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Article ; Online: Molecular mechanism of Streptococcus pneumoniae-targeting xenophagy recognition and evasion: Reinterpretation of pneumococci as intracellular bacteria.

Ogawa, Michinaga / Shizukuishi, Sayaka / Akeda, Yukihiro / Ohnishi, Makoto

2023 Volume 67, Issue 5, Page(s) 224–227

Abstract: Streptococcus pneumoniae is a major, encapsulated Gram-positive pathogen that causes diseases including community-acquired pneumonia, meningitis, and sepsis. This pathogen colonizes the nasopharyngeal epithelia asymptomatically but can often migrate to ... ...

Abstract	Streptococcus pneumoniae is a major, encapsulated Gram-positive pathogen that causes diseases including community-acquired pneumonia, meningitis, and sepsis. This pathogen colonizes the nasopharyngeal epithelia asymptomatically but can often migrate to sterile tissues and cause life-threatening invasive infections (invasive pneumococcal disease). Although multivalent pneumococcal polysaccharides and conjugate vaccines are available and effective, they also have major shortcomings with respect to the emergence of vaccine-resistant serotypes. Therefore, alternative therapeutic approaches are needed, and the molecular analysis of host-pathogen interactions and their applications to pharmaceutical development and clinical practice has recently received increased attention. In this review, we introduce pneumococcal surface virulence factors involved in pathogenicity and highlight recent advances in our understanding of host autophagy recognition mechanisms against intracellular S. pneumoniae and pneumococcal evasion from autophagy.
MeSH term(s)	Humans ; Streptococcus pneumoniae/genetics ; Macroautophagy ; Pneumococcal Infections/microbiology ; Virulence Factors ; Virulence ; Pneumococcal Vaccines
Chemical Substances	Virulence Factors ; Pneumococcal Vaccines
Language	English
Publishing date	2023-03-21
Publishing country	Australia
Document type	Journal Article ; Review
ZDB-ID	224792-6
ISSN	1348-0421 ; 0385-5600
ISSN (online)	1348-0421
ISSN	0385-5600
DOI	10.1111/1348-0421.13060
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Article ; Online: The multi-step mechanism and biological role of noncanonical autophagy targeting

Shizukuishi, Sayaka / Ogawa, Michinaga / Ryo, Akihide / Ohnishi, Makoto

Autophagy

2020 Volume 16, Issue 6, Page(s) 1152–1153

Abstract: Multiple autophagic processes are triggered in response to bacterial infection as the host attempts to eliminate intracellular invaders. However, it is still unclear how the mechanisms contributing to canonical macroautophagy/autophagy, including ... ...

Abstract	Multiple autophagic processes are triggered in response to bacterial infection as the host attempts to eliminate intracellular invaders. However, it is still unclear how the mechanisms contributing to canonical macroautophagy/autophagy, including xenophagy, coordinate with the more recently described features that are characteristic of noncanonical autophagy. Recently, we revealed that infection with
MeSH term(s)	Autophagosomes ; Autophagy ; Bacterial Proteins ; Phagosomes ; Streptococcus pneumoniae
Chemical Substances	Bacterial Proteins
Language	English
Publishing date	2020-03-21
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.1080/15548627.2020.1743937
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Article ; Online: Streptococcus pneumoniae

Shizukuishi, Sayaka / Ogawa, Michinaga / Ryo, Akihide / Ohnishi, Makoto

Autophagy

2020 Volume 16, Issue 8, Page(s) 1529–1531

Abstract: Streptococcus pneumoniae: is an opportunistic bacterial pathogen that can promote severe infection by overcoming the epithelial and blood-brain barrier. Pneumococcal cell-surface virulence factors, including cell wall-anchored choline-binding proteins ( ... ...

