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      Animal infection models using non‐mammals

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          Abstract

          The use of non‐human animal models for infection experiments is important for investigating the infectious processes of human pathogenic bacteria at the molecular level. Mammals, such as mice and rabbits, are also utilized as animal infection models, but large numbers of animals are needed for these experiments, which is costly, and fraught with ethical issues. Various non‐mammalian animal infection models have been used to investigate the molecular mechanisms of various human pathogenic bacteria, including Staphylococcus aureus, Streptococcus pyogenes, and Pseudomonas aeruginosa. This review discusses the desirable characteristics of non‐mammalian infection models and describes recent non‐mammalian infection models that utilize Caenorhabditis elegans, silkworm, fruit fly, zebrafish, two‐spotted cricket, hornworm, and waxworm.

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          A simple model host for identifying Gram-positive virulence factors.

          We demonstrate the use of the nematode Caenorhabditis elegans as a facile and inexpensive model host for several Gram-positive human bacterial pathogens. Enterococcus faecalis, Streptococcus pneumoniae, and Staphylococcus aureus, but not Bacillus subtilis, Enterococcus faecium, or Streptococcus pyogenes, kill adult C. elegans. Focusing our studies on the enterococcal species, we found that both E. faecalis and E. faecium kill C. elegans eggs and hatchlings, although only E. faecalis kills the adults. In the case of adults, a low inoculum of E. faecalis grows to a high titer in the C. elegans intestine, resulting in a persistent infection that cannot be eradicated by prolonged feeding on E. faecium. Interestingly, a high titer of E. faecium also accumulates in the nematode gut, but does not affect the longevity of the worms. Two E. faecalis virulence-related factors that play an important role in mammalian models of infection, fsr, a putative quorum-sensing system, and cytolysin, are also important for nematode killing. We exploit the apparent parallels between Gram-positive infection in simple and more complex organisms by using the nematode to identify an E. faecalis virulence factor, ScrB, which is relevant to mammalian pathogenesis.
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            Galleria mellonella as a model system to study Cryptococcus neoformans pathogenesis.

            Evaluation of Cryptococcus neoformans virulence in a number of nonmammalian hosts suggests that C. neoformans is a nonspecific pathogen. We used the killing of Galleria mellonella (the greater wax moth) caterpillar by C. neoformans to develop an invertebrate host model system that can be used to study cryptococcal virulence, host immune responses to infection, and the effects of antifungal compounds. All varieties of C. neoformans killed G. mellonella. After injection into the insect hemocoel, C. neoformans proliferated and, despite successful phagocytosis by host hemocytes, killed caterpillars both at 37 degrees C and 30 degrees C. The rate and extent of killing depended on the cryptococcal strain and the number of fungal cells injected. The sequenced C. neoformans clinical strain H99 was the most virulent of the strains tested and killed caterpillars with inocula as low as 20 CFU/caterpillar. Several C. neoformans genes previously shown to be involved in mammalian virulence (CAP59, GPA1, RAS1, and PKA1) also played a role in G. mellonella killing. Combination antifungal therapy (amphotericin B plus flucytosine) administered before or after inoculation was more effective than monotherapy in prolonging survival and in decreasing the tissue burden of cryptococci in the hemocoel. The G. mellonella-C. neoformans pathogenicity model may be a substitute for mammalian models of infection with C. neoformans and may facilitate the in vivo study of fungal virulence and efficacy of antifungal therapies.
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              Killing of Caenorhabditis elegans by Pseudomonas aeruginosa used to model mammalian bacterial pathogenesis.

              We show that a single clinical isolate of the human opportunistic pathogen Pseudomonas aeruginosa (strain PA14), which previously was shown to be pathogenic in mice and plants, also kills Caenorhabditis elegans. The rate of PA14-mediated killing of C. elegans depends on the composition of the agar medium on which PA14 is grown. When PA14 is grown on minimal medium, killing occurs over the course of several days and is referred to as "slow" killing. When PA14 is grown on high-osmolarity medium, killing occurs over the course of several hours and is referred to as "fast" killing. Several lines of evidence, including the fact that heat-killed bacteria are still capable of fast but not slow killing of C. elegans, indicate that fast and slow killing occur by distinct mechanisms. Slow killing involves an infection-like process and correlates with the accumulation of PA14 within worm intestines. Among 10 PA14 virulence-related mutants that had been shown previously to affect pathogenicity in plants and mice, 6 were less effective in killing C. elegans under both fast- and slow-killing conditions, indicating a high degree of commonalty among the P. aeruginosa factors required for pathogenicity in disparate eukaryotic hosts. Thus, we show that a C. elegans pathogenicity model that is genetically tractable from the perspectives of both host and pathogen can be used to model mammalian bacterial pathogenesis.
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                Author and article information

                Contributors
                ckaito@okayama-u.ac.jp
                Journal
                Microbiol Immunol
                Microbiol Immunol
                10.1111/(ISSN)1348-0421
                MIM
                Microbiology and Immunology
                John Wiley and Sons Inc. (Hoboken )
                0385-5600
                1348-0421
                22 August 2020
                September 2020
                : 64
                : 9 ( doiID: 10.1111/mim.v64.9 )
                : 585-592
                Affiliations
                [ 1 ] Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences Okayama University Okayama Japan
                Author notes
                [*] [* ] Correspondence Chikara Kaito, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University, 1‐1‐1 Tsushima‐naka, Kita‐ku, Okayama 700‐8530, Japan.

                Email: ckaito@ 123456okayama-u.ac.jp

                Author information
                http://orcid.org/0000-0002-2895-3386
                Article
                MIM12834
                10.1111/1348-0421.12834
                7590188
                32757288
                022f4276-1af3-4ac4-90e4-78e2da4d585a
                © 2020 The Authors. Microbiology and Immunology published by The Societies and John Wiley & Sons Australia, Ltd

                This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                : 18 June 2020
                : 17 July 2020
                : 27 July 2020
                Page count
                Figures: 2, Tables: 2, Pages: 8, Words: 5043
                Funding
                Funded by: JSPS Grants‐in‐Aid for Scientific Research
                Award ID: 19H03466
                Award ID: 19K22523
                Funded by: Ichiro Kanehara Foundation , open-funder-registry 10.13039/501100003837;
                Funded by: Takeda Science Foundation , open-funder-registry 10.13039/100007449;
                Categories
                Mini‐review
                Mini‐review
                Custom metadata
                2.0
                September 2020
                Converter:WILEY_ML3GV2_TO_JATSPMC version:5.9.3 mode:remove_FC converted:27.10.2020

                infection model,non‐mammals,pathogenic bacteria
                infection model, non‐mammals, pathogenic bacteria

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