Immunocytochemical detection of chitin in Pneumocystis carinii

Walker, Anna N.; Garner, Ronald E.; Horst, Michael N.

doi:10.1128/iai.58.2.412-415.1990

Cited by 46 publications

(10 citation statements)

References 20 publications

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“…The ␤-glucan appears to be necessary for viability since inhibitors of ␤-glucan synthetase can cure P. carinii pneumonia in animals (81,84). Other studies have reported the presence of material reactive with antibodies against chitin (32,110). Whatever its composition, the surface layer of trophic forms is insufficient to protect the cells from lysis under conditions that do not affect the integrity of conventional yeasts (41).…”

Section: P Carinii Is An Atypical Fungusmentioning

confidence: 99%

Pneumocystis carinii: what is it, exactly?

Stringer

1996

Clin Microbiol Rev

106

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The identity of Pneumocystis carinii has been uncertain for many years. Until recently, it was widely regarded to be a protozoan because it does not grow in culture and is not susceptible to antifungal drugs. Although these and a number of other phenotypic characteristics of P. carinii differ from those of typical fungi, analysis of DNA sequences has shown that P. carinii is a member of the fungal lineage of eukaryotes. However, a close phylogenetic relative of P. carinii has not yet been found. Analysis of gene sequences has also revealed that P. carinii is not a single entity but that the genus Pneumocystis contains a complex group of organisms. P. carinii organisms from one host species do not grow when introduced into another host species, and P. carinii isolates from different host species are more genetically divergent from one another than might be expected for members of the same species. Genetic variation of a lesser degree also occurs among P. carinii organisms from the same host species, suggesting that it may be possible to identify strains and to conduct transmission and epidemiological studies. Results of early studies exploiting genetic variation among P. carinii isolates from patients have suggested that recurrent P. carinii pneumonia may not always be caused by reactivation of latent organisms, as is commonly believed. However, other features of P. carinii suggest that this microbe has established a long-term relationship with its host. A striking new development in this regard is the discovery of a genetic system that is designed to allow variation in the structure of a major antigen on the surface of P. carinii.

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Section: P Carinii Is An Atypical Fungusmentioning

confidence: 99%

Pneumocystis carinii: what is it, exactly?

Stringer

1996

Clin Microbiol Rev

106

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“…Natural Ab to N ‐acetyl‐glucosamine, the sugar monomer of chitin, have been detected in various mouse strains with increased titers in aged mice 6. In addition, chitin‐specific Ab have been generated in rabbits 7. This demonstrates that the adaptive immune system can recognize and respond to chitin.…”

Section: Introductionmentioning

confidence: 98%

Chitin induces upregulation of B7‐H1 on macrophages and inhibits T‐cell proliferation

et al. 2010

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Chitin is a highly abundant glycopolymer, which serves as structural component in fungi, arthropods and crustaceans but is not synthesized by vertebrates. However, vertebrates express chitinases and chitinase-like proteins, some of which are induced by infection with helminths suggesting that chitinous structures may be targets of the immune system. The chitin-induced modulations of the innate and adaptive immune responses are not well understood. Here, we demonstrate that intranasal administration of OVA and chitin resulted in diminished T-cell expansion and Th2 polarization as compared with OVA administration alone. Chitin did not promote nor attenuate Th2 polarization in vitro. Chitin-exposed macrophages inhibited proliferation of CD4 1 T cells in a cell-cell contactdependent manner. Chitin induced upregulation of the inhibitory ligand B7-H1 (PD-L1) on macrophages independently of MyD88, TRIF, TLR2, TLR3, TLR4 and Stat6. Inhibition of T-cell proliferation was largely dependent on B7-H1, as the effect was not observed in cocultures with cells from B7-H1-deficient mice.Key words: B7-H1 . Chitin . Macrophages . T-cell proliferation Supporting Information available online IntroductionChitin, an N-acetyl-b-D-glucosamine polysaccharide, is a major structural component of fungal cell walls and the exoskeleton of crustaceans and insects. Vertebrates cannot synthesize chitin; however, their genomes contain genes for chitinases and chitinase-like proteins which might play a role in recognition and immune defense of fungi and helminth parasites [1][2][3]. Chitinase-like proteins are linked to genomic regions encoding MHC paralogous genes, suggesting that they might have been part of a ''proto MHC'' before the bilateral expansion [4,5]. Natural Ab to N-acetyl-glucosamine, the sugar monomer of chitin, have been detected in various mouse strains with increased titers in aged mice [6]. In addition, chitin-specific Ab have been generated in rabbits [7]. This demonstrates that the adaptive immune system can recognize and respond to chitin.Infections with helminths generally induce expression of the acidic mammalian chitinase (AMCase) and the chitinase-like proteins Ym1/Ym2 in an IL-4 or IL-13-dependent manner [8,9]. AMCase was also found to be induced after allergic provocation of the lung and pathology could be ameliorated by administration of the allosteric inhibitor allosamidin [10]. However, constitutive expression of AMCase in the lung of transgenic mice did not cause inflammation or airway hyper-reactivity and rather protected against chitin-induced recruitment of eosinophils and basophils [9].Macrophages and DC are probably the main cell types that recognize chitin and subsequently modulate the adaptive immune response. Potential transmembrane receptors for chitin include the mannose receptor [11], and the recently described fibrinogen C domain-containing protein 1 [13]. The modulation of immune responses by chitin is still poorly understood and may depend on particle size and route of administration. It has 2882been ...

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“…2 In addition, PC produces chitin in all three stages of its life cycle., i.e., cyst form, intracystic bodies, and trophozoites. 3 PC most commonly presents as pneumonia in patients with human immunodeficiency virus (HIV) infection. Extrapulmonary pneumocystosis is rare, and has been reported in lymph nodes, bone marrow, stomach, spleen, liver, small intestine, skin, pancreas, thyroid, choroid, and eye.…”

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confidence: 99%