Abstract	Streptococcus pneumoniae: is an opportunistic bacterial pathogen that can promote severe infection by overcoming the epithelial and blood-brain barrier. Pneumococcal cell-surface virulence factors, including cell wall-anchored choline-binding proteins (Cbps) play pivotal roles in promoting invasive disease. We reported previously that intracellular pneumococci were detected by hierarchical macroautophagic/autophagic processes that ultimately lead to bacterial elimination. However, whether intracellular pneumococci can evade autophagy by deploying Cbps remains unclear. In this study, we explore the biological functions of Cbps and reveal their roles in manipulating the autophagic process. Specifically, we found that CbpC-activated autophagy takes place via its interactions with ATG14 (autophagy related 14) and SQSTM1/p62 (sequestosome1). Importantly, CbpC dampens host autophagy by promoting ATG14 degradation via the ATG14-CbpC-SQSTM1/p62 axis. CbpC-induced reductions in ATG14 levels result in impaired ATG14-STX17 complex formation. In pneumococcal-infected cells, ATG14 levels are dramatically reduced in a CbpC-dependent manner that results in suppression of autophagy-mediated degradation and enhanced bacterial survival. Taken together, our results reveal a novel mechanism via which pneumococci can manipulate host autophagy responses, in this case, by employing CbpC as a trap to promote ATG14 depletion. Our findings highlight a novel and sophisticated tactic used by
Language	English
Publishing date	2020-06-17
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.1080/15548627.2020.1776475
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Article ; Online: Crosstalk between the innate immune system and selective autophagy in hepatitis B virus infection.

Miyakawa, Kei / Jeremiah, Sundararaj Stanleyraj / Ogawa, Michinaga / Nishi, Mayuko / Ohnishi, Makoto / Ryo, Akihide

Autophagy

2022 Volume 18, Issue 8, Page(s) 2006–2007

Abstract: Although the involvement of macroautophagy/autophagy in hepatitis B virus (HBV) infection has become clearer recently, whether selective autophagy plays an important role in suppressing HBV remains uncertain. We recently found that LGALS9 (galectin 9) is ...

Abstract	Although the involvement of macroautophagy/autophagy in hepatitis B virus (HBV) infection has become clearer recently, whether selective autophagy plays an important role in suppressing HBV remains uncertain. We recently found that LGALS9 (galectin 9) is an interferon (IFN)-inducible protein involved in the suppression of HBV replication. Expression of LGALS9 in HBV-infected cells causes the formation of cytoplasmic puncta that degrade the HBV core protein (HBc) in conjunction with RSAD2/viperin, another IFN-inducible protein. LGALS9 binds to HBc via RSAD2 and promotes the autoubiquitination of RNF13 (ring finger protein 13) to recruit SQSTM1/p62, resulting in the formation of LC3-positive autophagosomes that degrade HBc. Both LGALS9 and RSAD2 are encoded by IFN-stimulated genes that act synergistically to induce HBc proteolysis in HBV-infected hepatocytes in an IFN-dependent manner. These results reveal a crosstalk mechanism between the innate immune system and selective autophagy during viral infection.
MeSH term(s)	Autophagy ; Hepatitis B ; Hepatitis B virus ; Hepatocytes ; Humans ; Immune System ; Macroautophagy ; Virus Replication
Language	English
Publishing date	2022-04-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.1080/15548627.2022.2059747
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Article ; Online: Pneumococcal sialidase promotes bacterial survival by fine-tuning of pneumolysin-mediated membrane disruption.

Shizukuishi, Sayaka / Ogawa, Michinaga / Kuroda, Eisuke / Hamaguchi, Shigeto / Sakuma, Chisato / Kakuta, Soichiro / Tanida, Isei / Uchiyama, Yasuo / Akeda, Yukihiro / Ryo, Akihide / Ohnishi, Makoto

Cell reports

2024 Volume 43, Issue 3, Page(s) 113962

Abstract: Pneumolysin (Ply) is an indispensable cholesterol-dependent cytolysin for pneumococcal infection. Although Ply-induced disruption of pneumococci-containing endosomal vesicles is a prerequisite for the evasion of endolysosomal bacterial clearance, its ... ...

Abstract	Pneumolysin (Ply) is an indispensable cholesterol-dependent cytolysin for pneumococcal infection. Although Ply-induced disruption of pneumococci-containing endosomal vesicles is a prerequisite for the evasion of endolysosomal bacterial clearance, its potent activity can be a double-edged sword, having a detrimental effect on bacterial survivability by inducing severe endosomal disruption, bactericidal autophagy, and scaffold epithelial cell death. Thus, Ply activity must be maintained at optimal levels. We develop a highly sensitive assay to monitor endosomal disruption using NanoBiT-Nanobody, which shows that the pneumococcal sialidase NanA can fine-tune Ply activity by trimming sialic acid from cell-membrane-bound glycans. In addition, oseltamivir, an influenza A virus sialidase inhibitor, promotes Ply-induced endosomal disruption and cytotoxicity by inhibiting NanA activity in vitro and greater tissue damage and bacterial clearance in vivo. Our findings provide a foundation for innovative therapeutic strategies for severe pneumococcal infections by exploiting the duality of Ply activity.
MeSH term(s)	Humans ; Neuraminidase/metabolism ; Streptococcus pneumoniae/metabolism ; Streptolysins/metabolism ; Pneumococcal Infections ; Bacterial Proteins/metabolism
Chemical Substances	plY protein, Streptococcus pneumoniae ; Neuraminidase (EC 3.2.1.18) ; Streptolysins ; Bacterial Proteins
Language	English
Publishing date	2024-03-13
Publishing country	United States
Document type	Journal Article
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2024.113962
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Article ; Online: Clinical features relating to pneumococcal colony phase variation in hospitalized adults with pneumonia.

