Mycobacterium avium resists exposure to the acidic conditions of the stomach.

Organisms of the Mycobacterium avium complex are common pathogens in immunosuppressed patients such as individuals with AIDS. There is evidence that in AIDS patients, the main route for M. avium infection is the gastrointestinal tract.

Mycobacterium avium infection of epithelial cells results in inhibition or delay in the release of interleukin-8 and RANTES.

Mycobacterium avium is an opportunistic pathogen in AIDS patients, who acquire the infection mainly through the gastrointestinal tract. Previous studies in vitro have shown that M. avium invades epithelial cells of both intestinal and laryngeal origin.

Isolation of two subpopulations of Mycobacterium avium within human macrophages.

Mycobacterium avium is an intracellular pathogen that is associated with disseminated infection in acquired immunodeficiency syndrome (AIDS) patients. Human monocyte-derived macrophages were infected with M. avium strain 101 and a quinolone (Bay y 3118) was used at 8 micrograms ml-1, a concentration that kills growing bacteria but fails to eliminate static organisms.

Role of complement receptors in uptake of Mycobacterium avium by macrophages in vivo: evidence from studies using CD18-deficient mice.

Mycobacterium avium is an intracellular pathogen that has been shown to invade macrophages by using complement receptors in vitro, but mycobacteria released from one cell can enter a second macrophage by using receptors different from complement receptors. Infection of CD18 (beta(2) integrin) knockout mice and the C57 BL/6 control mice led to comparable levels of tissue infection at 1 day, 2 days, 1 week, and 3 weeks following administration of bacteria. A histopathological study revealed similar granulomatous lesions in the two mouse strains, with comparable numbers of organisms.

Mefloquine is active in vitro and in vivo against Mycobacterium avium complex.

Despite the development of several agents, new classes of antimicrobials with activity against the Mycobacterium avium complex (MAC) are needed. Based on a broad screening of compounds, we found that mefloquine has MICs of 8 to 16 microg/ml by the BACTEC system and 16 microg/ml by broth microdilution for five MAC strains tested. An expansion of the screening with broth microdilution to 24 macrolide-susceptible strains and 6 macrolide-resistant strains determined that the MIC for all strains was 16 microg/ml.

Neutrophils from Mycobacterium avium-infected mice produce TNF-alpha, IL-12, and IL-1 beta and have a putative role in early host response.

Recent evidence supports a role for neutrophils in the host defense against Mycobacterium avium. To determine whether the depletion of neutrophils has an effect on the outcome of infection in mice as determined by the number of bacteria in liver and spleen, we administered RB6-8C5 anti-neutrophil antibody intraperitoneally both early and late in the infection. Mice were then observed for 14 days and harvested.

Host defense against Mycobacterium avium does not have an absolute requirement for major histocompatibility complex class I-restricted T cells.

The role of CD8(+) T cells was evaluated in a mouse model of disseminated Mycobacterium avium infection. C57BL/6J and C57BL/6Jbeta2-/- (beta2-/-) mice were infected intravenously, and the number of viable bacteria in each liver and spleen was determined. No significant difference between the number of bacteria in the two strains of mice was observed at 2, 4, 6, and 8 weeks after infection.

Apoptosis of Mycobacterium avium-infected macrophages is mediated by both tumour necrosis factor (TNF) and Fas, and involves the activation of caspases.

Mycobacterium avium causes disseminated infection in AIDS patients and several forms of infection in immunocompetent hosts. Recent studies have shown that M. avium infection of macrophages in vitro leads to apoptosis of significant numbers of infected cells.

Mycobacterium avium infection of gut mucosa in mice associated with late inflammatory response and intestinal cell necrosis.

Mycobacterium avium is an intracellular pathogen that is associated with disseminated infection in acquired immunodeficiency syndrome (AIDS). Patients with AIDS appear to acquire M. avium mainly through the gastrointestinal tract.

Treatment with recombinant granulocyte colony-stimulating factor (Filgrastin) stimulates neutrophils and tissue macrophages and induces an effective non-specific response against Mycobacterium avium in mice.

A role of neutrophils in the host response against Mycobacterium avium (MAC) has recently been suggested. To investigate this matter further, we determined the effect of granulocyte colony-stimulating factor (G-CSF) on the outcome of MAC infection in mice. C57BL/6bg+/bg- black mice were intravenously infected with 1 x 10(7) MAC and then divided into four experimental groups to receive G-CSF as follows: (i) 10 micrograms/kg/day; (ii) 50 micrograms/kg/day; (iii) 100 micrograms/kg/day; (iv) placebo control.

Clarithromycin significantly improves interleukin-12-mediated anti-Mycobacterium avium activity and abolishes toxicity in mice.

Treatment of experimental murine Mycobacterium avium (MAC) infection with interleukin-12 (IL-12) significantly decreased MAC organisms in tissue but resulted in toxicity. Because IL-12-related toxicity was seen only in infected mice, IL-12 was combined with clarithromycin in an attempt to decrease bacterial burden. Clarithromycin (200 mg/kg/day) was administered alone to M.

CTL response to Mycobacterium tuberculosis: identification of an immunogenic epitope in the 19-kDa lipoprotein.

The successful resolution of infection with Mycobacterium tuberculosis (M.tb) is believed to involve the induction of CTLs that are capable of killing cells harboring this pathogen, although little information is known about the MHC restriction or fine specificity of such CTLs. In this study, we used knowledge of the HLA-A*0201-binding motif and an immunofluorescence-based peptide-binding assay to screen for potential HLA-A*0201-binding epitopes contained in the 19-kDa lipoprotein of M.

