ArticleInfection and immunity2001
Role of complement in Mycobacterium avium pathogenesis: in vivo and in vitro analyses of the host response to infection in the absence of complement component C3.
Article in Infection and immunity, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
18 citing papers in PubMed, 35 citations in OpenAlex.
- Pathogenesis of SARS-CoV-2 andFrontiers in immunology · 2022Review
- Specificity of the innate immune responses to different classes of non-tuberculous mycobacteria.Frontiers in immunology · 2022Article
- The Role of Complement System and the Immune Response to Tuberculosis Infection.Medicina (Kaunas, Lithuania) · 2021Review
- Mycobacterium avium MAV_2941 mimics phosphoinositol-3-kinase to interfere with macrophage phagosome maturation.Microbes and infection · 2015Article
- Complement, c1q, and c1q-related molecules regulate macrophage polarization.Frontiers in immunology · 2014Review
- The roles of complement receptor 3 and Fcγ receptors during Leishmania phagosome maturation.Journal of leukocyte biology · 2013Article
- Complement component C1q regulates macrophage expression of Mer tyrosine kinase to promote clearance of apoptotic cells.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Complement factor C7 contributes to lung immunopathology caused by Mycobacterium tuberculosis.Clinical & developmental immunology · 2012Article
- Oversulfated chondroitin sulfate inhibits the complement classical pathway by potentiating C1 inhibitor.PloS one · 2012Article
- A new role of the complement system: C3 provides protection in a mouse model of lung infection with intracellular Chlamydia psittaci.PloS one · 2012Article
- Tactics of Mycobacterium avium subsp. paratuberculosis for intracellular survival in mononuclear phagocytes.Journal of veterinary science · 2008Review
- Article
- Pathogenesis of Mycobacterium avium infection: typical responses to an atypical mycobacterium?Immunologic research · 2006Review
- Activation and mitogen-activated protein kinase regulation of transcription factors Ets and NF-kappaB in Mycobacterium-infected macrophages and role of these factors in tumor necrosis factor alpha and nitric oxide synthase 2 promoter function.Infection and immunity · 2005Article
- Differential activation of the transcription factor cyclic AMP response element binding protein (CREB) in macrophages following infection with pathogenic and nonpathogenic mycobacteria and role for CREB in tumor necrosis factor alpha production.Infection and immunity · 2005Article
- Complement protein C3 binding to Mycobacterium tuberculosis is initiated by the classical pathway in human bronchoalveolar lavage fluid.Infection and immunity · 2004Article
- Mycobacterium's arrest of phagosome maturation in macrophages requires Rab5 activity and accessibility to iron.Molecular biology of the cell · 2003Article
- Differential regulation of the mitogen-activated protein kinases by pathogenic and nonpathogenic mycobacteria.Infection and immunity · 2002Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We investigated the importance of the host complement system in the pathogenesis of disease mediated by the intramacrophage pathogen Mycobacterium avium. Mycobacteria opsonized with complement are efficiently ingested by macrophages through various complement receptors. Furthermore, unlike other bacteria, mycobacteria can activate both the alternative and classical complement pathways in the absence of specific antibodies. Therefore, to examine the role of complement in the mycobacterial infection process in vivo, mice deficient in complement component C3 were infected with M. avium. Surprisingly, C3-deficient mice infected intravenously with M. avium displayed no difference in bacterial burden or granulomatous response compared to wild-type control mice. C3-sufficient mice and C3-deficient mice were equally susceptible to infection by M. avium regardless of the genotype at the bcg locus, a locus known to confer susceptibility to infection with intracellular pathogens. In vitro studies using mouse bone marrow-derived macrophages resulted in significant M. avium invasion of macrophages in the absence of C3; however, the kinetics of infection were delayed compared to complement-mediated invasion. The data indicate that complement does not play an essential role in mediating M. avium infections in the mouse and suggest either that other invasion mechanisms can compensate for the absence of complement-mediated entry or that complement is not a major mycobacterial opsonin in vivo.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.