Ideguchi, Shuhei / Yamamoto, Kazuko / Takazono, Takahiro / Fukuda, Yuichi / Tashiro, Takahiro / Shizukuishi, Sayaka / Chang, Bin / Ogawa, Michinaga / Izumikawa, Koichi / Yanagihara, Katsunori / Yatera, Kazuhiro / Mukae, Hiroshi

Journal of medical microbiology

2024 Volume 73, Issue 1

Abstract: Background. ...

Abstract	Background.
MeSH term(s)	Animals ; Male ; Humans ; Aged ; Streptococcus pneumoniae ; Pneumonia, Pneumococcal ; Phase Variation ; Retrospective Studies ; Pneumococcal Infections
Language	English
Publishing date	2024-01-08
Publishing country	England
Document type	Journal Article
ZDB-ID	218356-0
ISSN	1473-5644 ; 0022-2615
ISSN (online)	1473-5644
ISSN	0022-2615
DOI	10.1099/jmm.0.001784
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Article ; Online: Individual Atg8 paralogs and a bacterial metabolite sequentially promote hierarchical CASM-xenophagy induction and transition.

Sakuma, Chisato / Shizukuishi, Sayaka / Ogawa, Michinaga / Honjo, Yuko / Takeyama, Haruko / Guan, Jun-Lin / Weiser, Jeffery / Sasai, Miwa / Yamamoto, Masahiro / Ohnishi, Makoto / Akeda, Yukihiro

Cell reports

2024 Volume 43, Issue 5, Page(s) 114131

Abstract: Atg8 paralogs, consisting of LC3A/B/C and GBRP/GBRPL1/GATE16, function in canonical autophagy; however, their function is controversial because of functional redundancy. In innate immunity, xenophagy and non-canonical single membranous autophagy called " ... ...

Abstract	Atg8 paralogs, consisting of LC3A/B/C and GBRP/GBRPL1/GATE16, function in canonical autophagy; however, their function is controversial because of functional redundancy. In innate immunity, xenophagy and non-canonical single membranous autophagy called "conjugation of Atg8s to single membranes" (CASM) eliminate bacteria in various cells. Previously, we reported that intracellular Streptococcus pneumoniae can induce unique hierarchical autophagy comprised of CASM induction, shedding, and subsequent xenophagy. However, the molecular mechanisms underlying these processes and the biological significance of transient CASM induction remain unknown. Herein, we profile the relationship between Atg8s, autophagy receptors, poly-ubiquitin, and Atg4 paralogs during pneumococcal infection to understand the driving principles of hierarchical autophagy and find that GATE16 and GBRP sequentially play a pivotal role in CASM shedding and subsequent xenophagy induction, respectively, and LC3A and GBRPL1 are involved in CASM/xenophagy induction. Moreover, we reveal ingenious bacterial tactics to gain intracellular survival niches by manipulating CASM-xenophagy progression by generating intracellular pneumococci-derived H
Language	English
Publishing date	2024-04-23
Publishing country	United States
Document type	Journal Article
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2024.114131
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Article ; Online: Invasive Streptococcus oralis Expressing Serotype 3 Pneumococcal Capsule, Japan.

Chang, Bin / Morita, Masatomo / Nariai, Akiyoshi / Kasahara, Kei / Kakutani, Akira / Ogawa, Michinaga / Ohnishi, Makoto / Oishi, Kazunori

Emerging infectious diseases

2022 Volume 28, Issue 8, Page(s) 1720–1722

Abstract: We report 2 adult cases of invasive disease in Japan caused by Streptococcus oralis that expressed the serotype 3 pneumococcal capsule and formed mucoid colonies. Whole-genome sequencing revealed that the identical serotype 3 pneumococcal capsule locus ... ...