Exposure to low oxygen tension and increased osmolarity enhance the ability of Mycobacterium avium to enter intestinal epithelial (HT-29) cells.

Current evidence indicates that Mycobacterium avium infection in patients with AIDS is acquired mostly through the gastrointestinal (GI) tract and that M. avium binds to and invades GI mucosal cells in vitro. Since M.

Interaction of Mycobacterium avium with environmental amoebae enhances virulence.

Environmental mycobacteria are a common cause of human infections. Recently, contaminated domestic water supplies have been suggested as a potential environmental source of several mycobacterial diseases. Since many of these mycobacterial species replicate best intracellularly, environmental hosts have been sought.

Mycobacterium avium infection in mice is associated with time-related expression of Th1 and Th2 CD4+ T-lymphocyte response.

Disseminated infection caused by organisms of Mycobacterium avium complex is common in acquired immune deficiency syndrome (AIDS) patients. M. avium is an intracellular bacterium that multiplies within macrophages.

Mycobacterium avium reduces expression of costimulatory/adhesion molecules by human monocytes.

Organisms of the Mycobacterium avium complex survive the hostile environment of their host cells, the macrophages, and evade immune response, in part, by interfering with processing and presentation of antigen. We studied the effect of infection with M. avium on the expression of the costimulatory/adhesion molecules (referred to herein as accessory molecules) because generating an efficient T cell response requires both the recognition of processed antigen and the participation of accessory molecules.

Therapy of sepsis.

The term 'sepsis' is often used synonymously with 'infection' or 'bacteremia'. Additional definitions, e.g.

Regulation of the expression of Mycobacterium avium complex proteins differs according to the environment within host cells.

Mycobacterium avium is an intracellular organism that can infect a number of cell types such as macrophages and epithelial cells. Each one of these cells represents a different environment that requires specific adaptation from the bacterium. The effect of uptake of M.

Effect of ethambutol on emergence of clarithromycin-resistant Mycobacterium avium complex in the beige mouse model.

An animal model was developed for studying macrolide-resistant Mycobacterium avium complex (MAC) and to measure the effect of ethambutol on resistance. MAC-infected beige mice were given clarithromycin daily; the frequency of clarithromycin-resistant MAC after 8 and 12 weeks was 10(-3) and 10(-2), respectively. Combined ethambutol plus clarithromycin did not increase anti-MAC activity, but clarithromycin-resistant MAC was less frequent (P < .

Interleukin-7 induces anti-Mycobacterium avium activity in human monocyte-derived macrophages.

To examine the modulatory role of interleukin (IL)-7 on intracellular growth of Mycobacterium avium complex (MAC), human macrophages were treated either before or after MAC infection with different concentrations of IL-7. At 100 pg/mL, 1 ng/mL, and 10 ng/mL, treatment with IL-7 before infection stimulated secretion of tumor necrosis factor-alpha (TNF-alpha) from MAC-infected macrophages (increase up to 40%) and resulted in dose-dependent reduction in the number of intracellular bacteria. Pretreatment with IL-7 did not inhibit the secretion of transforming growth factor-beta1 (TGF-beta1).

Epidermal growth factor-binding protein in Mycobacterium avium and Mycobacterium tuberculosis: a possible role in the mechanism of infection.

Epidermal growth factor (EGF) is a potent mitogen for a variety of eukaryotic cells. EGF is found in a number of tissues and is prevalent in necrotic tissues and granulomata. The biological effect of EGF on mammalian cells is initiated by the binding to a specific receptor.

Efficacy of azithromycin and rifabutin in preventing infection by Mycobacterium avium complex in beige mice.

We investigated the potential of the azalide, azithromycin, and rifabutin in preventing disseminated infection due to Mycobacterium avium complex (MAC) in beige mice. Azithromycin 200 mg/kg, rifabutin (30 mg/kg or 60 mg/kg) were administered by gavage 6 days before mice were challenged orally with 10(8) cfu MAC and daily for 10 days thereafter during which time the mice were again challenged with the same inoculum on alternate days (days +1, +3, +5, +7, and +9). Sixty-four days later, the presence of bacteria in the blood and the number of viable bacteria in liver, spleen and appendix were estimated.

Interleukin-12-stimulated natural killer cells can activate human macrophages to inhibit growth of Mycobacterium avium.

Interleukin-12 (IL-12) is a critical cytokine that affects many of the biological functions of NK cells and T cells. We have previously shown that both human and murine NK cells are important in host defense against Mycobacterium avium complex and act by secreting cytokines that induce macrophages to inhibit the growth of intracellular M. avium.

Signal requirements for production of luteinizing hormone releasing-hormone by human T cells.

We have previously demonstrated that both human CD4+ and CD8+ T lymphocytes produce enhanced levels of luteinizing hormone-releasing hormone (LHRH) mRNA and peptide upon stimulation with monoclonal antibody directed at the CD3 component of the T cell receptor for antigen (TCR) or mitogenic lectin. In the current study, we define the signaling pathways that control TCR-mediated LHRH production by using agents known to affect distinct signals, and compare the messenger systems required for LHRH response to other T-cell-associated activation responses, such as expression of CD69 and interleukin-2 receptor (IL-2R) molecules and production of interleukin-2 (IL-2). Results indicate that the activation of protein kinase C (PKC) is essential for LHRH production by previously nonstimulated T cells, not increased concentration of cytosolic-free calcium ([Ca2+]i).