Effect of CARD9 Deficiency on Neutrophil-Mediated Host Defense against Pulmonary Infection with Streptococcus pneumoniae
Shigenari IshizukaRin YokoyamaKo SatoRyuhei ShiromaAyako NakahiraHideki YamamotoTakano KazukiTakafumi KagesawaTomomitsu MiyasakaJun KasamatsuEmi KannoHiromasa TannoKeiko IshiiKazuyoshi Kawakami
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Streptococcus pneumoniae is a major causative bacterium of community-acquired pneumonia. Dendritic cell-associated C-type lectin-2 (dectin-2), one of the C-type lectin receptors (CLRs), was previously reported to play a pivotal role in host defense against pneumococcal infection through regulating phagocytosis by neutrophils while not being involved in neutrophil accumulation. In the present study, to elucidate the possible contribution of other CLRs to neutrophil accumulation, we examined the role of caspase recruitment domain-containing protein 9 (CARD9), a common adaptor molecule for signal transduction triggered by CLRs, in neutrophilic inflammatory response against pneumococcal infection. Wild-type (WT), CARD9 knockout (KO), and dectin-2 KO mice were infected intratracheally with pneumococcus, and the infected lungs were histopathologically analyzed to assess neutrophil accumulation at 24 h postinfection. Bronchoalveolar lavage fluids (BALFs) were collected at the same time point to count the neutrophils and assess the production of inflammatory cytokines and chemokines. Neutrophil accumulation was significantly decreased in CARD9 KO mice, but not in dectin-2 KO mice. Tumor necrosis factor alpha (TNF-α), keratinocyte-derived chemokine (KC), and macrophage inflammatory protein-2 (MIP-2) production in BALFs were also attenuated in CARD9 KO mice, but not in dectin-2 KO mice. Production of TNF-α and KC by alveolar macrophages stimulated with pneumococcal culture supernatants was significantly attenuated in CARD9 KO mice, but not in dectin-2 KO mice, compared to that in each group's respective control mice. In addition, pneumococcus-infected CARD9 KO mice showed larger bacterial burdens in the lungs than did WT mice. These data indicate that CARD9 is required for neutrophil migration after pneumococcal infection, as well as inflammatory cytokine and chemokine production by alveolar macrophages, and suggest that a CLR distinct from dectin-2 may be involved in this response.Keywords:
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Journal Article A Chimeric Lectin Formed from Bauhinia purpurea Lectin and Lens culinaris Lectin Recognizes a Unique Carbohydrate Structure Get access Kazuo Yamamoto, Kazuo Yamamoto 2 Laboratory of Molecular Medicine, Department of Integrated Biosciences, Graduate School of Frontier Sciences, The University of Tokyo7–3–1 Hongo, Bunkyo-ku, Tokyo 113–0033 2 To whom correspondence should be addressed. Tel +81-3-5841-4776, 8843, Fax: +81-03-5841-8923, E-mail:yamamoto@k.u-tokyo.ac.jp Search for other works by this author on: Oxford Academic PubMed Google Scholar Yukiko Konami, Yukiko Konami Laboratory of Molecular Medicine, Department of Integrated Biosciences, Graduate School of Frontier Sciences, The University of Tokyo7–3–1 Hongo, Bunkyo-ku, Tokyo 113–0033 Search for other works by this author on: Oxford Academic PubMed Google Scholar Toshiaki Osawa Toshiaki Osawa Laboratory of Molecular Medicine, Department of Integrated Biosciences, Graduate School of Frontier Sciences, The University of Tokyo7–3–1 Hongo, Bunkyo-ku, Tokyo 113–0033 Search for other works by this author on: Oxford Academic PubMed Google Scholar The Journal of Biochemistry, Volume 127, Issue 1, January 2000, Pages 129–135, https://doi.org/10.1093/oxfordjournals.jbchem.a022573 Published: 01 January 2000 Article history Received: 02 September 1999 Accepted: 25 October 1999 Published: 01 January 2000
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Streptococcus pneumoniae is one of most common causes of community-acquired pneumonia. We evaluated a newly available rapid immunochromatographic test to detect S. pneumoniae in urine samples verifying its importance in the diagnosis of pneumococcal pneumonia. Our data, obtained from 104 patients with community-acquired pneumonia, show that Now S. pneumoniae Urinary Test is characterized by a sensitivity value of 77.7%, a specifity of 98.8%: positive and negative predictive values are 93.3% and 95.5%, respectively. In conclusion, Now S. pneumoniae Urinary Test should be a useful test to establish the etiology of community-acquired pneumonia.
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Abstract The crystal structures of an L‐type lectin domain from Methanocaldococcus jannaschii in apo and mannose‐bound forms have been determined. A thorough investigation of L‐type lectin domains from several organisms provides insight into the differences in these domains from different kingdoms of life. While the overall fold of the L‐type lectin domain is conserved, differences in the lengths of the carbohydrate‐binding loops and significant variations in the Mn 2+ ‐binding site compared to the Ca 2+ ‐binding site are observed. Furthermore, the sequence and phylogenetic analyses suggest that the archaeal L‐type lectin domain is evolutionarily closer to the plant legume lectins than to its bacterial or animal counterparts. This is the first report of the biochemical, structural, sequence, and phylogenetic analyses of an L‐type lectin domain from archaea and serves to enhance our understanding of the species‐specific differences and evolution of L‐type lectin domains.
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Community-acquired pneumonia (CAP) is an important cause of morbidity and mortality in all age groups throughout the world. Bacterial pneumonia is the most described, with Streptococcus pneumoniae being the most important pathogen in all age groups. Viruses are also recognised as important causes of CAP both in children and adults. Viral pneumonia account for 13 - 50% of single pathogen diagnosed community-acquired pneumonia cases and 8 -27% of mixed bacterial-viral pneumonia.
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