dried powder of hot water extract obtained from twelve species of medical plants. An intraperitoneal (ip) injection with NIN 2 days before intravenous (iv) infection with Listeria monocytogenes (L. monocytogenes) accelerated elimination of viable bacteria in the spleen in the early stage of infection (from day 1) and protected mice from the lethal infection. It was suggested that the protective effect of NIN was mediated by the activation of nonimmune macrophages playing a principle role in resistance in the early stage of infection. Two days after ip injection with NIN just before infection, significantly increment in the number of monocytes in the peripheral blood was observed, though macrophage number in the spleen and their intracellular killing activity were unchanged. At 12 hours after infection with L. monocytogenes, a significantly enhanced increase of splenic macrophage number was observed in NIN-treated mice, compared to controls. After ip injection of NIN, interleukin-1 (IL-1), IL-6 and granulocyte macrophage-colony stimulating factor (GM-CSF) became detectable in the serum or peritoneal cavity. These results suggested that NIN stimulated macrophage-precursor cells in the bone marrow via the production of IL-1, IL-6, GM-CSF by macrophages, accelerated the supply of peripheral macrophages, and such macrophages accumulated into the site of infection in the very early stage of infection. Similar protective effects of NIN were observed by oral administration for 7 days till 1 day before iv infection with L. monocytogenes.

Adjuvants, Immunologic↗

PubMed2005

Simultaneous Th1-type cytokine expression is a signature of peritoneal CD4+ lymphocytes responding to infection with Listeria monocytogenes.

The robust murine response to infection with Listeria monocytogenes makes an excellent model to study the functional development of immune cells. We investigated the cellular immune response to i.p. infection using intracellular cytokine staining to identify Ag-specific lymphocytes. CD4(+) peritoneal exudate cells obtained 10 days postinfection predominantly coexpressed TNF-alpha, IFN-gamma, and IL-2 after polyclonal or Ag stimulation. A population of cells simultaneously making TNF-alpha and IFN-gamma was also detected but at a lower frequency. By following the kinetics of the response to Listeria, we found that CD4(+) lymphocytes coexpressing TNF-alpha and IFN-gamma dominated on day 6 postinfection and then declined. From days 10-27, TNF-alpha(+)IFN-gamma(+)IL-2(+) (triple-positive) was the most prevalent cytokine phenotype, and the frequency steadily declined. These characteristic cytokine expression patterns were observed in both primary and secondary responses to Listeria infection and developed even when infection was terminated with antibiotic treatment. A cytokine-assisted immunization procedure resulted in both double- and triple-positive cells, but the clear predominance of triple-positive cells required Listeria infection. Triple-positive cells were preferentially noted in the peritoneal cavity tissue site; spleen cells displayed a predominant population of double-positive T cells (TNF-alpha(+)IFN-gamma(+)). We speculate that the appearance of triple-positive cells represents a functionally significant subset important in host defense at nonlymphoid tissue sites.

Animals↗

PubMed1967

Mechanisms of pathogenesis in Listeria monocytogenes infection. II. Characterization of listeriosis in the CD-1 mouse and survey of biochemical lesions.

Several physiological and biochemical changes which occur in CD-1 pathogen-free mice during the course of infection with Listeria monocytogenes strain A4413 have been examined. Mice injected with 10(4) to 10(6) organisms by the intraperitoneal route displayed a significant depression in weight gain. In contrast, at 24 hr after infection an increment in total liver weight averaging 0.1 g was observed. The ratios of liver to body weight increased throughout the observation period. As the severity of the infection increased, food intake, as well as total liver protein and nitrogen, showed a corresponding decrease, with the diminution being most evident immediately prior to the death of the animals. Blood urea nitrogen remained relatively constant for 24 hr and then increased continuously as the infection progressed to the acute stage. Total liver lipid increased until the death of the animals. At 72 hr postinfection, a significant decrease in oxidative phosphorylation was observed. Xanthine dehydrogenase activity increased, with maximal values obtained 72 hr after infection. Uric acid levels remained constant for 24 hr, diminished at 48 hr, and then increased until the death of the animals. After 24 hr, uricase activity showed a slight increase. This activity returned to within normal ranges at 48 hr and decreased as the infection progressed to the acute stage at 72 hr. The results support the hypothesis that at least a part of the cause of death is a derangement in hepatic purine and carbohydrate metabolism. The data are also consistent with the possibility of changes in iron transport in the infected mice.

Animals↗