Abstract	We report 2 adult cases of invasive disease in Japan caused by Streptococcus oralis that expressed the serotype 3 pneumococcal capsule and formed mucoid colonies. Whole-genome sequencing revealed that the identical serotype 3 pneumococcal capsule locus and hyl fragment were recombined into the genomes of 2 distinct S. oralis strains.
MeSH term(s)	Adult ; Humans ; Japan ; Pneumococcal Infections ; Pneumococcal Vaccines ; Serogroup ; Streptococcus oralis/genetics ; Streptococcus pneumoniae/genetics
Chemical Substances	Pneumococcal Vaccines
Language	English
Publishing date	2022-07-25
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1380686-5
ISSN	1080-6059 ; 1080-6040
ISSN (online)	1080-6059
ISSN	1080-6040
DOI	10.3201/eid2808.212176
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Article: [Functional analysis of IcsB protein secreted via the type III secretion system of Shigella].

Ogawa, Michinaga

Nihon saikingaku zasshi. Japanese journal of bacteriology

2006 Volume 61, Issue 2, Page(s) 229–233

MeSH term(s)	Animals ; Autophagy/genetics ; Bacterial Proteins/genetics ; Bacterial Proteins/metabolism ; Bacterial Proteins/physiology ; Cells, Cultured ; Dogs ; Mice ; Mutation ; Shigella flexneri/metabolism ; Shigella flexneri/pathogenicity
Chemical Substances	Bacterial Proteins
Language	Japanese
Publishing date	2006-05-25
Publishing country	Japan
Document type	Journal Article ; Review
ZDB-ID	604101-2
ISSN	1882-4110 ; 0021-4930
ISSN (online)	1882-4110
ISSN	0021-4930
DOI	10.3412/jsb.61.229
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Article ; Online: Galectin-9 restricts hepatitis B virus replication via p62/SQSTM1-mediated selective autophagy of viral core proteins.

Miyakawa, Kei / Nishi, Mayuko / Ogawa, Michinaga / Matsunaga, Satoko / Sugiyama, Masaya / Nishitsuji, Hironori / Kimura, Hirokazu / Ohnishi, Makoto / Watashi, Koichi / Shimotohno, Kunitada / Wakita, Takaji / Ryo, Akihide

Nature communications

2022 Volume 13, Issue 1, Page(s) 531

Abstract: Autophagy has been linked to a wide range of functions, including a degradative process that defends host cells against pathogens. Although the involvement of autophagy in HBV infection has become apparent, it remains unknown whether selective autophagy ... ...

Abstract	Autophagy has been linked to a wide range of functions, including a degradative process that defends host cells against pathogens. Although the involvement of autophagy in HBV infection has become apparent, it remains unknown whether selective autophagy plays a critical role in HBV restriction. Here, we report that a member of the galectin family, GAL9, directs the autophagic degradation of HBV HBc. BRET screening revealed that GAL9 interacts with HBc in living cells. Ectopic expression of GAL9 induces the formation of HBc-containing cytoplasmic puncta through interaction with another antiviral factor viperin, which co-localized with the autophagosome marker LC3. Mechanistically, GAL9 associates with HBc via viperin at the cytoplasmic puncta and enhanced the auto-ubiquitination of RNF13, resulting in p62 recruitment to form LC3-positive autophagosomes. Notably, both GAL9 and viperin are type I IFN-stimulated genes that act synergistically for the IFN-dependent proteolysis of HBc in HBV-infected hepatocytes. Collectively, these results reveal a previously undescribed antiviral mechanism against HBV in infected cells and a form of crosstalk between the innate immune system and selective autophagy in viral infection.
MeSH term(s)	Antiviral Agents/pharmacology ; Autophagosomes/metabolism ; Autophagy/drug effects ; Galectins/genetics ; Galectins/metabolism ; Galectins/pharmacology ; Gene Expression ; HEK293 Cells ; Hep G2 Cells ; Hepatitis B ; Hepatitis B virus/drug effects ; Hepatitis B virus/metabolism ; Humans ; Macroautophagy/drug effects ; Proteolysis ; Sequestosome-1 Protein/genetics ; Sequestosome-1 Protein/metabolism ; Viral Core Proteins/metabolism ; Virus Replication/drug effects
Chemical Substances	Antiviral Agents ; Galectins ; LGALS9 protein, human ; SQSTM1 protein, human ; Sequestosome-1 Protein ; Viral Core Proteins
Language	English
Publishing date	2022-01-27
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-022-28171-5
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